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在小鼠皮肤伤口愈合过程中,progranulin通过与DNAJC3相互作用和上调来抑制纤维化

Shanshan Li¹, Jialin Liu¹, Jiamei Guo¹

¹Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu, China; Jiangsu Medical Engineering Research Center of Gene Detection, Xuzhou, Jiangsu, China.

Cellular signalling

|June 17, 2023

概括

进子素 (PGRN) 通过调高DNAJC3.3,在伤口愈合期间抑制皮肤纤维化. 这项研究阐明了PGRN减少纤维化基因表达的机制,为痕减少提供了洞察力.

科学领域:

皮肤病学和分子生物学
研究伤口愈合和痕形成的分子机制.

背景情况:

痕代表着一个重要的个人和社会负担.
之前的研究表明,降低的progranulin (PGRN) 水平在小鼠皮肤伤口愈合中促进纤维生成.
在纤维生成中PGRN作用的确切机制尚不清楚.

研究的目的:

阐明通过哪种分子机制的progranulin (PGRN) 在伤口修复过程中影响皮肤纤维化.
为了确定参与调节纤维化过程的PGRN下游目标.

主要方法:

使用小鼠皮肤伤口愈合模型.
在PGRN操纵后评估了益纤维基因 (αSMA,SRF,CTGF) 的表达.
采用生物信息学分析来预测PGRN下游目标.
使用分子生物学技术验证的相互作用和功能效应,包括敲击研究.

主要成果:

过度表达PGRN导致益肌基因的表达下降:α-平滑肌动蛋白 (αSMA),血清反应因子 (SRF) 和结缔组织生长因子 (CTGF).
生物信息学和实验数据确定DNAJC3 (Hsp40超级家族C3) 是由PGRN. upregulated的下游分子.
PGRN直接与DNAJC3.3相互作用并对其进行升级调节.
击败DNAJC3挽救了PGRN的抗纤维作用.

结论:

益格拉努林 (PGRN) 通过与DNAJC3.3相互作用和上调调节,在伤口愈合期间抑制皮肤纤维化.
这项研究为PGRN在皮肤伤口修复中抑制纤维生成的作用提供了机械解释.
PGRN-DNAJC3轴代表了减少痕形成的潜在治疗标.

关键词:

纤维化纤维化纤维化热冲击蛋白40超级家族C3 益格拉努林是一种Progranulin.血清反应因子的血清反应因子.皮肤伤口愈合的愈合

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