Gsα deficiency facilitates cardiac remodeling via CREB/ Bmp10-mediated signaling

Yin, Ping; Li, Dan; Zhao, Qi; Cai, Mingming; Wu, Zhenru; Shi, Yujun; Su, Li

doi:10.1038/s41420-021-00788-3

Cited by 8 publications

(7 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The endothelial Gsα deficiency or overexpression could affect CREB protein level, which was consistent with previous reports from our and other groups that Gsα deficiency in smooth muscle or cardiomyocytes resulted in CREB protein reduction (Qin et al, 2017;Yin et al, 2021). Phosphorylation at Ser133 in CREB may contribute to its protein stability (Costes et al, 2006;Mouravlev et al, 2007).…”

Section: Gsα Regulates Plvap Expression Via Creb-mediated Transcriptionsupporting

confidence: 91%

Stimulatory G-Protein α Subunit Modulates Endothelial Cell Permeability Through Regulation of Plasmalemma Vesicle-Associated Protein

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Endothelial cell leakage occurs in several diseases. Intracellular junctions and transcellular fashion are involved. The definite regulatory mechanism is complicated and not fully elucidated. The alpha subunit of the heterotrimeric G-stimulatory protein (Gsα) mediates receptor-stimulated production of cyclic adenosine monophosphate (cAMP). However, the role of Gsα in the endothelial barrier remains unclear. In this study, mice with knockout of endothelial-specific Gsα (GsαECKO) were generated by crossbreeding Gsαflox/flox mice with Cdh5-CreERT2 transgenic mice, induced in adult mice by tamoxifen treatment. GsαECKO mice displayed phenotypes of edema, anemia, hypoproteinemia and hyperlipoproteinemia, which indicates impaired microvascular permeability. Mechanistically, Gsα deficiency reduces the level of endothelial plasmalemma vesicle-associated protein (PLVAP). In addition, overexpression of Gsα increased phosphorylation of cAMP response element-binding protein (CREB) as well as the mRNA and protein levels of PLVAP. CREB could bind to the CRE site of PLVAP promoter and regulate its expression. Thus, Gsα might regulate endothelial permeability via cAMP/CREB-mediated PLVAP expression.

show abstract

Section: Gsα Regulates Plvap Expression Via Creb-mediated Transcriptionsupporting

confidence: 91%

Stimulatory G-Protein α Subunit Modulates Endothelial Cell Permeability Through Regulation of Plasmalemma Vesicle-Associated Protein

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Unlike TGFβ1, many BMPs have been shown to exert anti-fibrotic effects during cardiac injury, including BMP2, BMP7, and BMP9 [ 37 , 38 , 39 , 40 , 41 , 42 ]. In TAC-induced cardiac fibrosis, each recombinant BMP attenuates cardiac fibrosis.…”

Section: Molecular Mechanisms Involved In the Development Of Cardiac ...mentioning

confidence: 99%

Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis

Bertaud

Joshkon

Heim

et al. 2023

IJMS

View full text Add to dashboard Cite

Cardiac fibrosis constitutes irreversible necrosis of the heart muscle as a consequence of different acute (myocardial infarction) or chronic (diabetes, hypertension, …) diseases but also due to genetic alterations or aging. Currently, there is no curative treatment that is able to prevent or attenuate this phenomenon that leads to progressive cardiac dysfunction and life-threatening outcomes. This review summarizes the different targets identified and the new strategies proposed to fight cardiac fibrosis. Future directions, including the use of exosomes or nanoparticles, will also be discussed.

show abstract

“…Restoration of Gsα increases CREB1 expression and enhances the Bmp10-mediated signaling pathway. (Yin et al, 2021) Angiogenesis VEGF induces activation of CREB. (Mayo et al, 2001)…”

Section: Roles Of Creb In Cardiovascular Function and Remodelingmentioning

confidence: 99%

The Pleiotropic Face of CREB Family Transcription Factors

Chowdhury

Jeong

2023

Molecules and Cells

View full text Add to dashboard Cite

cAMP responsive element-binding protein (CREB) is one of the most intensively studied phosphorylation-dependent transcription factors that provide evolutionarily conserved mechanisms of differential gene expression in vertebrates and invertebrates. Many cellular protein kinases that function downstream of distinct cell surface receptors are responsible for the activation of CREB. Upon functional dimerization of the activated CREB to cis-acting cAMP responsive elements within the promoters of target genes, it facilitates signaldependent gene expression. From the discovery of CREB, which is ubiquitously expressed, it has been proven to be involved in a variety of cellular processes that include cell proliferation, adaptation, survival, differentiation, and physiology, through the control of target gene expression. In this review, we highlight the essential roles of CREB proteins in the nervous system, the immune system, cancer development, hepatic physiology, and cardiovascular function and further discuss a wide range of CREB-associated diseases and molecular mechanisms underlying the pathogenesis of these diseases.

show abstract

Gsα deficiency facilitates cardiac remodeling via CREB/ Bmp10-mediated signaling

Cited by 8 publications

References 35 publications

Stimulatory G-Protein α Subunit Modulates Endothelial Cell Permeability Through Regulation of Plasmalemma Vesicle-Associated Protein

Stimulatory G-Protein α Subunit Modulates Endothelial Cell Permeability Through Regulation of Plasmalemma Vesicle-Associated Protein

Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis

The Pleiotropic Face of CREB Family Transcription Factors

Contact Info

Product

Resources

About