Cardiac Nestin⁺ Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Abstract

SummaryDilated cardiomyopathy (DCM), as one of the common cardiomyopathies, is a disease of the heart muscle; however, the etiology and pathogenesis of DCM were still poorly understood. Nestin has been reported a special marker of stem/progenitor cells in various tissues, and the tissue resident Nestin + cells could promote the wound healing and tissue remodeling. However, it remains unclear whether Nestin + cells participate in the protection of cardiomyocytes during the pathogenesis of DCM. Here the model of mice DCM was induced by doxorubicin (DOX) intraperitoneal injection and observed heart failure and ventricular enlargement via echocardiography and histologic analysis, respectively. During DCM pathogenesis, the number of Nestin + cells showed a significant peak on day 6 after DOX treatment, which then gradually decreases to lower than normal levels after day 30 in the total population of the heart. Furthermore, we found that the isolated increased heart-derived Nestin + cells are mesenchymal property and could protect DOX-induced HL-1 cells toxicity in vitro by promoting their proliferation and inhibiting their apoptosis. Collectively, our results showed that Nestin + cells increased during DCM pathogenesis and played an important role in protecting against the DOX-induced HL-1 cells loss via regulating proliferation and apoptosis. Thus, the loss of Nestin + cells might be an etiology to DCM pathogenesis, and these cells could be a promising candidate cell source for study and treatment of DCM patients.(Int Heart J 2018; 59: 180-189)

The Inflammatory Transcription Factor C/EBPβ Plays a Critical Role in Cardiac Fibroblast Differentiation and a Rat Model of Cardiac Fibrosis Induced by Autoimmune Myocarditis

“…21) Echocardiography Four weeks after lentiviral infection, echocardiography was performed on the rats as described previously. 22,23) Briefly, the rats were anesthetized with chloral hydrate and subjected to transthoracic echocardiograms using a General Electric (GE, Vivid-5) imaging system equipped with a 1.7-3.6 MHz multi-frequency transducer in order to measure interventricular septal wall thickness at end diastole (IVS), left ventricular posterior wall thickness (LVPW), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), ejection fraction (EF), and fractional shortening (FS).…”

Trasplantation of Exosomes Derived From CD90 Positive Fibroblasts Reduce Apoptosis of Cardiomyocytes in Mice After Acute Myocardial Infarction

“…Considering the regenerative capacity of adult cardiomyocytes was extremely low and it was insufficient to meet the functional and structural requirements after the myocardium was injured, an increasing number of researches were focused on the preservation of cardiomyocytes through cellular transplantation with or without cytokines supplement (4,5). However, the number of exogenous cells that migrated and retained in the myocardium was not optimistic, because many cells were located in the lungs or spleens (6). Currently, researches indicated that cells from the auto tissues of the exact organs quickly and accurately facilitated organ repair after they were injured (7)(8)(9).…”