دورية أكاديمية
أعرض في EDS

Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure.

التفاصيل البيبلوغرافية
العنوان: Transient Cell Cycle Induction in Cardiomyocytes to Treat Subacute Ischemic Heart Failure.
المؤلفون: Abouleisa RRE; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Salama ABM; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY.; Faculty of Medicine (A.B.M.S.), Zagazig University, Egypt., Ou Q; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Tang XL; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Solanki M; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Guo Y; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Nong Y; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., McNally L; Envirome Institute, Diabetes and Obesity Center (L.M., P.K.L., D.J.C., B.G.H., T.M.A.M.), University of Louisville, KY., Lorkiewicz PK; Envirome Institute, Diabetes and Obesity Center (L.M., P.K.L., D.J.C., B.G.H., T.M.A.M.), University of Louisville, KY., Kassem KM; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Ahern BM; Department of Physiology, University of Kentucky, Lexington (B.M.A., J.S.)., Choudhary K; Gladstone Institute, San Francisco, CA (K.C., R.T., Y.H., D.S.)., Thomas R; Gladstone Institute, San Francisco, CA (K.C., R.T., Y.H., D.S.)., Huang Y; Gladstone Institute, San Francisco, CA (K.C., R.T., Y.H., D.S.)., Juhardeen HR; College of Medicine, Alfaisal University, Riyadh, Saudi Arabia (H.R.J., A.S., Z.I.)., Siddique A; College of Medicine, Alfaisal University, Riyadh, Saudi Arabia (H.R.J., A.S., Z.I.)., Ifthikar Z; College of Medicine, Alfaisal University, Riyadh, Saudi Arabia (H.R.J., A.S., Z.I.)., Hammad SK; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY.; Department of Biochemistry, Faculty of Pharmacy (S.K.H.), Zagazig University, Egypt., Elbaz AS; Department of Medicine, Department of Bioengineering, Speed School of Engineering (A.S.E., T.M.A.M.), University of Louisville, KY., Ivey KN; Tenaya Therapeutics, South San Francisco, CA (K.N.I.)., Conklin DJ; Envirome Institute, Diabetes and Obesity Center (L.M., P.K.L., D.J.C., B.G.H., T.M.A.M.), University of Louisville, KY., Satin J; Department of Physiology, University of Kentucky, Lexington (B.M.A., J.S.)., Hill BG; Envirome Institute, Diabetes and Obesity Center (L.M., P.K.L., D.J.C., B.G.H., T.M.A.M.), University of Louisville, KY., Srivastava D; Gladstone Institute, San Francisco, CA (K.C., R.T., Y.H., D.S.)., Bolli R; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY., Mohamed TMA; From the Institute of Molecular Cardiology (R.R.E.A., A.B.M.S., Q.O., X.-L.T., M.S., Y.G., Y.N., K.M.K., S.K.H., R.B., T.M.A.M.), University of Louisville, KY.; Envirome Institute, Diabetes and Obesity Center (L.M., P.K.L., D.J.C., B.G.H., T.M.A.M.), University of Louisville, KY.; Department of Medicine, Department of Bioengineering, Speed School of Engineering (A.S.E., T.M.A.M.), University of Louisville, KY.; Department of Pharmacology and Toxicology (T.M.A.M.), University of Louisville, KY.; Institute of Cardiovascular Sciences, University of Manchester, United Kingdom (T.M.A.M.).
المصدر: Circulation [Circulation] 2022 Apr 26; Vol. 145 (17), pp. 1339-1355. Date of Electronic Publication: 2022 Jan 21.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 0147763 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1524-4539 (Electronic) Linking ISSN: 00097322 NLM ISO Abbreviation: Circulation Subsets: MEDLINE
أسماء مطبوعة: Publication: Hagerstown, MD : Lippincott Williams & Wilkins
Original Publication: [Dallas, Tex., etc., American Heart Association, etc.]
مواضيع طبية MeSH: Heart Failure*/complications , Heart Failure*/genetics , Heart Failure*/therapy , Induced Pluripotent Stem Cells*/metabolism , Myocardial Infarction*/complications , Myocardial Infarction*/genetics , Myocardial Infarction*/therapy, Animals ; Cell Cycle ; Humans ; Mice ; Myocytes, Cardiac/metabolism ; Rats ; Stroke Volume ; Swine ; Ventricular Function, Left
مستخلص: Background: The regenerative capacity of the heart after myocardial infarction is limited. Our previous study showed that ectopic introduction of 4 cell cycle factors (4F; CDK1 [cyclin-dependent kinase 1], CDK4 [cyclin-dependent kinase 4], CCNB [cyclin B1], and CCND [cyclin D1]) promotes cardiomyocyte proliferation in 15% to 20% of infected cardiomyocytes in vitro and in vivo and improves cardiac function after myocardial infarction in mice.
Methods: Using temporal single-cell RNA sequencing, we aimed to identify the necessary reprogramming stages during the forced cardiomyocyte proliferation with 4F on a single cell basis. Using rat and pig models of ischemic heart failure, we aimed to start the first preclinical testing to introduce 4F gene therapy as a candidate for the treatment of ischemia-induced heart failure.
Results: Temporal bulk and single-cell RNA sequencing and further biochemical validations of mature human induced pluripotent stem cell-derived cardiomyocytes treated with either LacZ or 4F adenoviruses revealed full cell cycle reprogramming in 15% of the cardiomyocyte population at 48 hours after infection with 4F, which was associated mainly with sarcomere disassembly and metabolic reprogramming (n=3/time point/group). Transient overexpression of 4F, specifically in cardiomyocytes, was achieved using a polycistronic nonintegrating lentivirus (NIL) encoding 4F; each is driven by a TNNT2 (cardiac troponin T isoform 2) promoter (TNNT2-4Fpolycistronic-NIL). TNNT2-4Fpolycistronic-NIL or control virus was injected intramyocardially 1 week after myocardial infarction in rats (n=10/group) or pigs (n=6-7/group). Four weeks after injection, TNNT2-4Fpolycistronic-NIL-treated animals showed significant improvement in left ventricular ejection fraction and scar size compared with the control virus-treated animals. At 4 months after treatment, rats that received TNNT2-4Fpolycistronic-NIL still showed a sustained improvement in cardiac function and no obvious development of cardiac arrhythmias or systemic tumorigenesis (n=10/group).
Conclusions: This study provides mechanistic insights into the process of forced cardiomyocyte proliferation and advances the clinical feasibility of this approach by minimizing the oncogenic potential of the cell cycle factors owing to the use of a novel transient and cardiomyocyte-specific viral construct.
التعليقات: Comment in: Circulation. 2022 Apr 26;145(17):1356-1358. doi: 10.1161/CIRCULATIONAHA.122.059106. (PMID: 35467953)
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معلومات مُعتمدة: P50 HL120163 United States HL NHLBI NIH HHS; F32 HL149140 United States HL NHLBI NIH HHS; P30 GM127607 United States GM NIGMS NIH HHS; P01 HL078825 United States HL NHLBI NIH HHS; R01 HL130174 United States HL NHLBI NIH HHS; UM1 HL113530 United States HL NHLBI NIH HHS; R01 HL147921 United States HL NHLBI NIH HHS; R01 ES028268 United States ES NIEHS NIH HHS; U54 HL120163 United States HL NHLBI NIH HHS; R01 HL147844 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: cardiomyopathies; cell cycle; genetic therapy; heart failure; metabolism; sarcomeres
تواريخ الأحداث: Date Created: 20220121 Date Completed: 20220427 Latest Revision: 20240923
رمز التحديث: 20240923
مُعرف محوري في PubMed: PMC9038650
DOI: 10.1161/CIRCULATIONAHA.121.057641
PMID: 35061545
قاعدة البيانات: MEDLINE
الوصف
تدمد:1524-4539
DOI:10.1161/CIRCULATIONAHA.121.057641