Effect of bradykinin on bradykinin-B2 receptor in rat aortic vascular smooth muscle cells and the involved signal transduction pathways

Yang, Wen; Feng, Min; Wang, Peihua; Wang, Daowen

doi:10.1007/s11684-010-0003-z

Cited by 1 publication

(1 citation statement)

References 21 publications

(20 reference statements)

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“…35 Furthermore, the combined interactions among transcriptional factors or coactivators including p53, CREB, KLF-4, and CBP appeared to be critical in the regulation of B2R gene expression, particularly during terminal nephron differentiation. 35 In cultured rat aortic vascular smooth muscle cells, Yan et al 36 found that bradykinin could upregulate the expression of B2R through mitogen-activated protein kinase and phosphatidylinositol-3 0 -kinase/Akt signaling pathways. With regard to DN, Bodin et al 19 found that B1R and B2R gene expression was increased by diabetes in both WT and tissue kallikrein-null mice, so they ruled out the possibility of ligand-induced receptor upregulation.…”

Section: Discussionmentioning

confidence: 99%

Exogenous kallikrein protects against diabetic nephropathy

Liu

Yang

Liu

et al. 2016

Kidney International

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The kallikrein-kinin system has been shown to be involved in the development of diabetic nephropathy, but specific mechanisms are not fully understood. Here, we determined the renal-protective role of exogenous pancreatic kallikrein in diabetic mice and studied potential mechanisms in db/db type 2 diabetic and streptozotocin-induced type 1 diabetic mice. After the onset of diabetes, mice were treated with either pancreatic kallikrein (db/db+kallikrein, streptozotocin+kallikrein) or saline (db/db+saline, streptozotocin+saline) for 16 weeks, while another group of streptozotocin-induced diabetic mice received the same treatment after onset of albuminuria (streptozotocin'+kallikrein, streptozotocin'+saline). Db/m littermates or wild type mice were used as non-diabetic controls. Pancreatic kallikrein had no effects on body weight, blood glucose and blood pressure, but significantly reduced albuminuria among all three groups. Pathological analysis showed that exogenous kallikrein decreased the thickness of the glomerular basement membrane, protected against the effacement of foot process, the loss of endothelial fenestrae, and prevented the loss of podocytes in diabetic mice. Renal fibrosis, inflammation and oxidative stress were reduced in kallikrein-treated mice compared to diabetic controls. The expression of kininogen1, tissue kallikrein, kinin B1 and B2 receptors were all increased in the kallikrein-treated compared to saline-treated mice. Thus, exogenous pancreatic kallikrein both prevented and ameliorated diabetic nephropathy, which may be mediated by activating the kallikrein-kinin system.

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