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来自类细胞的小细胞外囊泡通过触发纤维细胞自来延缓糖尿病伤口愈合

Xiaosi Hong^1,2, Leiqin Cai^1,2, Lanlan Li^1,2

¹Department of Endocrinology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Archives of physiology and biochemistry

|June 3, 2024

概括

高葡萄糖基氨酸细胞中的小细胞外囊 (sEV) 通过运输LINC01435.35来阻碍糖尿病伤口愈合. 这种分子激活纤维细胞自,并减少原蛋白,阻碍修复.

科学领域:

细胞生物学细胞生物学
生物医学科学生物医学科学
伤口治愈研究研究伤口治愈研究

背景情况:

糖尿病的伤口愈合受到状细胞和纤维细胞功能障碍的影响.
小型细胞外囊泡 (sEVs) 介导细胞间通信和疾病的发病.
皮细胞衍生的sEVs可能会影响糖尿病伤口愈合过程.

研究的目的:

调查sEVs在糖尿病伤口愈合过程中角质细胞和纤维细胞之间的通信中的作用.
在糖尿病的背景下,阐明状细胞衍生的sEVs影响纤维细胞功能的特定机制.

主要方法:

用高葡萄糖皮细胞衍生的sEVs (HaCaT-HG-sEV) 对纤维细胞进行治疗,并操纵LINC01435水平.
评估纤维细胞原水平,迁移和自.
在体内研究使用糖尿病小鼠模型与HaCaT-HG-sEV治疗.

主要成果:

HaCaT-HG-sEV治疗和LINC01435过度表达减少了纤维细胞原蛋白和迁移,但增加了自.
自抑制抵消了由LINC01435.35诱导的纤维细胞原水平的下降.
在糖尿病小鼠中,HaCaT-HG-sEV治疗减少了伤口原蛋白和增加了自标志物 (Beclin-1,LC3),延迟了愈合.

结论:

在皮细胞衍生的sEV中,LINC01435促进纤维细胞自并抑制原蛋白合成.
这一过程会损害纤维细胞的功能,导致糖尿病伤口愈合延迟.
针对这种sEV介导的途径为糖尿病伤口提供了潜在的治疗策略.

关键词:

自自是一种自的过程.糖尿病伤口愈合的治疗方法林克拉纳林克拉纳小小的细胞外囊泡.

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