Poly(ADP-Ribose) Polymerase-1 Mediates Angiotensin II-Induced Expression of Plasminogen Activator Inhibitor-1 and Fibronectin in Rat Mesangial Cells

Zhu, Hengmei; Jiang, Zongpei; Lei, Ping; Huang, Weiyuan; Yu, Xueqing

doi:10.1159/000327344

Cited by 6 publications

(2 citation statements)

References 86 publications

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“…Aberrant activity and/or expression of PARP-1 are present in ECs under abnormally elevated levels of radical oxygen species (ROS), TNF-α, or angiotensin II to cause vascular inflammation (26)(27)(28). Such proinflammatory conditions are linked to decreases in AMPK activity and Bcl-6 expression.…”

Section: Discussionmentioning

confidence: 99%

AMPKα2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6

Gongol

Marin

Peng

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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B-cell lymphoma-6 protein (Bcl-6) is a corepressor for inflammatory mediators such as vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 and -3, which function to recruit monocytes to vascular endothelial cells upon inflammation. Poly [ADP ribose] polymerase 1 (PARP-1) is proinflammatory, in part through its binding at the Bcl-6 intron 1 to suppress Bcl-6 expression. We investigated the mechanisms by which PARP-1 dissociates from the Bcl-6 intron 1, ultimately leading to attenuation of endothelial inflammation. Analysis of the PARP-1 primary sequence suggested that phosphorylation of PARP-1 Serine 177 (Ser-177) by AMP-activated protein kinase (AMPK) is responsible for the induction of Bcl-6. Our results show that AMPK activation with treatment of 5-aminoimidazole-4-carboxamide ribonucleotide, metformin, or pulsatile shear stress induces PARP-1 dissociation from the Bcl-6 intron 1, increases Bcl-6 expression, and inhibits expression of inflammatory mediators. Conversely, AMPKα suppression or knockdown produces the opposite effects. The results demonstrate an anti-infamatory pathway linking AMPK, PARP-1, and Bcl-6 in endothelial cells.

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Section: Discussionmentioning

confidence: 99%

AMPKα2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6

Gongol

Marin

Peng

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…1 and 2) provides such a link between its dysregulation and pathogenesis of PH, suggesting that miR-19a/b may also contribute to PH via its target PAI-1. Previous studies shown that RAGE and PARP-1 are positive regulators of PAI-1 (47,58). We have found that miR-17~92 inhibits PAI-1 and RAGE, but not PARP-1 (Fig.…”

Section: L155mentioning

confidence: 55%

PAI-1 is a novel component of the miR-17~92 signaling that regulates pulmonary artery smooth muscle cell phenotypes

Chen

Huang

Dai

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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We have previously reported that miR-17~92 is critically involved in the pathogenesis of pulmonary hypertension (PH). We also identified two novel mR-17/20a direct targets, PDZ and LIM domain protein 5 (PDLIM5) and prolyl hydroxylase 2 (PHD2), and elucidated the signaling pathways by which PDLIM5 and PHD2 regulate functions of pulmonary artery smooth muscle cells (PASMCs). In addition, we have shown that plasminogen activator inhibitor-1 (PAI-1) is also downregulated in PASMCs that overexpress miR-17~92. However, it is unclear whether PAI-1 is a direct target of miR-17~92 and whether it plays a role in regulating the PASMC phenotype. In this study, we have identified PAI-1 as a novel target of miR-19a/b, two members of the miR-17~92 cluster. We found that the 3'-untranslated region (UTR) of PAI-1 contains a miR-19a/b binding site and that miR-19a/b can target this site to suppress PAI-1 protein expression. MiR-17/20a, two other members of miR-17~92, may also indirectly suppress PAI-1 expression through PDLIM5. PAI-1 is a negative regulator of miR-17~92-mediated PASMC proliferation. Silencing of PAI-1 induces Smad2/calponin signaling in PASMCs, suggesting that PAI-1 is a negative regulator of the PASMC contractile phenotype. We also found that PAI-1 is essential for the metabolic gene expression in PASMCs. Furthermore, although there is no significant change in PAI-1 levels in PASMCs isolated from idiopathic pulmonary arterial hypertension and associated pulmonary arterial hypertension patients, PAI-1 is downregulated in hypoxia/Sugen-induced hypertensive rat lungs. These results suggest that miR-17~92 regulates the PASMC contractile phenotype and proliferation coordinately and synergistically by direct and indirect targeting of PAI-1.

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XPO1-mediated nuclear export of RNF146 protects from angiotensin II-induced endothelial cellular injury

Zhang

Wang

et al. 2018

Biochemical and Biophysical Research Communications

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Poly(ADP-Ribose) Polymerase-1 Mediates Angiotensin II-Induced Expression of Plasminogen Activator Inhibitor-1 and Fibronectin in Rat Mesangial Cells

Cited by 6 publications

References 86 publications

AMPKα2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6

AMPKα2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6

PAI-1 is a novel component of the miR-17~92 signaling that regulates pulmonary artery smooth muscle cell phenotypes

XPO1-mediated nuclear export of RNF146 protects from angiotensin II-induced endothelial cellular injury

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