دورية أكاديمية
Urokinase-Type Plasminogen Activator Receptor Regulates Prosurvival and Angiogenic Properties of Cardiac Mesenchymal Stromal Cells.
العنوان: | Urokinase-Type Plasminogen Activator Receptor Regulates Prosurvival and Angiogenic Properties of Cardiac Mesenchymal Stromal Cells. |
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المؤلفون: | Dergilev K; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia., Tsokolaeva Z; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia.; Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 107031 Moscow, Russia., Goltseva Y; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia., Beloglazova I; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia., Ratner E; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia., Parfyonova Y; Institute of Experimental Cardiology Named after Academician V.N. Smirnov, Federal State Budgetary Institution National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Ministry of Health of the Russian Federation, 121552 Moscow, Russia.; Department of Biochemistry and Molecular Medicine, Faculty of Medicine, Lomonosov Moscow State University, 119192 Moscow, Russia. |
المصدر: | International journal of molecular sciences [Int J Mol Sci] 2023 Oct 25; Vol. 24 (21). Date of Electronic Publication: 2023 Oct 25. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: Basel, Switzerland : MDPI, [2000- |
مواضيع طبية MeSH: | Mesenchymal Stem Cells*/metabolism , Receptors, Urokinase Plasminogen Activator*/genetics , Receptors, Urokinase Plasminogen Activator*/metabolism , Myocardium*/cytology, Animals ; Mice ; Integrins ; Signal Transduction ; Urokinase-Type Plasminogen Activator/genetics ; Urokinase-Type Plasminogen Activator/metabolism |
مستخلص: | One of the largest challenges to the implementation of cardiac cell therapy is identifying selective reparative targets to enhance stem/progenitor cell therapeutic efficacy. In this work, we hypothesized that such a target could be an urokinase-type plasminogen activator receptor (uPAR)-a glycosyl-phosphatidyl-inositol-anchored membrane protein, interacting with urokinase. uPAR is able to form complexes with various transmembrane proteins such as integrins, activating intracellular signaling pathway and thus regulating multiple cell functions. We focused on studying the CD117+ population of cardiac mesenchymal progenitor cells (MPCs), expressing uPAR on their surface. It was found that the number of CD117+ MPCs in the heart of the uPAR-/- mice is lower, as well as their ability to proliferate in vitro compared with cells from wild-type animals. Knockdown of uPAR in CD117+ MPCs of wild-type animals was accompanied by a decrease in survival rate and Akt signaling pathway activity and by an increase in the level of caspase activity in these cells. That suggests the role of uPAR in supporting cell survival. After intramyocardial transplantation of uPAR(-) MPCs, reduced cell retention and angiogenesis stimulation were observed in mice with myocardial infarction model compared to uPAR(+) cells transplantation. Taken together, the present results appear to prove a novel mechanism of uPAR action in maintaining the survival and angiogenic properties of CD117+ MPCs. These results emphasize the importance of the uPAR as a potential pharmacological target for the regulation of reparative properties of myocardial mesenchymal progenitor cells. |
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معلومات مُعتمدة: | 23-15-00540 Russian Science Foundation |
فهرسة مساهمة: | Keywords: CD117; angiogenesis; cardiac mesenchymal cell; cardiac repair; cell survival; uPA; uPAR |
المشرفين على المادة: | 0 (Integrins) 0 (Receptors, Urokinase Plasminogen Activator) EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) 0 (Plaur protein, mouse) |
تواريخ الأحداث: | Date Created: 20231114 Date Completed: 20231129 Latest Revision: 20231129 |
رمز التحديث: | 20231130 |
مُعرف محوري في PubMed: | PMC10650341 |
DOI: | 10.3390/ijms242115554 |
PMID: | 37958542 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1422-0067 |
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DOI: | 10.3390/ijms242115554 |