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细胞外组织蛋白在小鼠血管光滑肌细胞中促进了依赖酸的化

Tomonori Hoshino^1,2, Davood Kharaghani^1,3, Shohei Kohno^1,4

¹Department of Calcified Tissue Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Journal of biochemistry

|February 1, 2024

概括

细胞外基因组通过促进细胞变化和增加DNA,使慢性病 (CKD) 的血管化恶化.

科学领域:

心血管研究研究心血管研究
腎臟病學 (nephrology) 是一種醫學.
细胞生物学细胞生物学

背景情况:

血管化是心血管事件的重要危险因素,特别是在慢性病 (CKD) 患者中.
这一过程涉及血管光滑肌细胞 (VSMCs) 转化为骨质母细胞类细胞.
与损伤相关的分子模式 (DAMPs),包括细胞外组织蛋白,都与化部位有关.

研究的目的:

为了研究细胞外组织素在血管化中的作用.
确定组织蛋白对VSMC分化和化的影响.
探索双链DNA (dsDNA) 在基因组介导血管化中的潜在参与.

主要方法:

评估了外部添加的组织蛋白对和无机酸盐诱导的化在小鼠VSMCs的影响.
测量了VSMC和骨质细胞标记基因的表达.
与用DNase I (降解dSDNA) 治疗的基因组相比,结石化与未经处理的基因组相比.
从CKD模型小鼠的血清中检测到dsDNA水平.

主要成果:

细胞外组织蛋白在VSMC中显著加剧了血管化.
基因组蛋白降低了VSMC标记基因表达和增加了骨质细胞标记基因表达.
基因组的DNase I处理减弱了化,这表明dSDNA参与.
在CKD模型小鼠中发现了高血清dsDNA水平.

结论:

细胞外组织蛋白促进血管化和VSMC骨质细胞转化.
双链DNA可能在基因素诱导的血管化中发挥关键作用.
细胞外组织蛋白是CKD相关的血管化中的潜在关键参与者.

关键词:

慢性脏疾病慢性脏疾病与损伤相关的分子模式.细胞外基因组的基因组.血管化血管化血管光滑肌肉细胞的细胞.

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