LincRNA-EPS通过诱导CCND1促进老年皮肤纤维细胞的增殖
Liping Zhang1, Iris C Wang1,2, Songmei Meng1
1Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
International journal of molecular sciences
|July 27, 2024
概括
在老皮肤细胞中减少长跨基因非编码RNA (lincRNA) -EPS会损害愈合. 恢复lincRNA-EPS促进细胞分裂和Cyclin D1,为伤口修复提供潜在的治疗点.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 皮肤病学 皮肤病学
背景情况:
- 衰老会改变皮肤纤维细胞的功能,影响皮肤的伤口愈合.
- 衰老的皮肤纤维细胞的特征是细胞增殖减少.
- 长跨基因非编码RNAs (lincRNAs),特别是LincRNA-EPS在老化纤维细胞中的作用尚不清楚.
研究的目的:
- 研究LincRNA-EPS在老化皮肤纤维细胞中的作用.
- 确定LincRNA-EPS对细胞循环调节器Cyclin D1 (CCND1) 和细胞增殖的影响.
- 探索LincRNA-EPS作为与年龄相关的皮肤伤口愈合的治疗点的潜力.
主要方法:
- 从年轻和老年小鼠中分离出初级皮肤纤维细胞.
- 使用等离子体转染,LincRNA-EPS被过度表达.
- 通过MTT测定来评估细胞增殖,并使用实时PCR量化基因表达.
主要成果:
- 老化皮肤纤维细胞显示LincRNA-EPS表达减少,CCND1水平降低,并减少了增殖.
- 在老化纤维细胞中LincRNA-EPS的过度表达上调了CCND1并显著增加了细胞增殖.
- LincRNA-EPS通过隔离miR-34a并准CCND1.1,促进CCND1的表达.
结论:
- LincRNA-EPS对于调节CCND1和促进老年皮肤纤维细胞增殖至关重要.
- 减少的LincRNA-EPS有助于老年皮肤中受损的伤口愈合.
- LincRNA-EPS是改善与年龄相关的皮肤伤口愈合的有希望的治疗点.
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