دورية أكاديمية
أعرض في EDS

Mir-30d Regulates Cardiac Remodeling by Intracellular and Paracrine Signaling.

التفاصيل البيبلوغرافية
العنوان: Mir-30d Regulates Cardiac Remodeling by Intracellular and Paracrine Signaling.
المؤلفون: Li J; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, China (J.L., X.M., J. Xiao)., Salvador AM; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Li G; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Valkov N; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Ziegler O; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Yeri A; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Yang Xiao C; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Meechoovet B; Neurogenomics Division, TGen, Phoenix, AZ (B.M., E.A., K.V.K.-J.)., Alsop E; Neurogenomics Division, TGen, Phoenix, AZ (B.M., E.A., K.V.K.-J.)., Rodosthenous RS; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Kundu P; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Huan T; The Framingham Heart Study and The Population Sciences Branch, Division of Intramural Research, National Heart, Lung and Blood Institute, NIH, Bethesda, MD (T.H., D.L.)., Levy D; The Framingham Heart Study and The Population Sciences Branch, Division of Intramural Research, National Heart, Lung and Blood Institute, NIH, Bethesda, MD (T.H., D.L.)., Tigges J; Division of Allergy and Inflammation, Beth Israel Deaconess Medical Center, Boston, MA (J.T., I.G.)., Pico AR; Gladstone Institutes, San Francisco, CA (A.R.P.)., Ghiran I; Division of Allergy and Inflammation, Beth Israel Deaconess Medical Center, Boston, MA (J.T., I.G.)., Silverman MG; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Meng X; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, China (J.L., X.M., J. Xiao)., Kitchen R; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Xu J; Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (J. Xu)., Van Keuren-Jensen K; Neurogenomics Division, TGen, Phoenix, AZ (B.M., E.A., K.V.K.-J.)., Shah R; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.)., Xiao J; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, China (J.L., X.M., J. Xiao)., Das S; Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.).
المصدر: Circulation research [Circ Res] 2021 Jan 08; Vol. 128 (1), pp. e1-e23. Date of Electronic Publication: 2020 Oct 22.
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: 0047103 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4571 (Electronic) Linking ISSN: 00097330 NLM ISO Abbreviation: Circ Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Baltimore, MD : Lippincott Williams & Wilkins
Original Publication: Baltimore, Md. Grune & Stratton.
مواضيع طبية MeSH: Paracrine Communication* , Ventricular Function, Left* , Ventricular Remodeling*, MicroRNAs/*metabolism , Myocardial Infarction/*metabolism , Myocardium/*metabolism, Animals ; Apoptosis ; Cells, Cultured ; Disease Models, Animal ; Extracellular Vesicles/genetics ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/pathology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosis ; Gene Expression Regulation ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs/genetics ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Rats, Sprague-Dawley ; Rats, Transgenic ; Signal Transduction ; NF-kappaB-Inducing Kinase ; Mice ; Rats
مستخلص: Rationale: Previous translational studies implicate plasma extracellular microRNA-30d (miR-30d) as a biomarker in left ventricular remodeling and clinical outcome in heart failure (HF) patients, although precise mechanisms remain obscure.
Objective: To investigate the mechanism of miR-30d-mediated cardioprotection in HF.
Methods and Results: In rat and mouse models of ischemic HF, we show that miR-30d gain of function (genetic, lentivirus, or agomiR-mediated) improves cardiac function, decreases myocardial fibrosis, and attenuates cardiomyocyte (CM) apoptosis. Genetic or locked nucleic acid-based knock-down of miR-30d expression potentiates pathological left ventricular remodeling, with increased dysfunction, fibrosis, and cardiomyocyte death. RNA sequencing of in vitro miR-30d gain and loss of function, together with bioinformatic prediction and experimental validation in cardiac myocytes and fibroblasts, were used to identify and validate direct targets of miR-30d. miR-30d expression is selectively enriched in cardiomyocytes, induced by hypoxic stress and is acutely protective, targeting MAP4K4 (mitogen-associate protein kinase 4) to ameliorate apoptosis. Moreover, miR-30d is secreted primarily in extracellular vesicles by cardiomyocytes and inhibits fibroblast proliferation and activation by directly targeting integrin α5 in the acute phase via paracrine signaling to cardiac fibroblasts. In the chronic phase of ischemic remodeling, lower expression of miR-30d in the heart and plasma extracellular vesicles is associated with adverse remodeling in rodent models and human subjects and is linked to whole-blood expression of genes implicated in fibrosis and inflammation, consistent with observations in model systems.
Conclusions: These findings provide the mechanistic underpinning for the cardioprotective association of miR-30d in human HF. More broadly, our findings support an emerging paradigm involving intercellular communication of extracellular vesicle-contained miRNAs (microRNAs) to transregulate distinct signaling pathways across cell types. Functionally validated RNA biomarkers and their signaling networks may warrant further investigation as novel therapeutic targets in HF.
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معلومات مُعتمدة: R01 CA218500 United States CA NCI NIH HHS; T32 HL007208 United States HL NHLBI NIH HHS; UH3 TR000901 United States TR NCATS NIH HHS; K23 HL127099 United States HL NHLBI NIH HHS; UG3 TR002878 United States TR NCATS NIH HHS; R35 HL150807 United States HL NHLBI NIH HHS; R01 HL122547 United States HL NHLBI NIH HHS; UH2 TR000901 United States TR NCATS NIH HHS; R01 HL102368 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: apoptosis; extracellular vesicle; fibrosis; heart failure; microRNA
المشرفين على المادة: 0 (MIRN30 microRNA, rat)
0 (MicroRNAs)
0 (Mirn30d microRNA, mouse)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
تواريخ الأحداث: Date Created: 20201023 Date Completed: 20210726 Latest Revision: 20240226
رمز التحديث: 20240226
مُعرف محوري في PubMed: PMC7790887
DOI: 10.1161/CIRCRESAHA.120.317244
PMID: 33092465
قاعدة البيانات: MEDLINE
الوصف
تدمد:1524-4571
DOI:10.1161/CIRCRESAHA.120.317244