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Jiang T, Zhou QS, Pi L, Huang B: [Role of angiotensin II and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion]. J Hand Surg Am. 2009 Dec;34(10):1785-94. Epub 2009 Nov 11.
OBJECTIVE: To investigate the effect of angiotensin (Ang) II and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury. METHODS: Models of acute ischemic reperfusion injury were established and the level of local AngII, a key element of renin-angiotensin system (RAS), in kidney was measured using radioimmunity technique. The expression of alpha-smooth muscle actin (alpha-SMA), a phenotype of mesenchymal cells, was detected by RT-PCR and immunohistochemistry methods. Renal tubule cells (NRK-52E) were cultured with various concentration of AngII, followed by blocking of PD123319, AngII receptor 2 antagonist, and AG490, an inhibitor of JAK2 signal pathway. RESULTS: AngII of kidney tissue increased immediately after acute ischemic-reperfusion injury, in time dependent fashion. Expression of alpha-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of AngII and was dose and time dependent. The peak of alpha-SMA expression was seen after 30 minute treatment at the dose of 10 (-9) mol/L, which was interrupted by both of PD123319 and AG490. CONCLUSIONS: Transdifferentiation of renal tubular epithelial cells occurs under acute ischemic-reperfusion injury. Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. |
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