Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

URI permanent per a aquesta col·leccióhttps://hdl.handle.net/2445/7189

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Impact of ocean acidification on skeletal structures in gilthead sea bream (Sparus aurata): In vitro and in vivo studies
(Elsevier B.V., 2026-01-01) Rodríguez Carretero, Inmaculada; García-Pérez, Isabel; Sadeghi, Nazanin; Montblanch, Manel; Gutiérrez Fruitós, Joaquín; Navarro Álvarez, Isabel; Capilla Campos, Encarnación; Garcia de la Serrana Castillo, Daniel
Ocean acidification is considered a significant risk to aquaculture, as it may adversely affect the growth and development of aquatic organisms. The effect of ocean acidification has been shown to impair the growth and survival of fish and to increase otoliths calcification in certain species; however, its effects on bone mineralization remain not well studied. The objective of the present study was to examine the effects of seawater acidification on the skeletal mineralization of gilthead sea bream juveniles, and to assess the direct impact of distinct pH levels on bone-derived cells development. After 68 days of exposure to low pH, fish exhibited a significantly reduced specific growth rate and elevated plasma pH levels, which influenced electrolyte concentrations such as potassium. Moreover, fish exposed to low pH showed increased otoliths size but no differences in shape. In bone, a higher vertebral length/height ratio was also observed, accompanied by significantly reduced opacity and increased expression of the osteoblast and osteoclast markers, alkaline phosphatase (alp) and matrix metalloproteinase 9 (mmp9), respectively, suggesting an elevated rate of bone turnover although reduced mineralization. In vitro, osteoblasts exposed to a low extracellular pH for 30 days exhibited increased viability and mineralization compared to cells maintained at a plasma pH or an alkaline pH. Additionally, the pH level significantly influenced the expression of several extracellular matrix components and osteoblast markers supporting those observations. Overall, these findings underscore the threat that ocean acidification poses to aquaculture, particularly through its impact on skeletal mineralization in gilthead sea bream, and highlight the importance of identifying approaches to farming resilient fish.
Characterization of myogenesis in European sea bass (Dicentrarchus labrax) using primary white muscle cell cultures
(Nature Publishing Group, 2025) García-Pérez, Isabel; Rodríguez, Inmaculada; Rubio, Albert; Díaz-Serrano, Carla; Capilla Campos, Encarnación; Navarro Álvarez, Isabel; Blasco Mínguez, Josefina; Gutiérrez Fruitós, Joaquín
This study presents the first characterization of a primary cell culture from white skeletal muscleof European sea bass (Dicentrarchus labrax). Using immunofluorescence and gene expressionanalyses over 12 days, cell activation, proliferation, differentiation, fusion, and maturation phaseswere described. During culture development, myogenic regulatory factors (myf5, myod1, myod2,myog, mrf4) were sequentially expressed. Proliferation peaked at days 4–6, with high Pcna andMyod immunodetection and gene expression of pax7, c-met, and pcna. Early downregulationof cell cycle regulators, cdkn1a and cdkn1cb, and mstnb may have contributed to proliferation,while cdkn1bb progressively increased, likely to promote differentiation. The Gh/Igf axis showeddifferential regulation, igf-1 decreasing early and igf-2, igf-1ra, igf-1rb, and igfbp-1a gradually rising.Differentiation, myotube formation, and maturation were marked by higher Myhc staining, sarcomeredevelopment, and upregulation of cdh15, cav3, mef2, mymk, mymx, myhcb, and wnt4. Anabolic (akt2,mtor, eif4ebp1) and proteolytic-related genes (foxo1a, murf1, mafbx, capn1, capn3b, atg12, map1lc3b)increased in later stages. Comparison with other vertebrates revealed both conserved and speciesspecificregulatory mechanisms of myogenesis. These findings provide a comprehensive molecularframework of skeletal muscle development in European sea bass and establish a valuable in vitromodel for studying fish muscle biology and potential aquaculture and biotechnology applications.
The Liver Clock Tunes Transcriptional Rhythms in Skeletal Muscle to Regulate Mitochondrial Function
(SAGE Publications, 2026-01-04) Sica, Valentina; Sato, Tomoki; Tsialtas, Ioannis; Hernandez, Sophia; Chen, Siwei; Baldi, Pierre; Muñoz Cánoves, Pura, 1962-; Sassone-Corsi, Paolo; Koronowski, Kevin B.; Smith, Jacob Anderson Giffen
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Development of Insulin and Leptin Resistance in the Mouse Brainstem with Age
(Humana Press., 2026-01-16) De Frutos González, Elvira; Lauzurica, Nuria; Ochoa Navarro, José Joaquín; García San Frutos, Miriam; Aguado Tomàs, Fernando; Fernández-Agulló, Teresa
Physiological aging involves a progressive deterioration of homeostatic mechanisms that cause obesity and defective glucose homeostasis, which develop age-related diseases increasing mortality risk and reducing lifespan. The brainstem is involved in glucose and metabolic homeostasis by integrating peripheral signals such as insulin and leptin. Here, we evaluated the brainstem response to intracerebroventricular administration of insulin or leptin and the relationship with physiological levels of key molecules implicated in their signal transduction pathway and inflammation in 3-, 6-, and 12-month-old mice which progressively increase adiposity and develop signs of insulin resistance. The initial steps of insulin and leptin signaling pathways decline with age, as well as the protein kinase B (Akt) phosphorylation response. Both hormones decrease the phosphorylation of AMP-activated protein kinase (AMPK) but, while the response to insulin increases with age, the response to leptin decreases in older animals. This insulin and leptin resistance is accompanied by changes in basal protein expression or phosphorylation of insulin and leptin receptors and insulin receptor substrates-1 (IRS-1), as well as the imbalance between basal levels of Akt-phosphorylated and non-phosphorylated protein, without changes in other serine kinases and/or inflammatory pathways such as glycogen-synthase-kinase-3 (GSK3), mammalian targets of rapamycin (mTOR), kinase-p70S6 (p70), protein kinase-C-ε (PKCε), p38 mitogen-activated protein kinase (p38), or c-Janus N-terminal kinase (JNK). High levels of proinflammatory cytokines and glial cell activation suggest the development of neuroinflammation in the brainstem with age, which could mediate the age-associated insulin and leptin resistance and the impairment in glucose and metabolic homeostasis commonly observed in the aging process.
Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions
(MDPI, 2026-01-19) Zimkowska, Karolina; Riu-Villanueva, Marc; Río Fernández, José Antonio del
Neuromechanobiology has emerged as a multidisciplinary field at the interface of neuroscience and mechanobiology, aiming to elucidate how mechanical forces influence the development, organization, and function of the nervous system. This review offers a comprehensive overview of the historical evolution of the discipline, its molecular and biophysical foundations, and the experimental strategies employed to investigate it. Recent advances have revealed the pivotal roles of substrate stiffness, mechanical signaling, and force transduction in neural stem proliferation, axon guidance, synapse formation, and neural circuit maturation. All these effects originate at the molecular level and extend to the mesoscopic scale. Disrupted mechanotransduction has been increasingly implicated in neurodevelopmental disorders and neurodegenerative diseases, underscoring its clinical relevance. Key unresolved questions and future directions are also highlighted, with emphasis on the need for integrative approaches to decipher the complex interplay between mechanical forces and neural function.
Immune-Derived Cardiac Autonomic Signatures: Predicting Autonomic Responses to Exercise from B-Cell Phenotypes
(Frontiers Media, 2026-01-15) Castillo-Aguilar, Matías; Viscor Carrasco, Ginés; Sarmiento, L.; Sepúlveda, J.; Navarrete M.; Núñez Espinosa, Cristian Andrés
Objective: Aging affects both immune and autonomic regulation, yet their interaction remains poorly characterized. This study investigated how aging B-cell subpopulations, defined by CD21/CD11c expression, are associated with autonomic nervous system (ANS) dynamics, as measured by heart rate variability (HRV) during exercise in older adults. Materials and methods: In this cross-sectional study, 81 community-dwelling older adults (mean age 70.7 ± 5.8 years) underwent immune flow cytometry profiling of total B cells and four CD21/CD11c phenotypes. Continuous R–R interval (RRi) data were recorded at rest, during a standardized Two-Minute Step Test (TMST), and over a 5-min recovery period. A coupled-logistic RRi-vs-time model capturing each participant’s cardiac autonomic signature (CAS) was obtained. Individual parameter estimates were regressed on standardized immune predictors using multivariate Bayesian models adjusted for age, sex and body composition. Results: Higher counts of CD21+CD11c>+ B cells were associated with elevated baseline RRi (resting vagal tone), an increased exercise-induced RRi drop, and an incomplete post-exercise recovery. Conversely, greater CD21−CD11c− B-cell counts were associated with lower resting RRi, a faster sympathetic-driven RRi decrease during exercise, and more complete vagal reactivation during recovery. High posterior probability (>90%) was observed for the aforementioned posterior estimates. Conclusion: CD21 + CD11c + and CD21−CD11c− aging B-cell subsets display opposite associations with ANS responsiveness to acute exercise, suggesting immunosenescence-linked autonomic modulation on the neuro-immune axis. Distinct B-cell phenotypes may serve as biomarkers of resilience or fragility in aging, supporting personalized interventions to optimize cardiovascular health in aging individuals.
Dense core vesicle markers in CSF and cortical tissues of patients with Alzheimer's disease
(BioMed Central, 2021-12-01) Barranco Muñoz, Neus; Plá, Virginia; Alcolea, Daniel; Sánchez Domínguez, Irene; Fischer-Colbrie, Reiner; Ferrer, Isidro (Ferrer Abizanda); Lleó Bisa, Alberto; Aguado Tomàs, Fernando
Background: New fluid biomarkers for Alzheimer's disease (AD) that reveal synaptic and neural network dysfunctions are needed for clinical practice and therapeutic trial design. Dense core vesicle (DCV) cargos are promising cerebrospinal fluid (CSF) indicators of synaptic failure in AD patients. However, their value as biomarkers has not yet been determined. Methods: Immunoassays were performed to analyze the secretory proteins prohormone convertases PC1/3 and PC2, carboxypeptidase E (CPE), secretogranins SgIII and SgII, and Cystatin C in the cerebral cortex (n = 45, provided by Bellvitge University Hospital) and CSF samples (n = 66, provided by The Sant Pau Initiative on Neurodegeneration cohort) from AD patients (n = 56) and age-matched controls (n = 55). Results: In AD tissues, most DCV proteins were aberrantly accumulated in dystrophic neurites and activated astrocytes, whereas PC1/3, PC2 and CPE were also specifically accumulated in hippocampal granulovacuolar degeneration bodies. AD individuals displayed an overall decline of secretory proteins in the CSF. Interestingly, in AD patients, the CSF levels of prohormone convertases strongly correlated inversely with those of neurodegeneration markers and directly with cognitive impairment status. Conclusions: These results demonstrate marked alterations of neuronal-specific prohormone convertases in CSF and cortical tissues of AD patients. The neuronal DCV cargos are biomarker candidates for synaptic dysfunction and neurodegeneration in AD.
Syntaxin-1 is necessary for UNC5A-C/Netrin-1-dependent macropinocytosis and chemorepulsion
(Frontiers Media, 2023-09-27) Martínez Mármol, Ramón; Soriano García, Eduardo; Muhaisen, Ashraf; Cotrufo, Tiziana; Roselló Busquets, Cristina; Ros i Torres, Oriol; Hernaiz Llorens, Marc; Pérez-Brangulí, Francesc; Andrés, Rosa María; Parcerisas Mosqueda, Antoni; Pascual Sánchez, Marta; Ulloa Darquea, Fausto Alexander
Introduction: Brain connectivity requires correct axonal guidance to drive axons to their appropriate targets. This process is orchestrated by guidance cues that exert attraction or repulsion to developing axons. However, the intricacies of the cellular machinery responsible for the correct response of growth cones are just being unveiled. Netrin-1 is a bifunctional molecule involved in axon pathfinding and cell migration that induces repulsion during postnatal cerebellar development. This process is mediated by UNC5 homolog receptors located on external granule layer (EGL) tracts. Methods: Biochemical, imaging and cell biology techniques, as well as syntaxin-1A/B (Stx1A/B) knock-out mice were used in primary cultures and brain explants. Results and discussion: Here, we demonstrate that this response is characterized by enhanced membrane internalization through macropinocytosis, but not clathrin-mediated endocytosis. We show that UNC5A, UNC5B, and UNC5C receptors form a protein complex with the t-SNARE syntaxin-1. By combining botulinum neurotoxins, an shRNA knock-down strategy and Stx1 knock-out mice, we demonstrate that this SNARE protein is required for Netrin1-induced macropinocytosis and chemorepulsion, suggesting that Stx1 is crucial in regulating Netrin-1-mediated axonal guidance.
Specific contribution of Reelin expressed by Cajal-Retzius cells or GABAergic interneurons to cortical lamination
(National Academy of Sciences, 2022-09-06) Vílchez Acosta, Alba del Valle; Manso Sanz, Yasmina; Cárdenas, Adrián; Elias-Tersa, Alba; Martínez-Losa, Magdalena; Pascual Sánchez, Marta; Alvarez-Dolado, Manuel; Nairn, Angus C.; Borrell Franco, Víctor; Soriano García, Eduardo
The extracellular protein Reelin, expressed by Cajal–Retzius (CR) cells at early stages of cortical development and at late stages by GABAergic interneurons, regulates radial migration and the “inside-out” pattern of positioning. Current models of Reelin functions in corticogenesis focus on early CR cell–derived Reelin in layer I. However, developmental disorders linked to Reelin deficits, such as schizophrenia and autism, are related to GABAergic interneuron–derived Reelin, although its role in migration has not been established. Here we selectively inactivated the Reln gene in CR cells or GABAergic interneurons. We show that CR cells have a major role in the inside-out order of migration, while CR and GABAergic cells sequentially cooperate to prevent invasion of cortical neurons into layer I. Furthermore, GABAergic cell–derived Reelin compensates some features of the reeler phenotype and is needed for the fine tuning of the layer-specific distribution of cortical neurons. In the hippocampus, the inactivation of Reelin in CR cells causes dramatic alterations in the dentate gyrus and mild defects in the hippocampus proper. These findings lead to a model in which both CR and GABAergic cell–derived Reelin cooperate to build the inside-out order of corticogenesis, which might provide a better understanding of the mechanisms involved in the pathogenesis of neuropsychiatric disorders linked to abnormal migration and Reelin deficits.
Editorial: The impact of lipid metabolism on cancer progression and metastasis
(Frontiers Media, 2025-12-10) Aydemir, Duygu; Martín Pérez, Miguel; Sunami, Yoshiaki
Recent advances in oncology, immunology, and metabolic medicine have increasingly positioned lipid metabolism as a central determinant of cancer initiation, progression, and therapeutic response. Across multiple domains, lipid metabolic pathways are now understood to intersect with endocrine regulation, immune cell function, and systemic metabolic homeostasis, thereby influencing tumor behavior at both cellular and organismal levels. This expanding body of evidence highlights lipid metabolism not as an isolated biochemical process, but as an integrative axis that coordinates metabolic, immunological, and endocrine signals within the tumor microenvironment and throughout the host. Such a multidimensional perspective underscores the importance of synthesizing cross-disciplinary findings to fully elucidate the mechanistic and translational relevance of lipid metabolic regulation in contemporary cancer research.
Association of Physical Fitness and Anthropometric Parameters With Lung Function in 7-Year-Old Children
(Human Kinetics, 2025-02-01) García Alday, Iker; San Millán Alonso, Marta; Cazorla-González, Jorge; Roman Viñas, Blanca; Serrano-Ferrer, Juan; Jòdar-Portas, Anna; Prats Puig, Anna; Font Lladó, Raquel
Purpose: Associations between health-related parameters and lung function remain unclear in childhood. The study aims toevaluate the relationship between physical fitness and anthropometric parameters with the lung function of healthy scholar-agedchildren. Method: A total of 418 children aged 7 years old participated in this study. The associations of physical fitness(handgrip strength, standing broad jump, and 800-m run) and anthropometric (waist circumference and body mass index)parameters with lung function (forced vital capacity and forced expiratory volume in 1 s) were analyzed using a mixed-linearregression model. Results: Girls had significantly lower forced vital capacity values (P = .006) and physical fitness (P < .030)compared to boys. On mixed-linear regression analyses, waist circumference (P = .003) was independently associated withforced vital capacity, explaining 34.6% of its variance, while handgrip strength (P = .042) and waist circumference (P = .010)were independently associated with forced expiratory volume in 1 second, accounting together for 26.5% of its variance in7-year-old healthy children. Conclusions: Handgrip strength and waist circumference were associated with lung function inhealthy children highlighting the influence of upper body muscular strength and trunk dimension on lung function. Our resultscorroborate the need to promote physical fitness during childhood to protect against lung complications in later on in life.
Pressure, Vibration, and Percussion in Athletic Recovery: With Great Power ComesGreat Responsibility
(Lippincott, Williams & Wilkins, 2024-07-01) Arrillaga, Beatriz; Konrad, Andreas; García Alday, Iker
Self-applied mechanical pressure on the body is instinctively performed by several mammals, such as camels, sheep, and horses. In recent years, humans have further sophisticated this behavior due to advances in engineering. Pressure and vibration applied via skin contact are the foundation of many new electronic and mechanical devices developed by the recovery industry. Some of these devices rely on percussive motion, distinct from both massage and vibration in its amplitude, frequency, and direction of pressure. They can offer a rapid and powerful stimulus applied at the will of the user to relieve tension in muscles (1). Considering the increase in the magnitude of the mechanical power, the question is, “How much impulse do we need to speed up recovery?”
Morphofunctional characterization of the three main adipose tissue depots in rainbow trout (Oncorhynchus mykiss)
(Elsevier Ltd., 2024-10-18) Rosell-Moll, Enrique; My, N. T. K.; Balbuena-Pecino, Sara; Montblanch, Manel; Rodríguez Carretero, Inmaculada; Gutiérrez Fruitós, Joaquín; Garcia de la Serrana Castillo, Daniel; Capilla Campos, Encarnación; Navarro Álvarez, Isabel
Visceral adipose tissue (VAT) is the primary fat reservoir and energy source in fish. Other relevant fat depots include subcutaneous adipose tissue (SAT), located under epithelial layers, and intramuscular adipose tissue (IMAT), found between the myotomes. The present study investigates the morphological, gene expression and functional characteristics of these different depots in rainbow trout (Oncorhynchus mykiss). Commercial rainbow trout of two different average weights were sampled for histology, lipid quantification and fatty acids profile. Mature adipocytes were isolated for gene expression analyses of lipid metabolic markers. Both VAT and SAT showed large adipocytes, and high total lipid content, suggesting hypertrophic growth. Adipocytes in IMAT were consistently smaller regardless of fish size. While fatty acid composition was similar across depots, SAT had lower levels of palmitic acid and higher levels of polyunsaturated fatty acids that act as precursors of phospholipids and eicosanoids such as eicosapentaenoic acid, compared to VAT and IMAT. Gene expression analyses revealed higher levels of fatty acid transporters, lipolysis and β-oxidation markers in VAT and SAT compared to IMAT, suggesting a more active lipid metabolism. These data support the role of VAT as the main energy depot, while SAT may act as a secondary reservoir, and IMAT potentially serves as an occasional energy source for muscles. This study provides valuable insights into the distinct properties of the different fat depots in fish, which may help to optimize strategies to modulate adiposity for improved health, metabolism, and product quality.
JNK signaling and its impact on neural cell maturation and differentiation
(Elsevier, 2024-05-25) Castro-Torres, Rubén Darío; Olloquequi, Jordi; Parcerisas, Antoni; Ureña, Jesús; Ettcheto Arriola, Miren; Beas Zárate, Carlos; Camins Espuny, Antoni; Verdaguer, Ester; Auladell i Costa, M. Carme
C-Jun-N-terminal-kinases (JNKs), members of the mitogen-activated-protein-kinase family, are significantly linked with neurological and neurodegenerative pathologies and cancer progression. However, JNKs serve key roles under physiological conditions, particularly within the central-nervous-system (CNS), where they are critical in governing neural proliferation and differentiation during both embryogenesis and adult stages. These processes control the development of CNS, avoiding neurodevelopment disorders. JNK are key to maintain the proper activity of neural-stem-cells (NSC) and neural-progenitors (NPC) that exist in adults, which keep the convenient brain plasticity and homeostasis. This review underscores how the interaction of JNK with upstream and downstream molecules acts as a regulatory mechanism to manage the self-renewal capacity and differentiation of NSC/NPC during CNS development and in adult neurogenic niches. Evidence suggests that JNK is reliant on non-canonical Wnt components, Fbw7-ubiquitin-ligase, and WDR62-scaffold-protein, regulating substrates such as transcription factors and cytoskeletal proteins. Therefore, understanding which pathways and molecules interact with JNK will bring knowledge on how JNK activation orchestrates neuronal processes that occur in CNS development and brain disorders.
Static Cold Storage and Machine Perfusion: Redefining the Role of Preservation and Perfusate Solutions
(MDPI, 2025-12-04) Panisello Roselló, Arnau; Carbonell i Camós, Teresa; Roselló Catafau, Juan; Vengohechea, Jordi; Hessheimer, Amelia; Adam, R. (René); Fondevila Campo, Constantino
Static cold storage (SCS) remains the most widely used method of liver graft preservation due to its simplicity, accessibility, and reduced cost in transplantation practice. Since the invention of the University of Wisconsin (UW) solution, several alternative preservation solutions—including histidine–tryptophan–ketoglutarate (HTK), Celsior, and more recently IGL-1 and IGL-2—have been formulated to optimize cellular and vascular protection during cold ischemia. More recently, the introduction of dynamic perfusion techniques, such as hypothermic oxygenated perfusion (HOPE) and normothermic machine perfusion (NMP), approximately fifteen years ago, has further enhanced transplantation protocols, being applied either alone or in combination with traditional SCS to ensure optimal graft preservation prior to implantation. Despite these technological advances, achieving fully effective dynamic perfusion remains a key challenge for improving outcomes in vulnerable grafts, particularly steatotic or marginal livers. This review details how Polyethylene Glycol 35 (PEG35)-based solutions activate multiple cytoprotective pathways during SCS, including AMP-activated protein kinase (AMPK), nitric oxide (NO) production, and the antioxidant transcription factor Nrf2. We propose that these molecular mechanisms serve as a form of preconditioning that is synergistically leveraged by HOPE to preserve mitochondrial function, endothelial glycocalyx integrity, and microvascular homeostasis. Furthermore, the oncotic and rheological properties of PEG35 reduce perfusate viscosity, mitigating shear stress and microcirculatory damage during dynamic perfusion—effects that are further enhanced by NO- and AMPK-mediated protection initiated during the SCS phase. This integrated approach provides a strong rationale for combining PEG35-mediated SCS with HOPE, particularly for grafts with high susceptibility to ischemia–reperfusion injury, such as fatty livers. Finally, we highlight emerging avenues in graft preservation, including the design of unified perfusion solutions that optimize endothelial, mitochondrial, and redox protection, with the potential to improve post-transplant outcomes and extend applicability to other solid organ grafts.
Effects of daily use of intermittent pneumatic compression in competitive handball players: A randomized controlled trial
(Institute of Sport – National Research Institute, 2025-06-24) Nuell Turon, Sergi; Rabassa Blanco, Jordi; Bárcena, Cristina; Espar Moya, Josep; Munné Rodríguez, Carles; García Alday, Iker
Intermittent sequential pneumatic compression (ISPC) is used to improve readiness and recovery in athletes. This study aimed to evaluate the effects of daily use of ISPC for 5 weeks on the performance, physiological, and psychological parameters in seventeen male handball players. Players were randomly assigned either to an experimental (EXP, n = 8) or a control (CON, n = 9) group. Before and after the intervention, we measured the countermovement jump (CMJ) and the agility test (T-test) as markers of sport-specific performance, the systolic blood pressure (SBP) in the brachial and ankle arteries to evaluate the hemodynamic function, and the tensiomyography of biceps femoral, gastrocnemius and vastus medialis to assess muscle function. During the intervention, the session rating of perceived effort (sRPE, 30 minutes after training) and perceived recovery status (PRS, 1 hour after waking-up the following morning) were registered to evaluate subjective recovery. Results showed that CON experienced a decrease in agility performance from pre- to post-intervention (p = 0.030). In contrast, EXP had a significant improvement in the muscle contraction delay time of the left biceps femoris (p = 0.002), and a significant decrease in ankle SBP after the intervention (p = 0.017). Regarding perceived fatigue and recovery, EXP had slightly higher values than CON in PRS (p = 0.047), while sRPE had no significant changes. Thus, daily use of intermittent pneumatic compression for 5 weeks during a training period slightly mitigates the fatigue induced effects of training, while enhancing hemodynamic regulation and subjective recovery in competitive handball players.
Biofilm formation of Tenacibaculum maritimum, a fish pathogenic bacteria, to evaluate the antimicrobial activity of fish skin mucus
(Frontiers Media, 2025-10-13) Tejero, Marc; Sanahuja Piera, Ignasi; Balsalobre Parra, Carlos; Ibarz i Valls, Antoni; Madrid Xufré, Cristina; Fernández-Alacid, Laura
Biofilms, defined as aggregates of microorganisms embedded in a self-produced matrix of extracellular polymeric substances (EPS), are formed by most bacteria in both natural and pathogenic ecosystems. In aquaculture, biofilms pose a dual challenge: they confer recalcitrance to antimicrobials treatments and contribute to persistent infections by forming on facility surfaces such as tanks, nets, cages, and equipment. Tenacibaculum maritimum, the causative agent of tenacibaculosis, is responsible for significant economic losses in fish farming. Although the antibacterial activity of fish skin mucus against this pathogen has been evaluated in vitro, its effects on T. maritimum biofilms have not yet been determined. In this study, we provide a simple methodology for the in vitro formation and quantification of T. maritimum biofilms to monitor antibacterial properties of different compounds or substances, such as fish skin mucus. For this purpose, biofilm formation was assessed under varying culture volumes (200, 300, and 400 µL) and incubation times (24, 48, and 72 hours) in 48-well microplates. Then, the effects of gilthead seabream (Sparus aurata) skin mucus were evaluated on planktonic growth, biofilm formation, and biofilm dispersion, measuring both biomass and metabolic activity. Based on the tested volumes and incubation times, the optimal condition for biofilm formation was defined as 24 hours in MB at 25 ºC using 200 µL culture volume. These conditions supported the development of a biofilm (OD570>1.5 after crystal violet staining) while conserving time and mucus. Seabream mucus significantly impaired T. maritimum planktonic growth and biofilm formation in a concentration-dependent manner. Non-diluted mucus completely inhibited planktonic growth and biofilm metabolic activity, and reduced biofilm biomass by 81.16 ± 2.54%. In contrast, its effect on mature biofilms was limited, with reductions of approximately 50% in metabolic activity and 40% in biomass. This study provides a platform to assess how different fish culture conditions affect the host’s susceptibility to T. maritimum infections, which is crucial for preventing economic losses in fish farming. Additionally, it opens the door to studies analyzing the components of fish skin mucus responsible for its antibacterial activity, aiming to develop novel therapeutic compounds for targeting biofilms formed by this pathogen.
Endogenous LXR signaling controls pulmonary surfactant homeostasis and prevents lung inflammation
(Springer Verlag, 2024-07-06) Hernández-Hernández, Irene; Rosa, Juan V. de la; Martín-Rodríguez, Patricia; Díaz-Sarmiento, Mercedes; Recio, Carlota; Guerra, Borja; Fernández-Pérez, Leandro; León Moreno, Theresa Elizabeth; Torres, Rosa; Font Díaz, Joan; Roig, Angela; Mora, Fernando de; Boscá, Lisardo; Díaz, Mario; Valledor Fernández, Annabel; Castrillo, Antonio; Tabraue, Carlos
Lung type 2 pneumocytes (T2Ps) and alveolar macrophages (AMs) play crucial roles in the synthesis, recycling and catabolism of surfactant material, a lipid/protein fluid essential for respiratory function. The liver X receptors (LXR), LXRα and LXRβ, are transcription factors important for lipid metabolism and inflammation. While LXR activation exerts anti-inflammatory actions in lung injury caused by lipopolysaccharide (LPS) and other inflammatory stimuli, the full extent of the endogenous LXR transcriptional activity in pulmonary homeostasis is incompletely understood. Here, using mice lacking LXRα and LXRβ as experimental models, we describe how the loss of LXRs causes pulmonary lipidosis, pulmonary congestion, fibrosis and chronic inflammation due to defective de novo synthesis and recycling of surfactant material by T2Ps and defective phagocytosis and degradation of excess surfactant by AMs. LXR-deficient T2Ps display aberrant lamellar bodies and decreased expression of genes encoding for surfactant proteins and enzymes involved in cholesterol, fatty acids, and phospholipid metabolism. Moreover, LXR-deficient lungs accumulate foamy AMs with aberrant expression of cholesterol and phospholipid metabolism genes. Using a house dust mite aeroallergen-induced mouse model of asthma, we show that LXR-deficient mice exhibit a more pronounced airway reactivity to a methacholine challenge and greater pulmonary infiltration, indicating an altered physiology of LXR-deficient lungs. Moreover, pretreatment with LXR agonists ameliorated the airway reactivity in WT mice sensitized to house dust mite extracts, confirming that LXR plays an important role in lung physiology and suggesting that agonist pharmacology could be used to treat inflammatory lung diseases.
Liver X receptors and inflammatory-induced C/EBPβ selectively cooperate to control CD38 transcription
(Karger, 2024-12-19) Glaría Percaz, Estibaliz; Rodríguez Martínez, Pol; Font Díaz, Joan; Rosa, Juan Vladimir de la; Castrillo, Antonio; Crawshaw, Dylan J.; Vidal Taboada, José Manuel; Saura Martí, Josep; Matalonga, Jonathan; Nunes Chini, Eduardo; Caelles Franch, Carme; Valledor Fernández, Annabel
Introduction: Macrophages abundantly express liver X receptors (LXRs), which are ligand-dependent transcription factors and sensors of several cholesterol metabolites. In response to agonists, LXRs promote the expression of key lipid homeostasis regulators. Cross talk between LXRs and inflammatory signals exists in a cell type- and gene-specific manner. A common feature in the macrophage response to inflammatory mediators is the induction of CCAAT/enhancer-binding protein beta (C/EBPβ), a master transcriptional regulator and lineage-determining transcription factor in monocytes/macrophages. Methods: Quantitative real-time PCR in control and C/EBPβ-deficient macrophages was used to explore the role of C/EBPβ in the cross talk between inflammatory mediators and the macrophage response to pharmacological LXR activation. The functional interaction between C/EBPβ and LXRs on selected genomic regions was further characterized by chromatin-immunoprecipitation (ChIP) and gene reporter studies. Results: Whereas inflammatory signaling repressed several LXR-regulated genes involved in lipid metabolism, these effects were conserved after deletion of C/EBPβ. In contrast, inflammatory mediators and LXRs synergistically induced the expression of the multifunctional protein CD38 in a C/EBPβ-dependent manner. C/EBPβ and LXRs bound to several regions with enhancer activity upstream and within the mouse Cd38 gene and their functional cooperation in macrophages required intact binding sites for LXR and C/EBPβ. Conclusion: This study reveals positive cross talk between C/EBPβ and LXRs during the macrophage inflammatory response, which selectively impacts CD38 expression.
Lung diffusing capacity after different modalities of exercise at sea level and hypobaric simulated altitude of 4000 m
(2023-09-30) García Alday, Iker; Drobnic, Franchek; Arrillaga, Beatriz; Cheng, Yinkiria; Javierre Garcés, Casimiro F.; Pons, Vicente; Viscor Carrasco, Ginés
Introduction: Lung diffusion capacity of carbon monoxide (DLCO) provides a measure of gas transfer in the lungs, which increase in relation to exercise and decrease in the presence of lung interstitial disease. The aim of this study is to evaluate the changes in lung diffusion after anaerobic and aerobic exercise in a cycle ergometer. Material and method: The participants were 11 healthy active subjects, including 8 females and 3 males (age: 24.3 ± 3.1 years). Lung diffusion capacity for carbon monoxide (DLCO) was studied under two different protocols: In the first day, DLCO was measured at SL at rest (SL-R), after 30-s maximal exercise (SL-ANA), and after 15-min moderate continuous exercise (SL-AER). In the second day, DLCO was evaluated at rest at SL, and then at HA (4,000 m) at rest (HA-R) and after 30-min of moderate interval exercise (HA-AER). Results: There was an increase in DLCO from rest to after SL-ANA (32.5 ± 6.4 to 40.3 ± 11.6 mL·min-1·mmHg-1, P = 0.027). In the second day, DLCO was evaluated at rest at SL, and then at HA (4,000 m) at rest (HA-R) and after 30-min of moderate interval exercise (HA-AER). During HA exposure, there was no changes in DLCO, either at HA-R, or after HA-AER. Conclusions: Lung diffusion capacity largely increased after 30-s maximal exercise in a cycle ergometer, although the O2 -dependence is small during this type of anaerobic exercise. Thus, exercise intensity may be a key modulator of the changes in lung diffusing capacity in relation to exercise.

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