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  RGS5 Attenuates Baseline Activity of ERK1/2 and Promotes Growth Arrest of Vascular Smooth Muscle Cells

Demirel, E., Arnold, C., Garg, J., Jaeger, M. A., Sticht, C., Li, R., et al. (2021). RGS5 Attenuates Baseline Activity of ERK1/2 and Promotes Growth Arrest of Vascular Smooth Muscle Cells. CELLS, 10(7): 1748. doi:10.3390/cells10071748.

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 Creators:
Demirel, Eda, Author
Arnold, Caroline, Author
Garg, Jaspal, Author
Jaeger, Marius Andreas, Author
Sticht, Carsten, Author
Li, Rui1, Author              
Kuk, Hanna, Author
Wettschureck, Nina1, Author              
Hecker, Markus, Author
Korff, Thomas, Author
Affiliations:
1Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591696              

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Free keywords: GTPASE-ACTIVATING PROTEINS; BLOOD-PRESSURE; GENE-EXPRESSION; KINASE; PHOSPHORYLATION; REGULATOR; DIFFERENTIATION; PKACell Biology; RGS proteins; G-protein signaling; VSMC phenotype; ERK1; 2; blood pressure;
 Abstract: The regulator of G-protein signaling 5 (RGS5) acts as an inhibitor of G alpha(q/11) and G alpha(i/o) activity in vascular smooth muscle cells (VSMCs), which regulate arterial tone and blood pressure. While RGS5 has been described as a crucial determinant regulating the VSMC responses during various vascular remodeling processes, its regulatory features in resting VSMCs and its impact on their phenotype are still under debate and were subject of this study. While Rgs5 shows a variable expression in mouse arteries, neither global nor SMC-specific genetic ablation of Rgs5 affected the baseline blood pressure yet elevated the phosphorylation level of the MAP kinase ERK1/2. Comparable results were obtained with 3D cultured resting VSMCs. In contrast, overexpression of RGS5 in 2D-cultured proliferating VSMCs promoted their resting state as evidenced by microarray-based expression profiling and attenuated the activity of Akt- and MAP kinase-related signaling cascades. Moreover, RGS5 overexpression attenuated ERK1/2 phosphorylation, VSMC proliferation, and migration, which was mimicked by selectively inhibiting G alpha(i/o) but not G alpha(q/11) activity. Collectively, the heterogeneous expression of Rgs5 suggests arterial blood vessel type-specific functions in mouse VSMCs. This comprises inhibition of acute agonist-induced G alpha(q/11)/calcium release as well as the support of a resting VSMC phenotype with low ERK1/2 activity by suppressing the activity of G alpha(i/o).

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Language(s): eng - English
 Dates: 2021-07-11
 Publication Status: Published online
 Pages: 20
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000676727500001
DOI: 10.3390/cells10071748
 Degree: -

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Title: CELLS
Source Genre: Journal
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Publ. Info: ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND : MDPI
Pages: - Volume / Issue: 10 (7) Sequence Number: 1748 Start / End Page: - Identifier: -