纤维细胞增强肥胖的乳腺纤维化
Genevra Kuziel1, Brittney N Moore2, Grace P Haugstad2
1Cancer Biology Program, University of Wisconsin-Madison, Madison, Wisconsin, USA.
概括
肥胖通过增加纤维细胞,一种免疫细胞,促进乳腺纤维化. 降低化学因子受体2型 (CCR2) 信号降低纤维化,这表明肥胖相关的乳腺癌的治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
背景情况:
- 肥胖与乳腺癌风险增加有关.
- 肥胖的乳腺脂肪表现出慢性炎症和纤维化.
- 乳腺纤维化可能会增加与肥胖相关的乳腺癌风险.
研究的目的:
- 为了研究肥胖引起的炎症如何驱动乳腺组织纤维化.
- 为了确定参与肥胖相关乳腺纤维化的免疫细胞群.
主要方法:
- 利用高脂肪饮食模型在小鼠中诱导肥胖.
- 研究了化学基因受体2型 (CCR2) 信号在免疫细胞招募和纤维化中的作用.
- 分析了免疫细胞种群,纤维细胞殖民地形成和基因表达.
主要成果:
- 肥胖增加了乳腺脂肪中的CD11b+细胞,与纤维细胞一致.
- 在CCR2-null小鼠中,乳腺纤维化和纤维细胞形成减少.
- 骨髓原生细胞的移植增加了肥胖CCR2-零小鼠的肌纤维细胞形成.
- 肥胖的骨髓原生细胞被丰富为参与原合成和细胞外矩阵重塑的基因.
结论:
- 肥胖会增加纤维细胞向乳腺的招募.
- 纤维细胞在乳腺组织中促进肥胖引起的纤维化.
- 向纤维细胞或CCR2信号可能提供一种降低与肥胖相关的乳腺癌风险的策略.
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