Suppr超能文献

miR-183-3p 通过抑制 GAB1 抑制银屑病角质形成细胞的增殖和迁移。

miR-183-3p suppresses proliferation and migration of keratinocyte in psoriasis by inhibiting GAB1.

机构信息

Department of Dermatology, Affiliated Hospital of North Sichuan Medical College, No. 1, Maoyuan South Road, Nanchong City, 637000, Sichuan Province, China.

出版信息

Hereditas. 2020 Jul 10;157(1):28. doi: 10.1186/s41065-020-00138-w.

Abstract

BACKGROUND

MicroRNAs (miRNAs) target genes involved in the hyperproliferation of keratinocytes or immune dysfunction of psoriasis. This study prospectively determined the involvement of miR-183-3p in the pathogenesis of psoriasis.

METHODS

Differentially expressed miR-183-3p between psoriatic lesional and non-lesional skin were determined by quantitative RT-PCR and in situ hybridization (ISH). CCK8 and wound healing assays were performed to assess cell viability and migration of human keratinocyte cell line (HaCaT). The target of miR-183-3p was validated by luciferase activity assay.

RESULTS

Lower miR-183-3p expression was observed in psoriatic lesional skin compared to psoriatic non-lesional skin. MiR-183-3p over-expression inhibited the viability and migration of HaCaT cells, while inhibition of miR-183-3p promoted the viability and migration of HaCaT cells. Moreover, miR-183-3p could bind to the 3' UTR of GAB1 (growth factor receptor binding 2-associated binding protein 1) and decrease the mRNA and protein expression of GAB1 in HaCaT cells. In addition, higher GAB1 expression was observed in psoriatic lesional skin than psoriatic non-lesional skin.

CONCLUSION

MiR-183-3p exhibited inhibition property in the proliferation and migration of HaCaT cells via down-regulation of GAB1, suggesting the potential therapeutic strategy for psoriasis.

摘要

背景

MicroRNAs (miRNAs) 靶向参与角质形成细胞过度增殖或银屑病免疫功能障碍的基因。本研究前瞻性确定 miR-183-3p 在银屑病发病机制中的作用。

方法

通过定量 RT-PCR 和原位杂交 (ISH) 确定银屑病病变和非病变皮肤之间差异表达的 miR-183-3p。CCK8 和划痕愈合实验评估人角质形成细胞系 (HaCaT) 的细胞活力和迁移。通过荧光素酶活性测定验证 miR-183-3p 的靶标。

结果

与银屑病非病变皮肤相比,银屑病病变皮肤中 miR-183-3p 的表达较低。miR-183-3p 过表达抑制 HaCaT 细胞的活力和迁移,而抑制 miR-183-3p 则促进 HaCaT 细胞的活力和迁移。此外,miR-183-3p 可以与 GAB1(生长因子受体结合 2 相关结合蛋白 1)的 3'UTR 结合并降低 HaCaT 细胞中 GAB1 的 mRNA 和蛋白表达。此外,与银屑病非病变皮肤相比,银屑病病变皮肤中 GAB1 的表达更高。

结论

miR-183-3p 通过下调 GAB1 表现出对 HaCaT 细胞增殖和迁移的抑制作用,提示其可能成为银屑病的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca7/7353791/a4061f52db4a/41065_2020_138_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验