PubMed · 14063149
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Z FEKETE, F KALZ. 1963. STUDIES IN CAPILLARY PERMEABILITY.. https://doi.org/10.1159/000254873
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Gap junction intercellular communication (GJIC) plays a significant role in the vascular system. Regulation of GJIC is a dynamic process, with alterations in connexin (Cx) protein expression and post-translational modification as contributing mechanisms. We hypothesized that the endothelial autacoid nitric oxide (NO) would reduce dye coupling in human umbilical vein endothelial cells (HUVECs). In our subsequent experiments, we sought to isolate the specific Cx isoform(s) targeted by NO or NO-activated signaling pathways. Since HUVEC cells variably express three Cx (Cx37, Cx40, and Cx43), this latter aim required the use of transfected HeLa cells (HeLaCx37, HeLaCx43), which do not express Cx proteins in their wild type form. Dye coupling was measured by injecting fluorescent dye (e.g., Alexa Fluor 488) into a single cell and determining the number of stained adjacent cells. Application of the NO donor SNAP (2 microM, 20 min) reduced dye coupling in HUVEC by 30%. In HeLa cells, SNAP did not reduce dye transfer of cells expressing Cx43, but decreased the dye transfer from Cx37-expressing cells to Cx43-expressing cells by 76%. The effect of SNAP on dye coupling was not mediated via cGMP. In contrast to its effect on dye coupling, SNAP had no effect on electrical coupling, measured by a double patch clamp in whole cell mode. Our results demonstrate that NO inhibits the intercellular transfer of small molecules by a specific influence on Cx37, suggesting a potential role of NO in controlling certain aspects of vascular GJIC.
BACKGROUND: Pulmonary endothelium is an active organ possessing numerous physiological, immunological, and metabolic functions. These functions may be altered early in acute lung injury (ALI) and further contribute to the development of acute respiratory distress syndrome (ARDS). Pulmonary endothelium is strategically located to filter the entire blood before it enters the systemic circulation; consequently its integrity is essential for the maintenance of adequate homeostasis in both the pulmonary and systemic circulations. Noxious agents that affect pulmonary endothelium induce alterations in hemodynamics and hemofluidity, promote interactions with circulating blood cells, and lead to increased vascular permeability and pulmonary edema formation. OBJECTIVE: We highlight pathogenic mechanisms of pulmonary endothelial injury and their clinical implications in ALI/ARDS patients.
OBJECTIVES: To analyze the morphometric composition of lesion components in exudative age-related macular degeneration and to study the relationships between individual lesion components and choroidal neovascularization (CNV) subtype, at 2 time points. METHODS: Morphometric analysis of 98 sets of angiograms separated by an interval of at least 3 weeks, with no treatment delivered in the intervening period between angiograms. Area measurements of individual lesion components were made from digitally captured angiograms. Choroidal neovascularizations were classified into subtypes based on the proportions of classic CNV. Fully corrected distance visual acuity measured on logMAR Early Treatment of Diabetic Retinopathy Study charts was available at baseline and at a subsequent visit in 78 subjects. Data were analyzed using parametric and nonparametric tests, linear regression, and McNemar test of equal proportions. RESULTS: Wholly and predominantly classic CNVs were significantly smaller at initial presentation than minimally classic or occult with no classic CNVs. Lesions containing blood and lipid were also significantly larger than lesions not exhibiting these features. Lesions containing any classic CNV expanded at a significantly greater rate than lesions without classic CNV. Approximately 40% of lesions categorized as wholly classic CNV converted to predominantly classic CNV between baseline and the next follow-up visit. CONCLUSION: The presence of classic leakage in exudative age-related macular degeneration is the most important risk factor for rapid expansion of CNV.