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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.

التفاصيل البيبلوغرافية
العنوان: 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.
المؤلفون: Ritter ML; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Deng G; Medical College of Wisconsin, Milwaukee. Department of Pharmacology and Neuroscience (G.D., Y.D., S.A.S., H.C.), University of Iowa, Iowa City., Reho JJ; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Comprehensive Rodent Metabolic Phenotyping Core (J.J.R., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Deng Y; Medical College of Wisconsin, Milwaukee. Department of Pharmacology and Neuroscience (G.D., Y.D., S.A.S., H.C.), University of Iowa, Iowa City., Sapouckey SA; Medical College of Wisconsin, Milwaukee. Department of Pharmacology and Neuroscience (G.D., Y.D., S.A.S., H.C.), University of Iowa, Iowa City., Opichka MA; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Balapattabi K; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Wackman KK; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Brozoski DT; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Lu KT; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Paradee WJ; Genome Editing Core Facility (W.J.P.), University of Iowa, Iowa City., Gibson-Corley KN; Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, TN (K.N.G.-C.)., Cui H; Medical College of Wisconsin, Milwaukee. Department of Pharmacology and Neuroscience (G.D., Y.D., S.A.S., H.C.), University of Iowa, Iowa City., Nakagawa P; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Cardiovascular Center (P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Morselli LL; Department of Medicine, Division of Endocrinology (L.L.M.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee., Sigmund CD; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Cardiovascular Center (P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee (C.D.S., J.L.G.)., Grobe JL; Department of Physiology (M.L.R., J.J.R., M.A.O., K.B., K.K.W., D.T.B., K.-T.L., P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Comprehensive Rodent Metabolic Phenotyping Core (J.J.R., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Cardiovascular Center (P.N., C.D.S., J.L.G.), Neuroscience Research Center, Medical College of Wisconsin, Milwaukee.; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee (C.D.S., J.L.G.).; Department of Biomedical Engineering (J.L.G.), University of Iowa, Iowa City.
المصدر: Hypertension (Dallas, Tex. : 1979) [Hypertension] 2022 Dec; Vol. 79 (12), pp. 2843-2853. Date of Electronic Publication: 2022 Oct 19.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Lippincott, Williams & Wilkins Country of Publication: United States NLM ID: 7906255 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4563 (Electronic) Linking ISSN: 0194911X NLM ISO Abbreviation: Hypertension Subsets: MEDLINE
أسماء مطبوعة: Publication: : Hagerstown, MD : Lippincott, Williams & Wilkins
Original Publication: [Dallas, Tex.] : [American Heart Association], [©1979]-
مواضيع طبية MeSH: Hypertension*/genetics , RGS Proteins*/genetics, Animals ; Mice ; Agouti-Related Protein ; Mice, Knockout ; Mice, Transgenic ; Receptor, Angiotensin, Type 1/genetics ; Recombinases
مستخلص: 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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معلومات مُعتمدة: K01 HL153101 United States HL NHLBI NIH HHS; R01 HL134850 United States HL NHLBI NIH HHS; T32 HL007638 United States HL NHLBI NIH HHS; R01 HL153274 United States HL NHLBI NIH HHS; R35 HL144807 United States HL NHLBI NIH HHS; P01 HL084207 United States HL NHLBI NIH HHS; UL1 TR001436 United States TR NCATS NIH HHS; R01 DK133121 United States DK NIDDK NIH HHS; R01 HL127673 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: G protein coupled receptor; GTPase-activating proteins; animal model; mouse; second-messenger
المشرفين على المادة: 0 (Agouti-Related Protein)
0 (Receptor, Angiotensin, Type 1)
0 (Recombinases)
0 (RGS Proteins)
تواريخ الأحداث: Date Created: 20221019 Date Completed: 20221115 Latest Revision: 20231202
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9649888
DOI: 10.1161/HYPERTENSIONAHA.122.20169
PMID: 36259376
قاعدة البيانات: MEDLINE
الوصف
تدمد:1524-4563
DOI:10.1161/HYPERTENSIONAHA.122.20169