Cardiac Hypertrophy is Positively Regulated by MicroRNA‑24 in Rats / 中华医学杂志(英文版)

<p><b>Background</b>MicroRNA-24 (miR-24) plays an important role in heart failure by reducing the efficiency of myocardial excitation-contraction coupling. Prolonged cardiac hypertrophy may lead to heart failure, but little is known about the role of miR-24 in cardiac hypertrophy. This study aimed to preliminarily investigate the function of miR-24 and its mechanisms in cardiac hypertrophy.</p><p><b>Methods</b>Twelve Sprague-Dawley rats with a body weight of 50 ± 5 g were recruited and randomly divided into two groups: a transverse aortic constriction (TAC) group and a sham surgery group. Hypertrophy index was measured and calculated by echocardiography and hematoxylin and eosin staining. TargetScans algorithm-based prediction was used to search for the targets of miR-24, which was subsequently confirmed by a real-time polymerase chain reaction and luciferase assay. Immunofluorescence labeling was used to measure the cell surface area, and H-leucine incorporation was used to detect the synthesis of total protein in neonatal rat cardiac myocytes (NRCMs) with the overexpression of miR-24. In addition, flow cytometry was performed to observe the alteration in the cell cycle. Statistical analysis was carried out with GraphPad Prism v5.0 and SPSS 19.0. A two-sided P < 0.05 was considered as the threshold for significance.</p><p><b>Results</b>The expression of miR-24 was abnormally increased in TAC rat cardiac tissue (t = -2.938, P < 0.05). TargetScans algorithm-based prediction demonstrated that CDKN1B (p27, Kip1), a cell cycle regulator, was a putative target of miR-24, and was confirmed by luciferase assay. The expression of p27 was decreased in TAC rat cardiac tissue (t = 2.896, P < 0.05). The overexpression of miR-24 in NRCMs led to the decreased expression of p27 (t = 4.400, P < 0.01), and decreased G0/G1 arrest in cell cycle and cardiomyocyte hypertrophy.</p><p><b>Conclusion</b>MiR-24 promotes cardiac hypertrophy partly by affecting the cell cycle through down-regulation of p27 expression.</p>

Proliferation of neural progenitor cells in the subventricular zone and around the hematoma after intracerebral hemorrhage in adult rat / 南方医科大学学报

<p><b>OBJECTIVE</b>To examine the proliferation of the neural progenitor cells in the subventricular zone (SVZ) and around the hematoma after intracerebral hemorrhage (ICH) in adult rats.</p><p><b>METHODS</b>ICH was induced by stereotactic injection of type VII collagenase into the corpus striatum of adult rats, followed by pulse or continuous intrapenitoneal injection of bromodeoxyuridine (Brdu) to label the proliferating cells. The rats were sacrificed on days 2, 7, 14 and 28 following the ICH for immunohistochemistry of the tissues in the SVZ and around the hemotoma to determine the number of Brdu- immunoreactive cells.</p><p><b>RESULTS</b>With pulse Brdu labeling, a significant increase in the number of Brdu-immunoreactive cells in the ipsilateral and contralateral tissues in the SVZ and around the hematoma was observed 2-14 days, and the cell number reached the maximum on day 7 after ICH as compared with that of the sham-operated group. With continuous Brdu injection, the increase was observed on day 14 after ICH, and till day 28, the Brdu-immunoreactive cells in the SVZ decreased to the control level, but some positive cells still persisted in the tissues around the hematoma.</p><p><b>CONCLUSION</b>ICH induces transient and regional increase in the cell proliferation in the ipilateral and contraletral SVZ and tissues around the hematoma, and the proliferating cells in the SVZ may migrate towards the hematoma area.</p>