Publications by authors named "W N Duran"

S-nitrosylation of Cx43 gap junction channels critically regulates communication between smooth muscle cells and endothelial cells. This posttranslational modification also induces the opening of undocked Cx43 hemichannels. However, its specific impact on vasomotor regulation remains unclear.

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Objective: The endothelium regulates crucial aspects of vascular function, including hemostasis, vasomotor tone, proliferation, immune cell adhesion, and microvascular permeability. Endothelial cells (ECs), especially in arterioles, are pivotal for flow distribution and peripheral resistance regulation. Investigating vascular endothelium physiology, particularly in microvascular ECs, demands precise isolation and culturing techniques.

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Background: Nitric oxide is produced by different nitric oxide synthases isoforms. NO activates two signaling pathways, one dependent on soluble guanylate cyclase and protein kinase G, and other where NO post-translationally modifies proteins through S-nitrosylation, which is the modification induced by NO in free-thiol cysteines in proteins to form S-nitrosothiols. High levels of NO have been detected in blood of breast cancer patients and increased NOS activity has been detected in invasive breast tumors compared to benign or normal breast tissue, suggesting a positive correlation between NO biosynthesis, degree of malignancy and metastasis.

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Article Synopsis
  • Microvascular hyperpermeability, which is a key characteristic of inflammation, can have harmful effects if it lasts too long, leading to the proposal of targeted therapies to manage its duration.
  • The study tested how inflammatory signals like platelet-activating factor (PAF) and vascular endothelial growth factor (VEGF) cause hyperpermeability and whether activating the cAMP-dependent pathway through Epac1 could help reverse this process.
  • Results showed that stimulation of Epac1 effectively reduced hyperpermeability in both mouse tissues and human cells, with the mechanism involving the translocation of eNOS and a delayed increase in cAMP levels linked to nitric oxide production.
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