Heart remodeling occurs as a compensation mechanism for the massive loss of tissue during initial heart failure and the consequent inflammation process. During heart remodeling fibroblasts differentiate to myofibroblasts activate their secretion functions and produce elevated amounts, of extracellular matrix (ECM) proteins, mostly collagen, that form scar tissue and alter the normal degradation of ECM. Scar formation does replace the damaged tissue structurally; however, it impedes the normal contractive function of cardiomyocytes (CMs) and results in long-lasting effects after heart failure. Besides CMs and cardiac fibroblasts, endothelial cells (ECs) and circulating endothelial progenitor cells (cEPCs) contribute to heart repair. This review summarizes the current knowledge of EC-CM crosstalk in cardiac fibrosis (CF), the role of cEPCs in heart regeneration and the contribution of Endothelial-mesenchymal transition (EndoMT).
- MeSH
- endoteliální buňky fyziologie MeSH
- endoteliální progenitorové buňky fyziologie MeSH
- interakce mezi receptory a ligandy MeSH
- kardiomyocyty fyziologie MeSH
- lidé MeSH
- regenerace * MeSH
- remodelace komor * MeSH
- srdce fyziologie MeSH
- transdiferenciace buněk * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Adiponectin (APN), an adipose tissue-excreted adipokine, plays protective roles in metabolic and cardiovascular diseases. In this study, the effects and mechanisms of APN on biological functions of rat vascular endothelial progenitor cells (VEPCs) were investigated in vitro. After administrating APN in rat VEPCs, the proliferation was measured by methyl thiazolyl tetrazolium (MTT) method, the apoptotic rate was test by Flow cytometry assay, mRNA expression of B-cell lymphoma-2 (Bcl-2) and vascular endothelial growth factor (VEGF) was determined by real-time reverse transcriptase polymerase chain reaction (RT-PCR), and protein expression of mechanistic target of rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 (pSTAT3) was analyzed by Western blot. It was suggested that APN promoted the optical density (OD) value of VEPCs, enhanced mRNA expression of Bcl-2 and VEGF, and inhibited cell apoptotic rate. Furthermore, protein expression of pSTAT3 was also increased in the presence of APN. Moreover, APN changed-proliferation, apoptosis and VEGF expression of VEPCs were partially suppressed after blocking the mTOR-STAT3 signaling pathway by the mTOR inhibitor XL388. It was indicated that APN promoted biological functions of VEPCs through targeting the mTOR-STAT3 signaling pathway.
- MeSH
- adiponektin farmakologie MeSH
- buněčné linie MeSH
- cévní endotel účinky léků metabolismus MeSH
- endoteliální progenitorové buňky účinky léků fyziologie MeSH
- krysa rodu Rattus MeSH
- proliferace buněk účinky léků fyziologie MeSH
- signální transdukce účinky léků fyziologie MeSH
- sulfony farmakologie MeSH
- TOR serin-threoninkinasy antagonisté a inhibitory biosyntéza MeSH
- transkripční faktor STAT3 antagonisté a inhibitory biosyntéza MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adiponektin MeSH
- mTOR protein, rat MeSH Prohlížeč
- Stat3 protein, rat MeSH Prohlížeč
- sulfony MeSH
- TOR serin-threoninkinasy MeSH
- transkripční faktor STAT3 MeSH
- XL388 MeSH Prohlížeč
BACKGROUND: Continuous blood flow could have deleterious effects on endothelium and vascular health. This could have serious consequences in patients with heart failure treated with continuous flow left ventricular assist devices (LVAD). Therefore, we studied effect of LVAD on three circulating vascular biomarkers: stem cells (SC), endothelial progenitor cells (EPC) and microparticles (MP). METHODS: In 23 patients (5 women) with end-stage heart failure, SC, EPC and MP were measured before, and 3 and 6months after implantation of LVAD (HeartMate II). SC were defined using determination of surface antigen expression as mononuclear CD34+/CD45low+ cells and EPC as mononuclear CD34+/CD45low+/KDR+ cells. MP concentrations were determined by ELISA method. RESULTS: Three months after LVAD implantation numbers of SC and EPC significantly decreased (p=0.01 and p=0.001, respectively). On the contrary, between 3rd and 6th month after implantation they significantly increased (p=0.006 and p=0.003, respectively).MP did not change significantly during the study despite exerting similar trend as SC and EPC. CONCLUSIONS: Observed biphasic changes of SC and EPC might reflect two processes. First, shortly after LVAD implantation, improved tissue perfusion could lead to decrease in ischemic stimuli and ensuing decrease of SC and EPC. Second, continuous flow between 3rd and 6th month produced by LVAD could lead to increase of SC and EPC through activation of endothelium. This explanation could be supported also by similar trend in the changes of concentrations of MP.
- Klíčová slova
- Endothelial progenitor cells, Microparticles, Stem cells, Vascular function, Ventricular assist device,
- MeSH
- časové faktory MeSH
- cévní endotel cytologie fyziologie MeSH
- dospělí MeSH
- endoteliální progenitorové buňky fyziologie MeSH
- kmenové buňky fyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- longitudinální studie MeSH
- mladý dospělý MeSH
- následné studie MeSH
- počet buněk trendy MeSH
- podpůrné srdeční systémy trendy MeSH
- prospektivní studie MeSH
- senioři MeSH
- srdeční komory * MeSH
- srdeční selhání krev patofyziologie terapie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- pozorovací studie MeSH
