Title: Change in gap junctional intercellular communication in cultured human endothelial cells with hypoxia/reoxygenation and effect of tyrosine kinase inhibitor on its change
Abstract: Objective: To study the tyrosine kinase inhibitor (genistein) prevents the gap junctional intercellular communication (GJIC) abnormality induced by hypoxia/reoxygenation. Methods: After human umbilical vein endothelial cells (ECs) had grown to confluence, they were divided to three groups and exposed to different conditions. ECs in group Ⅰ were incubated in normal oxygenic condition. ECs in group Ⅱ were exposed to hypoxia (PO21%) for 12-14 hours and then were returned to normal atmospheric condition for reoxygenation. ECs in group Ⅲ were incubated with genistein and were exposed to hypoxia/reoxygenation. GJIC was measured by means of a fluorescence recovery after photobleaching (FRAP) technique and was represented by the fluorescence recovery rate. Results: The genistein (10μM. 50μM) completely blocked the fluorescence recovery rate decrease of ECs after two hours reoxygenation (P0. 05). Conclusion: The tyrosine kinase inhibitor genistein protect the GJIC from hypoxia/reoxygenation injury. This study suggests that hypoxia/reoxygenation induce a transient endothelial GJIC abnormality through a tyrosine kinase pathway.
Publication Year: 2003
Publication Date: 2003-01-01
Language: en
Type: article
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