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Microglia-Derived NLRP3 Activation Mediates the Pressor Effect of prorenin in the Rostral Ventrolateral Medulla of Stress-Induced Hypertensive Rats

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Neuroscience Bulletin 2020年第5期36卷 475-492页

作者： Li Hu Shutian Zhang Kokwin Ooi Xuehai Wu Jiaxiang Wu Jian Cai Yinggang Sun Jijiang Wang Danian Zhu Fuxue Chen Chunmei Xia Laboratory of Neuropharmacology and Neurotoxicology Shanghai Key Laboratory of Bio-Energy CropsCollege of Life ScienceShanghai UniversityShanghai 200444China Department of Physiology and Pathophysiology Basic Medicine CollegeFudan UniversityShanghai 200032China Department of Neurosurgery Huashan HospitalFudan UniversityShanghai 200040China Department of Neurology Renji HospitalShanghai Jiaotong UniversityShanghai 200240China Department of Cardiovascular Diseases Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China

Increased microglial activation and neuroinflammation within autonomic brain regions such as the rostral ventrolateral medulla(RVLM)have been implicated in stress-induced hypertension(SIH).prorenin,a member of the brain renin-angiotensin system(RAS),can directly activate microglia.The present study aimed to investigate the effects of prorenin on microglial activation in the RVLM of SIH rats.Rats were subjected to intermittent electric foot-shocks plus noise,this stress was administered for 2 h twice daily for 15 consecutive days,and mean arterial pressure(MAP)and renal sympathetic nerve activity(RSNA)were monitored.The results showed that MAP and RSNA were augmented,and this paralleled increased pro-inflammatory phenotype(M1)switching.prorenin and its receptor(PRR)expression and the NLR family pyrin domain containing 3(NLRP3)activation were increased in RVLM of SIH rats.In addition,PLX5622(a microglial depletion agent),MCC950(a NLRP3 inhibitor),and/or PRO20(a(Pro)renin receptor antagonist)had antihypertensive effects in the rats.The NLRP3 expression in the RVLM was decreased in SIH rats treated with PLX5622.Mito-tracker staining showed translocation of NLRP3 from mitochondria to the cytoplasm in proreninstimulated microglia.prorenin increased the ROS-triggering M1 phenotype-switching and NLRP3 activation,while MCC950 decreased the M1 polarization.In conclusion,upregulated prorenin in the RVLM may be involved in the pathogenesis of SIH,mediated by activation of the microglia-derived NLRP3 inflammasome.The link between prorenin and NLRP3 in microglia provides insights for the treatment of stress-related hypertension.

关键词： Stress NLRP3 prorenin Microglia Hypertension

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Renin and cardiovascular disease:Worn-out path,or new direction?

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World Journal of Cardiology 2011年第3期3卷 72-83页

作者： Gaurav Alreja Jacob Joseph Department of Medicine Boston University School of Medicine Cardiology Section(111) VA Boston Healthcare SystemWest Roxbury Department of Medicine Brigham and Women's Hospital and Harvard Medical School

Inhibition of the renin angiotensin system has beneficial effects in cardiovascular prevention and treatment. The advent of orally active direct renin inhibitors adds a novel approach to antagonism of the renin-angiotensin system.Inhibition of the first and rate-limiting step of the renin angiotensin cascade offers theoretical advantages over downstream blockade.However,the recent discovery of the(pro)renin receptor which binds both renin and prorenin,and which can not only augment catalytic activity of both renin and prorenin in converting angiotensinogen to angiotensinⅠ,but also signal intracellularly via various pathways to modulate gene expression,adds a significant level of complexity to the field.In this review,we will examine the basic and clinical data on renin and its inhibition in the context of cardiovascular pathophysiology.

关键词： Renin Angiotensin Cardiovascular disease Renin receptor prorenin receptor

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