Molecular mechanisms in H 2 O 2 -induced increase in AT1 receptor gene expression in cardiac fibroblasts: A role for endogenously generated Angiotensin II

Anupama, V.; George, Mereena; Dhanesh, Sivadasan Bindu; Chandran, Aneesh; James, Jackson; Shivakumar, K.

doi:10.1016/j.yjmcc.2016.05.010

Cited by 21 publications

(26 citation statements)

References 53 publications

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“…In the current study, reinforcing the role of AT1 receptors in inflammatory condition, we demonstrated that Olme prevented the lipid peroxidation, as evidenced by MDA assay, associated with increased GSH levels and SOD enzyme activities, when compared with the untreated group. These results indicate that AT1 receptor blockade decreases the oxidative stress, consistent with prior findings …”

Section: Discussionsupporting

confidence: 92%

Protective effect of angiotensin II receptor blocker against oxidative stress and inflammation in an oral mucositis experimental model

Araújo

Medeiros

et al. 2018

J Oral Pathology Medicine

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Section: Discussionsupporting

confidence: 92%

Protective effect of angiotensin II receptor blocker against oxidative stress and inflammation in an oral mucositis experimental model

Araújo

Medeiros

et al. 2018

J Oral Pathology Medicine

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“…Further experiments also showed that H 2 O 2 induced the activation of NF-κB and activator protein 1 (AP-1) in cardiac fibroblasts and that preincubation of these cells for 60 min with the NF-κB inhibitor BAY-11-7085 or with the AP-1 inhibitor SR11302 prior to H 2 O 2 treatment attenuated the AT 1 mRNA and protein expression. These data demonstrate that the H 2 O 2 -induced increase of AT 1 receptor mRNA and protein expression in cardiac fibroblasts involves the activation of NF-κB and AP-1 [22]. In subsequent experiments, H 2 O 2 was also shown to increase by threefold the local secretion of Ang II.…”

Section: Ros and Ang Receptorssupporting

confidence: 53%

Regulation of the Renin-Angiotensin-Aldosterone System by Reactive Oxygen Species

Morato¹,

Reina‐Couto²,

Pinho³

et al. 2017

Renin-Angiotensin System - Past, Present and Future

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Angiotensin II (Ang II), the major effector of the renin-angiotensin-aldosterone system (RAAS), stimulates the production of reactive oxygen species (ROS) which are critically involved in Ang II-induced effects. Noteworthy, accumulating evidence indicates that ROS also regulate the activation of RAAS, contributing to the fine-tuning of this system under physiological conditions or to the amplification of the deleterious signaling in several pathologies. This chapter aims at giving an overview of the role of ROS in the regulation of expression, secretion and/or activity of several RAAS components.

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“…We had reported earlier that cIAP2, induced in response to H 2 O 2 , protects cardiac fibroblasts against oxidative damage (Philip and Shivakumar, 2013). Additionally, we 7 had also shown that H 2 O 2 treatment promotes Ang II production in cardiac fibroblasts (Anupama et al, 2016). Pursuing these observations, we found that blocking the Ang II receptor, AT1, with candesartan attenuated cIAP2 expression ( Figure 3A.)…”

Section: Ddr2-dependent Ciap2 Expression Protects Cardiac Fibroblastssupporting

confidence: 70%

Co-ordinated regulation of cell survival and cell cycle pathways by DDR2-dependent SRF transcription factor in cardiac fibroblasts

Titus

Harikrishnan

Kailasam

2019

Preprint

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Relative resistance to apoptosis and the ability to proliferate and produce a collagenrich scar determine the critical role of cardiac fibroblasts in wound healing and tissue remodeling following myocardial injury. Identification of cardiac fibroblast-specific factors and mechanisms underlying these aspects of cardiac fibroblast function is therefore of considerable scientific and clinical interest. In the present study, gene knockdown and over-expression approaches, and promoter binding assays, showed that DDR2, a mesenchymal cell-specific collagen receptor tyrosine kinase localized predominantly in fibroblasts in the heart, acts via ERK1/2 MAPK-activated SRF transcription factor to enhance the expression of anti-apoptotic cIAP2 in cardiac fibroblasts, conferring resistance against oxidative injury. Further, DDR2 was found to act via ERK1/2 MAPK-activated SRF to transcriptionally up-regulate Skp2 that in turn facilitated post-translational degradation of p27, the cyclin-dependent kinase 2 inhibitor that causes cell cycle arrest, to promote G1-S transition, as evidenced by Rb phosphorylation, increased PCNA levels and flow cytometry. DDR2dependent ERK1/2 MAPK activation also suppressed FoxO3a-mediated transcriptional induction of p27. Notably, DDR2 levels positively correlated with SRF, cIAP2 and PCNA levels in cardiac fibroblasts from Spontaneously Hypertensive Rats. To conclude, DDR2-mediated ERK1/2 MAPK activation facilitates coordinated regulation of cell survival and cell cycle progression in cardiac fibroblasts via SRF.

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Molecular mechanisms in H 2 O 2 -induced increase in AT1 receptor gene expression in cardiac fibroblasts: A role for endogenously generated Angiotensin II

Cited by 21 publications

References 53 publications

Protective effect of angiotensin II receptor blocker against oxidative stress and inflammation in an oral mucositis experimental model

Protective effect of angiotensin II receptor blocker against oxidative stress and inflammation in an oral mucositis experimental model

Regulation of the Renin-Angiotensin-Aldosterone System by Reactive Oxygen Species

Co-ordinated regulation of cell survival and cell cycle pathways by DDR2-dependent SRF transcription factor in cardiac fibroblasts

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