Role of angiotensin II and JAK2 signal pathway in transdifferentation of renal tubular cells in mice after acute ischemic followed by reperfusion / 中华病理学杂志
Chinese Journal of Pathology
;
(12): 466-471, 2009.
Artigo
em Chinês
| WPRIM
| ID: wpr-249128
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Farmacologia
/
Piridinas
/
Sistema Renina-Angiotensina
/
RNA Mensageiro
/
Angiotensina II
/
Traumatismo por Reperfusão
/
Transdução de Sinais
/
Diferenciação Celular
/
Linhagem Celular
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Pathology
Ano de publicação:
2009
Tipo de documento:
Artigo
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