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造血生长因子通过趋化因子受体 CCR5 调节单核细胞进入成年大脑。

Hematopoietic Growth Factors Regulate the Entry of Monocytes into the Adult Brain via Chemokine Receptor CCR5.

机构信息

Department of Neurology, Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.

Department of Neurosurgery, The State University of New York Upstate Medical University, Syracuse, NY 13210, USA.

出版信息

Int J Mol Sci. 2024 Aug 15;25(16):8898. doi: 10.3390/ijms25168898.

Abstract

Monocytes are circulating macrophage precursors generated from bone marrow hematopoietic stem cells. In adults, monocytes continuously replenish cerebral border-associated macrophages under physiological conditions. Monocytes also rapidly infiltrate the brain in pathological settings. The mechanisms of recruiting monocyte-derived macrophages into the brain under pathological conditions have been extensively studied. However, it remains unclear how monocytes enter the brain to renew border-associated macrophages under physiological conditions. Using both in vitro and in vivo approaches, this study reveals that a combination of two hematopoietic growth factors, stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF), complementarily and synergistically enhances the adhesion of monocytes to cerebral endothelial cells in a dose-dependent manner. Cysteine-cysteine chemokine receptor 5 (CCR5) in brain endothelial cells, but not the cell adhesion molecules mediating neuroinflammation-related infiltration of monocyte-derived macrophages, modulates SCF+G-CSF-enhanced monocyte-endothelial cell adhesion. Blocking CCR5 or genetically deleting CCR5 reduces monocyte-endothelial cell adhesion induced by SCF+G-CSF. The SCF+G-CSF-enhanced recruitment of bone marrow-derived monocytes/macrophages into the cerebral perivascular space is also reduced in adult CCR5 knockout mice. This study demonstrates the role of SCF and G-CSF in regulating the entry of monocytes into the adult brain to replenish perivascular macrophages.

摘要

单核细胞是循环巨噬细胞前体,由骨髓造血干细胞生成。在成人中,单核细胞在生理条件下持续补充脑边缘相关巨噬细胞。单核细胞也在病理条件下迅速浸润大脑。单核细胞衍生的巨噬细胞在病理条件下招募到大脑中的机制已被广泛研究。然而,单核细胞如何在生理条件下进入大脑更新边缘相关巨噬细胞仍不清楚。本研究采用体外和体内方法,揭示了两种造血生长因子,干细胞因子(SCF)和粒细胞集落刺激因子(G-CSF)的组合,以剂量依赖性方式互补协同增强单核细胞与脑内皮细胞的黏附。脑内皮细胞中的半胱氨酸-半胱氨酸趋化因子受体 5(CCR5),而不是介导单核细胞衍生的巨噬细胞神经炎症相关浸润的细胞黏附分子,调节 SCF+G-CSF 增强的单核细胞-内皮细胞黏附。阻断 CCR5 或基因敲除 CCR5 可减少 SCF+G-CSF 诱导的单核细胞-内皮细胞黏附。SCF+G-CSF 增强的骨髓源性单核细胞/巨噬细胞招募到大脑血管周围间隙也减少了成年 CCR5 敲除小鼠。本研究证明了 SCF 和 G-CSF 在调节单核细胞进入成年大脑以补充血管周围巨噬细胞中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e4e/11354986/a7e09c81d4a8/ijms-25-08898-g001.jpg

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