دورية أكاديمية
أعرض في EDS

RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.

التفاصيل البيبلوغرافية
العنوان: RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.
المؤلفون: Joshi IV; Lung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA., Chan EC; Lung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA., Lack JB; NIAID Collaborative Bioinformatics Resource, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA., Liu C; Transgenic Core, NHLBI/NIH, Bethesda, Maryland, USA., Druey KM; Lung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: kdruey@niaid.nih.gov.
المصدر: The Journal of biological chemistry [J Biol Chem] 2024 Apr; Vol. 300 (4), pp. 107127. Date of Electronic Publication: 2024 Mar 02.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1083-351X (Electronic) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE
أسماء مطبوعة: Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology
Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology
مواضيع طبية MeSH: Asthma*/metabolism , Asthma*/genetics , Asthma*/pathology , RGS Proteins*/metabolism , RGS Proteins*/genetics, Animals ; Humans ; Mice ; Bronchoconstriction/genetics ; Dinoprostone/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Mice, Knockout ; Phosphatidylinositol 3-Kinases/metabolism ; Respiratory Hypersensitivity/metabolism ; Respiratory Hypersensitivity/genetics ; Respiratory Hypersensitivity/pathology ; Cell Line
مستخلص: Regulators of G protein signaling (RGS) proteins constrain G protein-coupled receptor (GPCR)-mediated and other responses throughout the body primarily, but not exclusively, through their GTPase-activating protein activity. Asthma is a highly prevalent condition characterized by airway hyper-responsiveness (AHR) to environmental stimuli resulting in part from amplified GPCR-mediated airway smooth muscle contraction. Rgs2 or Rgs5 gene deletion in mice enhances AHR and airway smooth muscle contraction, whereas RGS4 KO mice unexpectedly have decreased AHR because of increased production of the bronchodilator prostaglandin E2 (PGE2) by lung epithelial cells. Here, we found that knockin mice harboring Rgs4 alleles encoding a point mutation (N128A) that sharply curtails RGS4 GTPase-activating protein activity had increased AHR, reduced airway PGE2 levels, and augmented GPCR-induced bronchoconstriction compared with either RGS4 KO mice or WT controls. RGS4 interacted with the p85α subunit of PI3K and inhibited PI3K-dependent PGE2 secretion elicited by transforming growth factor beta in airway epithelial cells. Together, these findings suggest that RGS4 affects asthma severity in part by regulating the airway inflammatory milieu in a G protein-independent manner.
Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
References: Nat Med. 1998 Dec;4(12):1449-52. (PMID: 9846587)
Br J Pharmacol. 2000 Sep;131(1):152-9. (PMID: 10960082)
Front Immunol. 2023 Jun 12;14:1149203. (PMID: 37377958)
Am J Respir Cell Mol Biol. 2009 Jul;41(1):40-9. (PMID: 19059885)
Cell. 2013 May 9;153(4):910-8. (PMID: 23643243)
Cell Death Dis. 2022 Jul 28;13(7):656. (PMID: 35902557)
J Asthma Allergy. 2023 Jul 21;16:755-774. (PMID: 37496824)
Allergy. 2023 Mar;78(3):714-730. (PMID: 36181709)
J Gen Virol. 2023 Aug;104(8):. (PMID: 37561118)
Front Physiol. 2023 Jan 19;14:1113100. (PMID: 36744026)
J Allergy Clin Immunol. 2023 Oct;152(4):835-840. (PMID: 37531979)
Kidney Int. 2006 Sep;70(5):901-9. (PMID: 16820791)
Pharmacol Biochem Behav. 2010 May;95(3):315-24. (PMID: 20170671)
J Allergy Clin Immunol. 2014 Aug;134(2):451-9. (PMID: 24666695)
Endocrinology. 2008 Nov;149(11):5706-12. (PMID: 18635652)
Sci Signal. 2018 Jun 12;11(534):. (PMID: 29895615)
Cell Commun Signal. 2020 Jun 9;18(1):86. (PMID: 32517689)
J Exp Clin Cancer Res. 2020 May 5;39(1):76. (PMID: 32370786)
Sci Signal. 2017 Jul 04;10(486):. (PMID: 28676490)
Mol Cell Endocrinol. 2021 Feb 5;521:111098. (PMID: 33278490)
Cell Mol Life Sci. 2021 Sep;78(17-18):6305-6318. (PMID: 34292354)
J Biol Chem. 2009 Aug 7;284(32):21719-27. (PMID: 19509421)
Respir Res. 2017 Jun 19;18(1):123. (PMID: 28629359)
Pharmacol Ther. 2023 Jan;241:108313. (PMID: 36427569)
Mol Cell Biochem. 2002 Sep;238(1-2):11-8. (PMID: 12349897)
Br J Pharmacol. 2023 Mar 25;:. (PMID: 36964984)
PeerJ. 2023 Jan 17;11:e14695. (PMID: 36684665)
Int J Mol Sci. 2017 Dec 06;18(12):. (PMID: 29211014)
Endocrinology. 2013 May;154(5):1768-79. (PMID: 23515290)
Front Immunol. 2022 Aug 18;13:935114. (PMID: 36059455)
Mol Pharmacol. 2020 Dec;98(6):751-760. (PMID: 32973086)
Hippocampus. 2023 Mar;33(3):166-181. (PMID: 36541898)
Mol Cell Endocrinol. 1987 Oct;53(3):169-76. (PMID: 3499356)
J Biol Chem. 2000 Jun 23;275(25):18962-8. (PMID: 10747990)
J Biol Chem. 2018 Aug 17;293(33):12690-12702. (PMID: 29929985)
PLoS One. 2017 Jan 20;12(1):e0170269. (PMID: 28107494)
J Allergy Clin Immunol. 2020 Nov;146(5):1152-1164.e13. (PMID: 32199913)
Cancer Cell Int. 2023 Apr 28;23(1):81. (PMID: 37118788)
EBioMedicine. 2023 Aug;94:104717. (PMID: 37442061)
Pharmacol Ther. 2021 Jul;223:107818. (PMID: 33600853)
Cell. 2020 Oct 15;183(2):503-521.e19. (PMID: 33007266)
BMC Pulm Med. 2019 Nov 20;19(1):218. (PMID: 31747880)
PLoS One. 2012;7(1):e28504. (PMID: 22253691)
Gene. 2019 Apr 15;692:9-16. (PMID: 30641218)
Mol Biol Cell. 2000 Sep;11(9):3155-68. (PMID: 10982407)
Genome Res. 2003 Jul;13(7):1744-53. (PMID: 12840049)
Cell Signal. 2006 May;18(5):579-91. (PMID: 16226429)
Prog Mol Biol Transl Sci. 2015;133:13-30. (PMID: 26123300)
Front Immunol. 2023 May 15;14:1155421. (PMID: 37256149)
J Allergy Clin Immunol. 2022 Sep;150(3):721-726.e1. (PMID: 35398411)
Nat Immunol. 2008 Jan;9(1):73-80. (PMID: 18026105)
Allergol Int. 2023 Oct;72(4):493-506. (PMID: 37544851)
فهرسة مساهمة: Keywords: G proteins; PGE2; RGS proteins; TGF beta; asthma
المشرفين على المادة: K7Q1JQR04M (Dinoprostone)
0 (GTPase-Activating Proteins)
EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
0 (RGS Proteins)
175335-35-0 (RGS4 protein)
تواريخ الأحداث: Date Created: 20240303 Date Completed: 20240427 Latest Revision: 20240509
رمز التحديث: 20240509
مُعرف محوري في PubMed: PMC11065749
DOI: 10.1016/j.jbc.2024.107127
PMID: 38432633
قاعدة البيانات: MEDLINE
الوصف
تدمد:1083-351X
DOI:10.1016/j.jbc.2024.107127