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In ischemic vascular diseases, leukocyte recruitment and polarization are crucial for revascularization and tissue repair. We investigated the role of vasodilator-stimulated phosphoprotein (VASP) in vascular repair. After hindlimb ischemia induction, blood flow recovery, angiogenesis, arteriogenesis, and leukocyte infiltration into ischemic muscles in VASP-/- mice were accelerated. VASP deficiency also elevated the polarization of the macrophages through increased signal transducer and activator of transcription (STAT) signaling, which augmented the release of chemokines, cytokines, and growth factors to promote leukocyte recruitment and vascular repair. Importantly, VASP deletion in bone marrow--derived cells was sufficient to mimic the increased blood flow recovery of global VASP-/- mice. In chemotaxis experiments, VASP-/- neutrophils/monocytes were significantly more responsive to M1-related chemokines than wild-type controls. Mechanistically, VASP formed complexes with the chemokine receptor CCR2 and β-arrestin-2, and CCR2 receptor internalization was significantly reduced in VASP-/- leukocytes. Our data indicate that VASP is a major regulator of leukocyte recruitment and polarization in postischemic revascularization and support a novel role of VASP in chemokine receptor trafficking. [ABSTRACT FROM AUTHOR]

Background. Understanding of reproduction of the Egyptian sole, Solea aegyptiaca, has been considered a major step toward understanding its population dynamics, especially in the eastern Mediterranean Sea. In Egypt this species has highly commercial value and it has recently been successfully bred in aquaculture, but more data on the reproductive biology is still needed. So, the present work aimed to study the population structure and the reproductive dynamics of S. aegyptiaca over an annual reproductive cycle. Materials and Methods. A total of 594 specimens of S. aegyptiaca were obtained from October 2004 to September 2005 in a monthly basis from the commercial catch. Sex ratio, age, and length at first maturity, gonado-somatic index, maturity stage, oocyte diameter, and fecundity were analysed in order to increase our knowledge on the reproductive dynamics of S. aegyptiaca. Results. The overall ratio between males and females was 1.0 : 1.15 and showed no significant deviation from the expected 1 : 1 ratio, males are dominant among small size, while females are dominant among larger size. Females attained their maturity at the length of about 15.0 cm. The reproductive activity of S. aegyptiaca took place between January and June with a peak on January, when the majority of oocyte growth (> 400 μm in diameter) occurred. Hydrated oocytes reach 1000 μm immediately before spawning. Absolute fecundity ranged from 9898 to 38505 and can be expressed as a function of total length. Conclusion. S. aegyptiaca is a winter spawner, and the female attains its maturity at 15.0 cm of total length. So, fishing should be prohibited during the period from January to June to conserve the existing stock of the target species. Regulations should also be directed to reduce the fishing potential of 18.0 cm total length. It is important to give each fish the chance to reproduce at least once in its lifetime. [ABSTRACT FROM AUTHOR]

Aims: Chronic hypoxia causes detrimental structural alterations in the lung, which may cause pulmonary hypertension and are partially mediated by the endothelium. While its relevance for the development of hypoxia-associated lung diseases is well known, determinants controlling the initial adaptation of the lung endothelium to hypoxia remain largely unexplored., Methods and Results: We revealed that hypoxia activates the transcription factor nuclear factor of activated T-cells 5 (NFAT5) and studied its regulatory function in murine lung endothelial cells (MLECs). EC-specific knockout of Nfat5 (Nfat5(EC)-/-) in mice exposed to normobaric hypoxia (10% O2) for 21 days promoted vascular fibrosis and aggravated the increase in pulmonary right ventricular systolic pressure as well as right ventricular dysfunction as compared with control mice. Microarray- and single-cell RNA-sequencing-based analyses revealed an impaired growth factor-, energy-, and protein-metabolism-associated gene expression in Nfat5-deficient MLEC after exposure to hypoxia for 7 days. Specifically, loss of NFAT5 boosted the expression and release of platelet-derived growth factor B (Pdgfb)-a hypoxia-inducible factor 1 alpha (HIF1α)-regulated driver of vascular smooth muscle cell (VSMC) growth-in capillary MLEC of hypoxia-exposed Nfat5(EC)-/- mice, which was accompanied by intensified VSMC coverage of distal pulmonary arteries., Conclusion: Collectively, our study shows that early and transient subpopulation-specific responses of MLEC to hypoxia may determine the degree of organ dysfunction in later stages. In this context, NFAT5 acts as a protective transcription factor required to rapidly adjust the endothelial transcriptome to cope with hypoxia. Specifically, NFAT5 restricts HIF1α-mediated Pdgfb expression and consequently limits muscularization and resistance of the pulmonary vasculature., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)