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Internal associations and dynamic expression of c-kit and nanog genes in ventricular remodelling induced by adriamycin

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the dynamic expression of the c-kit and nanog genes in rats with left ventricular remodelling induced by adriamycin (ADR), and explore its internal association and mechanism of action. Sprague-Dawley male rats were randomly divided into a normal control group and a heart failure model group. Heart failure was induced by a single intraperitoneal injection of ADR (4 mg/kg) weekly for six weeks. The normal control group was given the same amount of saline. At the eighth week, rat cardiac function was examined to demonstrate the formation of heart failure. The rat hearts were harvested frozen and sectioned, and the expression levels of the nanog and c-kit genes in the myocardial tissue samples were detected using immunohistochemistry, immunofluorescence and reverse transcription-polymerase chain reaction (RT-PCR). Hematoxylin and eosin staining demonstrated various pathological changes in the myocardial cells in the heart failure model group, whereas myocardial infarction was not observed in the normal control group. Immunohistochemistry and immunofluorescence demonstrated that nanog-positive cells were predominantly expressed in the vascular endothelium, with a few myocardial cells and stem cells in normal myocardium. The expression levels of c-kit and nanog in the myocardium of the rats with heart failure decreased significantly. c-kit-positive cells clustered together in the epicardium and its vicinity, and c-kit expression significantly decreased in the myocardium of rats with heart failure, as compared with normal rats. In both groups, some cells co-expressed both the c-kit and nanog genes. The RT-PCR results demonstrated that the expression levels of the two genes in the heart failure model group were significantly lower compared with those in the normal control group (P<0.05). In conclusion, the c-kit- and nanog-positive stem cells decreased in the myocardium of the rats with left ventricular remodelling induced by ADR. Their abnormal expression was significantly correlated with left ventricular remodelling, thereby indicating an internal association (influences of two indexes in the experimental group and control group) between them.

No MeSH data available.


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(A) Staining with DAPI and immunofluorescence staining of (B) nanog and (C) c-kit in the myocardial tissue samples of rats with heart failure. (D) Merged images of the stains. Magnification, ×400. Images are magnifications of positive regions. Arrows indicate positive expression cells which were scattered or in clusters.
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f5-etm-0-0-3522: (A) Staining with DAPI and immunofluorescence staining of (B) nanog and (C) c-kit in the myocardial tissue samples of rats with heart failure. (D) Merged images of the stains. Magnification, ×400. Images are magnifications of positive regions. Arrows indicate positive expression cells which were scattered or in clusters.

Mentions: Fluorescence microscopy revealed that in the myocardial tissue samples of the normal group nanog protein expression was increased, specifically in the cardiomyocytes, vascular endothelium and small round cells. Cells with strong positive expression were unevenly distributed. Nanog-positive cells in the myocardial tissue samples of rats with heart failure were predominantly distributed in the subendocardial myocardium and subepicardial myocardium. The expression of nanog in the subendocardial myocardium and subepicardial myocardium was markedly lower compared with that of the normal myocardium, and its expression in the subendocardial myocardium was downregulated compared with that in the subepicardial myocardium (Fig. 4). The c-kit protein was predominantly expressed in small cells, which were often in clusters distributed in the myocardium rather than evenly distributed. c-kit-positive cells were predominantly located in the myocardium of the subepicardial myocardium. Compared with normal myocardial tissue, the number of c-kit-positive cells in the rats with heart failure was markedly reduced. c-kit fluorescence was not observed in cardiomyocytes and endothelial cells. Furthermore, a small number of cells co-expressed both the c-kit and nanog genes (Fig. 5).


Internal associations and dynamic expression of c-kit and nanog genes in ventricular remodelling induced by adriamycin
(A) Staining with DAPI and immunofluorescence staining of (B) nanog and (C) c-kit in the myocardial tissue samples of rats with heart failure. (D) Merged images of the stains. Magnification, ×400. Images are magnifications of positive regions. Arrows indicate positive expression cells which were scattered or in clusters.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998031&req=5

f5-etm-0-0-3522: (A) Staining with DAPI and immunofluorescence staining of (B) nanog and (C) c-kit in the myocardial tissue samples of rats with heart failure. (D) Merged images of the stains. Magnification, ×400. Images are magnifications of positive regions. Arrows indicate positive expression cells which were scattered or in clusters.
Mentions: Fluorescence microscopy revealed that in the myocardial tissue samples of the normal group nanog protein expression was increased, specifically in the cardiomyocytes, vascular endothelium and small round cells. Cells with strong positive expression were unevenly distributed. Nanog-positive cells in the myocardial tissue samples of rats with heart failure were predominantly distributed in the subendocardial myocardium and subepicardial myocardium. The expression of nanog in the subendocardial myocardium and subepicardial myocardium was markedly lower compared with that of the normal myocardium, and its expression in the subendocardial myocardium was downregulated compared with that in the subepicardial myocardium (Fig. 4). The c-kit protein was predominantly expressed in small cells, which were often in clusters distributed in the myocardium rather than evenly distributed. c-kit-positive cells were predominantly located in the myocardium of the subepicardial myocardium. Compared with normal myocardial tissue, the number of c-kit-positive cells in the rats with heart failure was markedly reduced. c-kit fluorescence was not observed in cardiomyocytes and endothelial cells. Furthermore, a small number of cells co-expressed both the c-kit and nanog genes (Fig. 5).

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the dynamic expression of the c-kit and nanog genes in rats with left ventricular remodelling induced by adriamycin (ADR), and explore its internal association and mechanism of action. Sprague-Dawley male rats were randomly divided into a normal control group and a heart failure model group. Heart failure was induced by a single intraperitoneal injection of ADR (4 mg/kg) weekly for six weeks. The normal control group was given the same amount of saline. At the eighth week, rat cardiac function was examined to demonstrate the formation of heart failure. The rat hearts were harvested frozen and sectioned, and the expression levels of the nanog and c-kit genes in the myocardial tissue samples were detected using immunohistochemistry, immunofluorescence and reverse transcription-polymerase chain reaction (RT-PCR). Hematoxylin and eosin staining demonstrated various pathological changes in the myocardial cells in the heart failure model group, whereas myocardial infarction was not observed in the normal control group. Immunohistochemistry and immunofluorescence demonstrated that nanog-positive cells were predominantly expressed in the vascular endothelium, with a few myocardial cells and stem cells in normal myocardium. The expression levels of c-kit and nanog in the myocardium of the rats with heart failure decreased significantly. c-kit-positive cells clustered together in the epicardium and its vicinity, and c-kit expression significantly decreased in the myocardium of rats with heart failure, as compared with normal rats. In both groups, some cells co-expressed both the c-kit and nanog genes. The RT-PCR results demonstrated that the expression levels of the two genes in the heart failure model group were significantly lower compared with those in the normal control group (P<0.05). In conclusion, the c-kit- and nanog-positive stem cells decreased in the myocardium of the rats with left ventricular remodelling induced by ADR. Their abnormal expression was significantly correlated with left ventricular remodelling, thereby indicating an internal association (influences of two indexes in the experimental group and control group) between them.

No MeSH data available.


Related in: MedlinePlus