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LncRNA MALAT1促进BM-MSCs分化为内皮细胞,并通过miR-206/CDC42/PAK1/paxillin信号轴改善勃起功能障碍

Longhua Luo¹, Zixin Wang¹, Xuxian Tong²

¹Jiangxi Provincial Key Laboratory of Urinary System Diseases, Department of Urology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Zheng Street, Nanchang, 330006, China.

Reproductive biology and endocrinology : RB&E

|June 25, 2024

概括

血管内皮生长因子 (VEGFA) 通过MALAT1/miR-206/CDC42通路促进骨髓衍生的中介质干细胞 (BM-MSC) 通过MALAT1/miR-206/CDC42通路分化为内皮细胞 (EC),改善勃起功能障碍 (ED). 这项研究揭示了MALAT1

科学领域:

再生医学是一种再生医学.
分子生物学分子生物学
泌尿器科泌尿器科泌尿器科泌尿器科

背景情况:

勃起功能障碍 (ED) 是一种普遍的疾病,发病率越来越高,治疗效果往往有限.
目前对ED的治疗策略在有效性和患者结果方面面临挑战.

研究的目的:

研究MALAT1在血管内皮生长因子 (VEGFA) 诱导的骨髓衍生中介质干细胞 (BM-MSCs) 转化为内皮细胞 (ECs) 中的作用.
阐明潜在的分子机制,包括miR-206/CDC42/PAK1/paxillin通路,参与BM-MSC差异化和随后的勃起功能改善.

主要方法:

对于BM-MSCs的VEGFA治疗,细胞迁移的Transwell测定,内皮细胞标志物表达的qRT-PCR和西部斑块 (vWF,VE-cadherin,eNOS).
使用si-MALAT1,CDC42和PAK1过度表达和蛋白质免疫沉来研究MALAT1-CDC42/PAK1/帕克西林通路.
路西法酶测定以确认MALAT1,miR-206和CDC42之间的相互作用.
在体内研究使用糖尿病引起的勃起功能障碍 (DMED) 鼠标模型来评估勃起功能 (ICP/MAP比) 和阴茎组织变化.

主要成果:

在VEGFA刺激下,MALAT1通过CDC42/PAK1/paxillin轴调节BM-MSC分化为EC.
与MALAT1或CDC42表达的干扰抑制了BM-MSC分化.
MALAT1与CDC42 3'-UTR在miR-206结合方面进行竞争,从而影响BM-MSC的分化.
与对照组相比,BM-MSC治疗在DMED大鼠模型中显著改善了勃起功能 (ICP/MAP比率).

结论:

MALAT1通过miR-206/CDC42/PAK1/paxillin通路促进BM-MSC分化为EC,为ED提供了一种新的治疗方法.
这些发现突显了MALAT1在BM-MSC介导的勃起功能修复中的关键作用,并为治疗DMED提供了机制性见解.

关键词:

在BM-MSCs中使用.糖尿病勃起功能障碍糖尿病勃起功能障碍马拉特语马拉特语在 miR-206/CDC42/PAK1/paxillin 信号通路中,我们可以看到

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Mesenchymal Stem Cells

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