Gsα Regulates Macrophage Foam Cell Formation During Atherosclerosis.

atherosclerosis cholesterol foam cell luciferase macrophage

Journal

Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103

Informations de publication

Date de publication:
20 Feb 2024
Historique:
medline: 20 2 2024
pubmed: 20 2 2024
entrez: 20 2 2024
Statut: aheadofprint

Résumé

Many cardiovascular pathologies are induced by signaling through G-protein-coupled receptors via Gsα (G protein stimulatory α subunit) proteins. However, the specific cellular mechanisms that are driven by Gsα and contribute to the development of atherosclerosis remain unclear. High-throughput screening involving data from single-cell and bulk sequencing were used to explore the expression of Gsα in atherosclerosis. The differentially expression and activity of Gsα were analyzed by immunofluorescence and cAMP measurements. Macrophage-specific Gsα knockout (Mac-Gsα ScRNA-seq showed elevated Gsα activation is enhanced during atherosclerotic progression and increases lipid uptake and foam cell formation. The genetic or chemical inactivation of Gsα inhibit the development of atherosclerosis in mice, suggesting that drugs targeting Gsα may be useful in the treatment of atherosclerosis.

Sections du résumé

BACKGROUND UNASSIGNED
Many cardiovascular pathologies are induced by signaling through G-protein-coupled receptors via Gsα (G protein stimulatory α subunit) proteins. However, the specific cellular mechanisms that are driven by Gsα and contribute to the development of atherosclerosis remain unclear.
METHODS UNASSIGNED
High-throughput screening involving data from single-cell and bulk sequencing were used to explore the expression of Gsα in atherosclerosis. The differentially expression and activity of Gsα were analyzed by immunofluorescence and cAMP measurements. Macrophage-specific Gsα knockout (Mac-Gsα
RESULTS UNASSIGNED
ScRNA-seq showed elevated
CONCLUSIONS UNASSIGNED
Gsα activation is enhanced during atherosclerotic progression and increases lipid uptake and foam cell formation. The genetic or chemical inactivation of Gsα inhibit the development of atherosclerosis in mice, suggesting that drugs targeting Gsα may be useful in the treatment of atherosclerosis.

Identifiants

pubmed: 38375634
doi: 10.1161/CIRCRESAHA.123.323156
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

Chang Ma (C)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Yihui Li (Y)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).
Department of Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. (Y.L.).

Mi Tian (M)

Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, China (M.T.).

Qiming Deng (Q)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Qin Xiaoteng (Q)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Hanlin Lu (H)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Jiangang Gao (J)

School of Life Science and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan, China. (J.G.).

Min Chen (M)

Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD (M.C., L.S.W.).

Lee S Weinstein (LS)

Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD (M.C., L.S.W.).

Mei Zhang (M)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Peili Bu (P)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Jianmin Yang (J)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Yun Zhang (Y)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Cheng Zhang (C)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Wencheng Zhang (W)

National Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).

Classifications MeSH