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miRNA-122 的表达有助于 H9C2 心肌细胞的凋亡。

Expression of microRNA-122 contributes to apoptosis in H9C2 myocytes.

机构信息

Division of Cardiology, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China.

出版信息

J Cell Mol Med. 2012 Nov;16(11):2637-46. doi: 10.1111/j.1582-4934.2012.01577.x.

DOI:10.1111/j.1582-4934.2012.01577.x
PMID:22453009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4118232/
Abstract

The microRNAs (miRNAs) can post-transcriptionally regulate gene expression and heart development. The Pax-8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays demonstrated differential expression of microRNAs between Pax-8(-/-) and Pax-8(+/-) mice, confirmed by real-time PCR. The miR-122 was up-regulated by 1.92 folds in Pax-8(-/-) mice. There were ventricular septum defects in Pax-8(-/-) mice, and increased numbers of apoptotic cells in the left ventricular wall and interventricular septum in Pax-8(-/-) mice. In H9C2 myocytes, treatment with miR-122 mimics or miR-122 inhibitor affects the expression of CCK-8 and activity of Caspase-3. The miR-122 is up-regulated in the myocytes of Pax-8(-/-) mice and may participate in the apoptotic gene expression and pathogenesis of heart development defect.

摘要

微小 RNA（miRNAs）可以在后转录水平上调节基因表达和心脏发育。Pax-8 基因敲除小鼠具有明显的心脏异常。本研究探讨了 miRNAs 在调节心脏凋亡和发育中的作用在敲除小鼠中。miRNA 微阵列显示 Pax-8(-/-)和 Pax-8(+/-)小鼠之间存在 miRNAs 的差异表达，实时 PCR 证实了这一点。miR-122 在 Pax-8(-/-)小鼠中上调 1.92 倍。Pax-8(-/-)小鼠存在室间隔缺损，左心室壁和室间隔的凋亡细胞数量增加。在 H9C2 心肌细胞中，用 miR-122 模拟物或 miR-122 抑制剂处理会影响 CCK-8 的表达和 Caspase-3 的活性。miR-122 在 Pax-8(-/-)小鼠的心肌细胞中上调，可能参与凋亡基因表达和心脏发育缺陷的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/61af7f8a755c/jcmm0016-2637-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/0cb7960d97f9/jcmm0016-2637-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/97294fceeda2/jcmm0016-2637-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/ec394b8facbc/jcmm0016-2637-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/7b87db392ea8/jcmm0016-2637-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/b3dcbc3c6f98/jcmm0016-2637-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/970a1d921f56/jcmm0016-2637-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/fcbe67f8e460/jcmm0016-2637-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/61af7f8a755c/jcmm0016-2637-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/0cb7960d97f9/jcmm0016-2637-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/97294fceeda2/jcmm0016-2637-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/ec394b8facbc/jcmm0016-2637-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/7b87db392ea8/jcmm0016-2637-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/b3dcbc3c6f98/jcmm0016-2637-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/970a1d921f56/jcmm0016-2637-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/fcbe67f8e460/jcmm0016-2637-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820d/4118232/61af7f8a755c/jcmm0016-2637-f8.jpg

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