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- 题目:
- RGS4 inhibits angiotensin II signaling and macrophage localization during renal reperfusion injury independent of vasospasm.
- 作者:
- Pang(Paul),Jin(Xiaohua),Proctor(Brandon M),Farley(Michelle),Roy(Nilay),Chin(Matthew S),von Andrian(Ulrich H),Vollmann(Elisabeth),Perro(Mario),Hoffman(Ryan J),Chung(Joseph),Chauhan(Nikita),Mistri(Murti),Muslin(Anthony J),Bonventre(Joseph V),Siedlecki(Andrew M)
- 状态:
- 发布时间2015-04-01 , 更新时间 2016-10-19
- 期刊:
- Kidney Int
- 摘要:
- Vascular inflammation is a major contributor to the severity of acute kidney injury. In the context of vasospasm-independent reperfusion injury we studied the potential anti-inflammatory role of the Gα-related RGS protein, RGS4. Transgenic RGS4 mice were resistant to 25 min injury, although post-ischemic renal arteriolar diameter was equal to the wild type early after injury. A 10 min unilateral injury was performed to study reperfusion without vasospasm. Eighteen hours after injury, blood flow was decreased in the inner cortex of wild-type mice with preservation of tubular architecture. Angiotensin II levels in the kidneys of wild-type and transgenic mice were elevated in a sub-vasoconstrictive range 12 and 18 h after injury. Angiotensin II stimulated pre-glomerular vascular smooth muscle cells (VSMCs) to secrete the macrophage chemoattractant RANTES, a process decreased by angiotensin II R2 (AT2) inhibition. However, RANTES increased when RGS4 expression was suppressed implicating Gα protein activation in an AT2-RGS4-dependent pathway. RGS4 function, specific to VSMC, was tested in a conditional VSMC-specific RGS4 knockout showing high macrophage density by T2 MRI compared with transgenic and non-transgenic mice after the 10 min injury. Arteriolar diameter of this knockout was unchanged at successive time points after injury. Thus, RGS4 expression, specific to renal VSMC, inhibits angiotensin II-mediated cytokine signaling and macrophage recruitment during reperfusion, distinct from vasomotor regulation.
- 语言:
- eng
- DOI:
DataTable pData
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