矩阵刚度通过CXCL13调节脂肪细胞/巨细胞/内皮细胞通过CXCL13的三元通信
Arthur Choisez1, Seiichiro Ishihara2, Takuro Ishii3
1Department of Biosignals and Inheritance, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Division of Biomedical Engineering for Health and Welfare, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Japan.
Journal of lipid research
|August 16, 2024
概括
矩阵刚度会影响脂肪组织细胞. 软矩阵减少炎症,而硬矩阵增加炎症,通过CXCL13信号介导,提供对代谢疾病治疗的见解.
科学领域:
- 生物医学工程 生物医学工程
- 细胞生物学 细胞生物学
- 组织工程是组织工程.
背景情况:
- 脂肪组织重塑涉及脂肪细胞,巨细胞,内皮细胞和细胞外基质 (ECM).
- 炎症和纤维化会破坏脂肪组织的功能,并改变ECM的机械特性.
- 了解ECM细胞通信对于脂肪组织功能至关重要.
研究的目的:
- 为了研究矩阵刚度对脂肪组织成分细胞的影响.
- 探索硬性在脂肪组织中细胞间通信中的作用.
- 为了确定脂肪组织中机械传递的机制.
主要方法:
- 从C57BL/6J小鼠中分离出初级脂肪细胞,巨细胞和内皮细胞.
- 细胞被培养在不同硬度的基因交叉连接的原体凝上.
- 共同培养实验是为了评估细胞间的通信.
主要成果:
- 硬矩阵诱导炎症基因表达,而软矩阵促进所有细胞类型的抗炎症基因表达.
- 对脂肪细胞的度诱导的影响被传递给其他脂肪组织细胞.
- 硬质矩阵刺激脂肪细胞的CXCL13分泌,这是硬度传播的关键媒介.
结论:
- 矩阵刚度显著影响脂肪组织细胞的行为和通信.
- CXCL13调解脂肪细胞,巨细胞和内皮细胞之间的度诱导的通信.
- 控制矩阵刚度可能为代谢性疾病中的慢性炎症提供治疗策略.
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