YAP-galectin-3 signaling mediates endothelial dysfunction in angiotensin II-induced hypertension in mice.

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Abstract

Vascular endothelial dysfunction is regarded as an early event of hypertension. Galectin-3 (Gal-3) is known to participate in various pathological processes. Whilst previous studies showed that inhibition of Gal-3 effectively ameliorates angiotensin II (Ang II)-induced atherosclerosis or hypertension, it remains unclear whether Ang II regulates Gal-3 expression and actions in vascular endothelium.

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A role for mitochondria in NLRP3 inflammasome activation.

Rongbin Zhou, Amir S Yazdi, Philippe Menu … (2011)

An inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host 'danger', including infection and metabolic dysregulation. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.

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Reactive oxygen species in inflammation and tissue injury.

Manish Mittal, Mohammad Rizwan Siddiqui, Khiem Vinh Tran … (2014)

Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.

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Regulation of the Hippo-YAP pathway by G-protein-coupled receptor signaling.

Fa-Xing Yu, Bin Zhao, Nattapon Panupinthu … (2012)

The Hippo pathway is crucial in organ size control, and its dysregulation contributes to tumorigenesis. However, upstream signals that regulate the mammalian Hippo pathway have remained elusive. Here, we report that the Hippo pathway is regulated by G-protein-coupled receptor (GPCR) signaling. Serum-borne lysophosphatidic acid (LPA) and sphingosine 1-phosphophate (S1P) act through G12/13-coupled receptors to inhibit the Hippo pathway kinases Lats1/2, thereby activating YAP and TAZ transcription coactivators, which are oncoproteins repressed by Lats1/2. YAP and TAZ are involved in LPA-induced gene expression, cell migration, and proliferation. In contrast, stimulation of Gs-coupled receptors by glucagon or epinephrine activates Lats1/2 kinase activity, thereby inhibiting YAP function. Thus, GPCR signaling can either activate or inhibit the Hippo-YAP pathway depending on the coupled G protein. Our study identifies extracellular diffusible signals that modulate the Hippo pathway and also establishes the Hippo-YAP pathway as a critical signaling branch downstream of GPCR. Copyright © 2012 Elsevier Inc. All rights reserved.

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Author and article information

Journal

Journal ID (iso-abbrev): Cell Mol Life Sci

Title: Cellular and molecular life sciences : CMLS

Publisher: Springer Science and Business Media LLC

ISSN (Electronic): 1420-9071

ISSN (Print): 1420-682X

Publication date (Electronic): Jan 11 2023

Volume: 80

Issue: 2

Affiliations

[1 ] Department of Physiology and Pathophysiology, Cardiovascular Research Centre, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China.

[2 ] Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China.

[3 ] School of Basic and Medical Sciences, Xi'an Medical University, 1 Xinwang Road, Xi'an, 710021, Shaanxi, China.

[4 ] Department of Cardiac Surgery, The First Affiliated Hospital, Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, 710061, Shaanxi, China.

[5 ] Department of Physiology and Pathophysiology, Cardiovascular Research Centre, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China. xiao-jun.du@baker.edu.au.

[6 ] Department of Physiology and Pathophysiology, Cardiovascular Research Centre, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China. dengxl@mail.xjtu.edu.cn.

[7 ] Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China. dengxl@mail.xjtu.edu.cn.

Article

Publisher Item ID: 10.1007/s00018-022-04623-5

DOI: 10.1007/s00018-022-04623-5

PubMed ID: 36629913

SO-VID: 4220f3f1-85db-4b3b-8a8c-1b79cc8e554e

History

Keywords: Galectin-3,Endothelial dysfunction,Angiotensin II,YAP,Oxidative stress,Hypertension

Data availability:

Keywords: Galectin-3, Endothelial dysfunction, Angiotensin II, YAP, Oxidative stress, Hypertension

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YAP-galectin-3 signaling mediates endothelial dysfunction in angiotensin II-induced hypertension in mice.

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Most cited references 39

A role for mitochondria in NLRP3 inflammasome activation.

Reactive oxygen species in inflammation and tissue injury.

Regulation of the Hippo-YAP pathway by G-protein-coupled receptor signaling.

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