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首页> 外文期刊>American Journal of Physiology >Long non-coding RNA HOXA11-AS induces type I collagen synthesis to stimulate keloid formation via sponging miR-124-3p and activation of Smad5 signaling
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Long non-coding RNA HOXA11-AS induces type I collagen synthesis to stimulate keloid formation via sponging miR-124-3p and activation of Smad5 signaling

机译:长期非编码RNA HOXA11--如诱导I型I型胶原合成,通过冲水MIR-124-3P刺激瘢痕疙瘩形成和SMAD5信号传导的激活

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摘要

Keloid, characterized by exuberant collagen deposition and invasive growth beyond original wound margins, results from abnormal wound healing. A recent microarray analysis identified homeobox (HOX) All antisense (HOXAII-AS) as a keloid-specific long non-coding RNA, although its potential role in keloid formation remains elusive. In this study, hematoxylin-eosin, Masson, and immunohistochemical staining of type I collagen (Coll) revealed abnormal arrangement and hyperplasia of fibers in keloid tissues along with increased Coll level. qRT-PCR and Western blot showed that HOXA11-AS and Coll were significantly upregulated, while miR-124-3p was decreased in both keloid tissues and human keloid fibroblasts (HKFs). Knockdown of HOXA11-AS inhibited cell proliferation (by CCK-8 and immunoflu-orescence staining of Ki67) and cell migration (by wound healing and transwell assays).
机译:瘢痕疙瘩,其特征在于较旺克胶原沉积和超越原始伤口边缘的侵袭性生长,从异常伤口愈合产生。 最近的微阵列分析鉴定了Homeobox(Hox)所有反义(Hoxaii-As)作为瘢痕疙瘩特异性的长非编码RNA,尽管其在瘢痕疙瘩形成中的潜在作用仍然是难以捉摸的。 在本研究中,I型胶原蛋白(Coll)的血毒素 - 曙红,Masson和免疫组织化学染色揭示了瘢痕疙瘩组织中的纤维的异常布置和增生,以及增加的电压水平。 QRT-PCR和Western印迹显示出显着上调Hoxa11-AS和Coll,而MiR-124-3P在瘢痕疙瘩组织和人瘢蛋白成纤维细胞(HKF)中降低。 Hoxa11的敲低 - 作为抑制细胞增殖(通过CCK-8和Ki67的免疫雾染色)和细胞迁移(通过伤口愈合和转发测定)。

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