Stromal cell-derived factor-1 (SDF1)-dependent recruitment of bonemarrow-derived renal endothelium-like cells in a mouse model of acute kidneyinjury

Journal of Veterinary Medical Science

Takashi KATO¹  Hiroyuki OHNISHI¹  Yoko MIZUNO-HORIKAWA¹  Shinya MIZUNO¹ 

[1] Department of Biochemistry, Osaka University Graduate School of Medicine, 2�?2 Yamadaoka, Suita 565�?0871, Japan

关键词: acute kidney injury;    bone marrow-derived cell;    chemokine (C-X-C motif) receptor-4;    endothelial cell;    stromal cell-derived factor-1;   

DOI  :  10.1292/jvms.14-0562

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

References(33)Ischemic acute kidney injury (AKI) is the most key pathological event for acceleratingprogression to chronic kidney disease through vascular endothelial injury or dysfunction.Thus, it is critical to elucidate the molecular mechanism of endothelial protection andregeneration. Emerging evidence indicates that bone marrow-derived cells (BMCs) contributeto tissue reconstitution in several types of organs post-injury, but little is knownwhether and how BMCs contribute to renal endothelial reconstitution, especially in anearly-stage of AKI. Using a mouse model of ischemic AKI, we provide evidence thatincorporation of BMCs in vascular components (such as endothelial and smooth muscle cells)becomes evident within four days after renal ischemia and reperfusion, associated with anincrease in stromal cell-derived factor-1 (SDF1) in endothelium and that inCXCR4/SDF1-receptor in BMCs. Notably, anti-CXCR4 antibody decreased the numbers ofinfiltrated BMCs and BMC-derived endothelium-like cells, but not of BMC-derived smoothmuscle cell-like cells. These results suggest that reconstitution of renal endotheliumpost-ischemia partially depends on a paracrine loop of SDF1-CXCR4 between residentendothelium and BMCs. Such a chemokine ligand-receptor system may be attributable forselecting a cellular lineage (s), required for renal vascular protection, repair andhomeostasis, even in an earlier phase of AKI.

【 授权许可】

Unknown