PDF(Pubmed)
Abstract：
UNASSIGNED: and design Mild vascular inflammation promotes the pathogenesis of hypertension. Asprosin, a newly discovered adipokine, is closely associated with metabolic diseases. We hypothesized that asprosin might led to vascular inflammation in hypertension via NLRP3 inflammasome formation. This study shows the importance of asprosin in the vascular inflammation of hypertension.
UNASSIGNED: Primary vascular smooth muscle cells (VSMCs) were obtained from the aorta of animals, including spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), NLRP3-/- and wild-type mice. Studies were performed in VSMCs in vitro, as well as WKY and SHR in vivo.
UNASSIGNED: Asprosin expressions were up-regulated in VSMCs and media of arteries in SHR. Asprosin overexpression promoted NLRP3 inflammasome activation via Toll-like receptor 4 (TLR4), accompanied with activation of NFκB signaling pathway in VSMCs. Exogenous asprosin protein showed similar roles in promoting NLRP3 inflammasome activation. Knockdown of asprosin restrained NLRP3 inflammasome and p65-NFκB activation in VSMCs of SHR. NLRP3 inhibitor MCC950 or NFκB inhibitor BAY11-7082 attenuated asprosin-caused VSMC proliferation and migration. Asprosin-induced interleukin-1β production, proliferation and migration were attenuated in NLRP3-/- VSMCs. Local asprosin knockdown in common carotid artery of SHR attenuated inflammation and vascular remodeling.
UNASSIGNED: Asprosin promoted NLRP3 inflammasome activation in VSMCs by TLR4-NFκB pathway, and thereby stimulates VSMCs proliferation, migration, and vascular remodeling of SHR.
UNASSIGNED: Primary vascular smooth muscle cells (VSMCs) were obtained from the aorta of animals, including spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), NLRP3-/- and wild-type mice. Studies were performed in VSMCs in vitro, as well as WKY and SHR in vivo.
UNASSIGNED: Asprosin expressions were up-regulated in VSMCs and media of arteries in SHR. Asprosin overexpression promoted NLRP3 inflammasome activation via Toll-like receptor 4 (TLR4), accompanied with activation of NFκB signaling pathway in VSMCs. Exogenous asprosin protein showed similar roles in promoting NLRP3 inflammasome activation. Knockdown of asprosin restrained NLRP3 inflammasome and p65-NFκB activation in VSMCs of SHR. NLRP3 inhibitor MCC950 or NFκB inhibitor BAY11-7082 attenuated asprosin-caused VSMC proliferation and migration. Asprosin-induced interleukin-1β production, proliferation and migration were attenuated in NLRP3-/- VSMCs. Local asprosin knockdown in common carotid artery of SHR attenuated inflammation and vascular remodeling.
UNASSIGNED: Asprosin promoted NLRP3 inflammasome activation in VSMCs by TLR4-NFκB pathway, and thereby stimulates VSMCs proliferation, migration, and vascular remodeling of SHR.
摘要：
■并设计轻度血管炎症促进高血压的发病机制。Asprosin,一种新发现的脂肪因子,与代谢性疾病密切相关。我们假设asprosin可能通过NLRP3炎性体形成导致高血压血管炎症。这项研究显示了在高血压的血管炎症中的作用。
■从动物的主动脉获得原代血管平滑肌细胞（VSMC），包括自发性高血压大鼠（SHR），Wistar-Kyoto大鼠（WKY），NLRP3-/-和野生型小鼠。在体外VSMC中进行了研究，以及体内的WKY和SHR。
■在SHR的VSMC和动脉中膜中，Asprosin表达上调。Asprosin过表达通过Toll样受体4（TLR4）促进NLRP3炎性体激活，在VSMCs中伴有NFκB信号通路的激活。外源性反胰岛素蛋白在促进NLRP3炎性体激活中显示出相似的作用。抑制SHRVSMC中NLRP3炎性体和p65-NFκB的激活。NLRP3抑制剂MCC950或NFκB抑制剂BAY11-7082减弱了asprosin引起的VSMC增殖和迁移。天门冬氨酸诱导的白细胞介素-1β的产生，NLRP3-/-VSMC的增殖和迁移减弱。SHR颈总动脉中局部的asprosin敲除减轻了炎症和血管重塑。
■Asprosin通过TLR4-NFκB途径促进VSMC中NLRP3炎性体的激活，从而刺激VSMC增殖，迁移,和SHR的血管重塑。
■从动物的主动脉获得原代血管平滑肌细胞（VSMC），包括自发性高血压大鼠（SHR），Wistar-Kyoto大鼠（WKY），NLRP3-/-和野生型小鼠。在体外VSMC中进行了研究，以及体内的WKY和SHR。
■在SHR的VSMC和动脉中膜中，Asprosin表达上调。Asprosin过表达通过Toll样受体4（TLR4）促进NLRP3炎性体激活，在VSMCs中伴有NFκB信号通路的激活。外源性反胰岛素蛋白在促进NLRP3炎性体激活中显示出相似的作用。抑制SHRVSMC中NLRP3炎性体和p65-NFκB的激活。NLRP3抑制剂MCC950或NFκB抑制剂BAY11-7082减弱了asprosin引起的VSMC增殖和迁移。天门冬氨酸诱导的白细胞介素-1β的产生，NLRP3-/-VSMC的增殖和迁移减弱。SHR颈总动脉中局部的asprosin敲除减轻了炎症和血管重塑。
■Asprosin通过TLR4-NFκB途径促进VSMC中NLRP3炎性体的激活，从而刺激VSMC增殖，迁移,和SHR的血管重塑。
