Regulator of G Protein Signaling 2

Osei‐Owusu, Patrick; Blumer, Kendall J.

doi:10.1016/bs.pmbts.2015.02.001

Cited by 29 publications

(18 citation statements)

References 79 publications

(103 reference statements)

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“…Our findings are consistent with a previous report showing that ANP and a cGMP analogue hyperpolarized cultured mesangial cells and that this hyperpolarization was inhibited by potassium channel blocker. 34 Recently, Osei-Owusu et al 25,27 demonstrated that endothelial-specific deletion of Rgs2 markedly inhibits EDHF-dependent relaxation of mouse mesenteric arteries. We found that ANP significantly increased Rgs2 mRNA expression levels in HUVECs and that ANPmediated hyperpolarization of HUVECs was abolished under Rgs2 siRNA transfection.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Osei-Owusu et al 25,27 demonstrated that endothelial-specific deletion of Rgs2 markedly inhibits EDHF-dependent relaxation of mouse mesenteric arteries. We found that ANP significantly increased Rgs2 mRNA expression levels in HUVECs and that ANP-mediated hyperpolarization of HUVECs was abolished under Rgs2 siRNA transfection.…”

Section: Discussionmentioning

confidence: 99%

“…Regulator of G-Protein Signaling 2 Plays a Key Role in the Hypotensive Effect of ANP RGS2 (regulator of G-protein signaling 2) is a GTPaseactivating protein for the G q/11 α and G i/o α subunits. 25 Rgs2-knockout mice (Rgs2-KO) exhibit hypertension. 26 Recently, it has been reported that RGS2 deficiency in endothelial cells causes impairment of EDHF-dependent vascular relaxation.…”

Section: Anp Hyperpolarizes Cultured Endothelial Cells Via a Cgmp-dep...mentioning

confidence: 99%

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Endothelial Natriuretic Peptide Receptor 1 Play Crucial Role for Acute and Chronic Blood Pressure Regulation by Atrial Natriuretic Peptide

et al. 2022

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Background: ANP (atrial natriuretic peptide), acting through NPR1 (natriuretic peptide receptor 1), provokes hypotension. Such hypotension is thought to be due to ANP inducing vasodilation via NPR1 in the vasculature; however, the underlying mechanism remains unclear. Here, we investigated the mechanisms of acute and chronic blood pressure regulation by ANP. Methods and Results: Immunohistochemical analysis of rat tissues revealed that NPR1 was abundantly expressed in endothelial cells and smooth muscle cells of small arteries and arterioles. Intravenous infusion of ANP significantly lowered systolic blood pressure in wild-type mice. ANP also significantly lowered systolic blood pressure in smooth muscle cell–specific Npr1 –knockout mice but not in endothelial cell–specific Npr1 –knockout mice. Moreover, ANP significantly lowered systolic blood pressure in Nos3 -knockout mice. In human umbilical vein endothelial cells, treatment with ANP did not influence nitric oxide production or intracellular Ca 2+ concentration, but it did hyperpolarize the cells. ANP-induced hyperpolarization of human umbilical vein endothelial cells was inhibited by several potassium channel blockers and was also abolished under knockdown of RGS2 (regulator of G-protein signaling 2), an GTPase activating protein in G-protein α-subunit. ANP increased Rgs2 mRNA expression in human umbilical vein endothelial cells but failed to lower systolic blood pressure in Rgs2 -knockout mice. Endothelial cell–specific Npr1 -overexpressing mice exhibited lower blood pressure than did wild-type mice independent of RGS2, and showed dilation of arterial vessels on synchrotron radiation microangiography. Conclusions: Together, these results indicate that vascular endothelial NPR1 plays a crucial role in ANP-mediated blood pressure regulation, presumably by a mechanism that is RGS2-dependent in the acute phase and RGS2-independent in the chronic phase.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Anp Hyperpolarizes Cultured Endothelial Cells Via a Cgmp-dep...mentioning

confidence: 99%

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Endothelial Natriuretic Peptide Receptor 1 Play Crucial Role for Acute and Chronic Blood Pressure Regulation by Atrial Natriuretic Peptide

et al. 2022

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“…RGS1 functions to regulate B lymphocyte maturation induced by chemokines and can also be found in T lymphocytes, natural killer (NK) cells, dendritic cells, and monocytes (4,38,94,113,169). The next RGS protein, Rgs2, is ubiquitously expressed, with expression documented in the CNS, heart, vasculature, kidney, immune system, lungs, bone and ovaries (13,89,98,125,163). The main function of RGS2 is to regulate G ␣q and G ␣i signaling (64,89,92,180).…”

Section: The B/r4 Family Of Rgs Proteinsmentioning

confidence: 99%

Regulators of G protein signaling in cardiovascular function during pregnancy

Perschbacher

Deng

Fisher

et al. 2018

Physiological Genomics

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G protein-coupled receptor signaling mechanisms are implicated in many aspects of cardiovascular control, and dysfunction of such signaling mechanisms is commonly associated with disease states. Investigators have identified a large number of regulator of G protein signaling (RGS) proteins that variously contribute to the modulation of intracellular second-messenger signaling kinetics. These many RGS proteins each interact with a specific set of second-messenger cascades and receptor types and exhibit tissue-specific expression patterns. Increasing evidence supports the contribution of RGS proteins, or their loss, in the pathogenesis of cardiovascular dysfunctions. This review summarizes the current understanding of the functional contributions of RGS proteins, particularly within the B/R4 family, in cardiovascular disorders of pregnancy including gestational hypertension, uterine artery dysfunction, and preeclampsia.

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“…Expression of RGS2 is inversely related to blood pressure (BP), as subjects with hypotension (ie, Bartter’s or Gitelman’s syndromes) exhibit increased RGS2 but those with hypertension exhibit reduced RGS2 levels. 7 Rodent models support a critical role for RGS2 in the function of the vasculature, 8–11 control of blood pressure, 12 and the development and function of adipose 13 and placenta. 14…”

mentioning

confidence: 99%

Cardiometabolic Consequences of Deleting the Regulator of G protein Signaling-2 ( Rgs2 ) From Cells Expressing Agouti-Related Peptide or the ANG (Angiotensin) II Type 1A Receptor in Mice

et al. 2022

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BACKGROUND: RGS (regulator of G protein signaling) family members catalyze the termination of G protein signaling cascades. Single nucleotide polymorphisms in the RGS2 gene in humans have been linked to hypertension, preeclampsia, and anxiety disorders. Mice deficient for Rgs2 ( Rgs2 Null ) exhibit hypertension, anxiety, and altered adipose development and function. METHODS: To study cell-specific functions of RGS2, a novel gene-targeted mouse harboring a conditional allele for the Rgs2 gene ( Rgs2 Flox ) was developed. These mice were bred with mice expressing Cre-recombinase via the Agouti-related peptide locus ( Agrp -Cre) to cause deletion of Rgs2 from all cells expressing Agrp ( Rgs2 Agrp-KO ), or a novel transgenic mouse expressing Cre-recombinase via the ANG (angiotensin) type 1A receptor ( Agtr1a / AT 1A ) promoter encoded in a bacterial artificial chromosome (BAC-AT 1A -Cre) to delete Rgs2 in all Agtr1a -expressing cells ( Rgs2 AT1A-KO ). RESULTS: Whereas Rgs2 Flox , Rgs2 Agrp-KO , and BAC-AT 1A -Cre mice exhibited normal growth and survival, Rgs2 AT1A-KO exhibited pre-weaning lethality. Relative to littermates, Rgs2 Agrp-KO exhibited reduced fat gains when maintained on a high fat diet, associated with increased energy expenditure. Similarly, surviving adult Rgs2 AT1A-KO mice also exhibited increased energy expenditure. Surprisingly, given the hypertensive phenotype previously reported for Rgs2 Null mice and evidence supporting a role for RGS2 in terminating AT 1A signaling in various cell types, Rgs2 AT1A-KO mice exhibited normal blood pressure, ingestive behaviors, and renal functions, both before and after chronic infusion of ANG (490 ng/kg/min, sc). CONCLUSIONS: These results demonstrate the development of a novel mouse with conditional expression of Rgs2 and illustrate the role of Rgs2 within selected cell types for cardiometabolic control.

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Regulator of G Protein Signaling 2

Cited by 29 publications

References 79 publications

Endothelial Natriuretic Peptide Receptor 1 Play Crucial Role for Acute and Chronic Blood Pressure Regulation by Atrial Natriuretic Peptide

Endothelial Natriuretic Peptide Receptor 1 Play Crucial Role for Acute and Chronic Blood Pressure Regulation by Atrial Natriuretic Peptide

Regulators of G protein signaling in cardiovascular function during pregnancy

Cardiometabolic Consequences of Deleting the Regulator of G protein Signaling-2 ( Rgs2 ) From Cells Expressing Agouti-Related Peptide or the ANG (Angiotensin) II Type 1A Receptor in Mice

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