The appropriate guidance and patterning of vessels during vascular development is critical for proper tissue function. The loss of these guidance mechanisms can lead to abnormal vascularization and a number of pathological conditions. The molecular basis of endothelial cell guidance and subsequent tissue specific vascular patterning remains largely unknown in spite of its clinical relevance and biological importance. In this regard, retinal vascular development offers many advantages for studying endothelial cell guidance and the mechanisms by which characteristic vascular patterns are formed. In this review, we will provide an overview of the known mechanisms that mediate vascular patterning during mouse retinal development, synthesizing these data to formulate a model of how growth factors, cellular adhesion molecules, and vascular-associated cells mediate directed endothelial cell migration and appropriate vascular remodeling. Finally, we will discuss the many aspects of retinal vascular development that remain unknown and cite evidence that many of these gaps may be addressed by further studying the guidance cues shared by vascular and neuronal elements in the retina and other parts of the central nervous system.
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http://dx.doi.org/10.1016/j.preteyeres.2006.01.001 | DOI Listing |
Biochem Biophys Res Commun
January 2025
Department of Ultrasonography, Fuwai Yunnan Hospital, Chinese Academy of Medical, Sciences/Affiliated Cardiovascular Hospital of Kunming Medical University, Kunming, 650102, China. Electronic address:
Pulmonary arterial hypertension (PAH) is a syndrome characterized by increased pulmonary vascular resistance and elevated pulmonary artery pressure, ultimately leading to right heart failure and even death. Increasing evidence implicates the fat mass and obesity-associated protein (FTO) in various metabolic and inflammatory pathways; however, its role in pulmonary endothelial function and PAH remains largely unexplored. In this study, we examined the effects of endothelial cell-specific FTO knockout on PAH development.
View Article and Find Full Text PDFBiol Reprod
January 2025
Department of Animal Sciences, University of Florida, Gainesville, FL 32611-0910, USA.
Optimal embryonic development depends upon cell-signaling molecules released by the maternal reproductive tract called embryokines. Identity of specific embryokines that enhance competence of the embryo for sustained survival is largely lacking. The current objective was to evaluate effects of three putative embryokines in cattle on embryonic development to the blastocyst stage.
View Article and Find Full Text PDFPLoS One
January 2025
Pharmaceutical Medicinal Chemistry & Drug Design Department, Faculty of Pharmacy (Boys), Al-Azhar University, Cairo, Egypt.
This study presents T-1-NBAB, a new compound derived from the natural xanthine alkaloid theobromine, aimed at inhibiting VEGFR-2, a crucial protein in angiogenesis. T-1-NBAB's potential to interacts with and inhibit the VEGFR-2 was indicated using in silico techniques like molecular docking, MD simulations, MM-GBSA, PLIP, essential dynamics, and bi-dimensional projection experiments. DFT experiments was utilized also to study the structural and electrostatic properties of T-1-NBAB.
View Article and Find Full Text PDFPLoS One
January 2025
Institute of Medical Biochemistry, Center for Molecular Biology of Inflammation, University of Muenster, Muenster, Germany.
Weibel-Palade bodies (WPB) are secretory organelles exclusively found in endothelial cells and among other cargo proteins, contain the hemostatic von-Willebrand factor (VWF). Stimulation of endothelial cells results in exocytosis of WPB and release of their cargo into the vascular lumen, where VWF unfurls into long strings of up to 1000 µm and recruits platelets to sites of vascular injury, thereby mediating a crucial step in the hemostatic response. The function of VWF is strongly correlated to its structure; in order to fulfill its task in the vascular lumen, VWF has to undergo a complex packing/processing after translation into the ER.
View Article and Find Full Text PDFInt J Surg
January 2025
Division of Cardiology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Background: This study tested the hypothesis that extracorporeal shockwave therapy (ECSWT) effectively rescues critical limb ischemia (CLI) in mice through the upregulation of GPR120, which protects against inflammation and angiogenesis to restore blood flow in the ischemic area.
Methods And Results: Compared with the control, ECSWT-induced GPR120-mediated anti-inflammatory effects significantly suppressed the expression of inflammatory signaling biomarkers (TAK1/MAPK family/NF-κB/IL-1β/IL-6/TNF-α/MCP-1) in HUVECs, and these effects were abolished by silencing GPR120 or by the GPR120 antagonist AH7614 (all P < 0.001).
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