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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Vet+Med+Sci
2015 ; 77
(3
): 313-9
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Stromal cell-derived factor-1 (SDF1)-dependent recruitment of bone marrow-derived
renal endothelium-like cells in a mouse model of acute kidney injury
#MMPMID25833353
Ohnishi H
; Mizuno S
; Mizuno-Horikawa Y
; Kato T
J Vet Med Sci
2015[Mar]; 77
(3
): 313-9
PMID25833353
show ga
Ischemic acute kidney injury (AKI) is the most key pathological event for
accelerating progression to chronic kidney disease through vascular endothelial
injury or dysfunction. Thus, it is critical to elucidate the molecular mechanism
of endothelial protection and regeneration. Emerging evidence indicates that bone
marrow-derived cells (BMCs) contribute to tissue reconstitution in several types
of organs post-injury, but little is known whether and how BMCs contribute to
renal endothelial reconstitution, especially in an early-stage of AKI. Using a
mouse model of ischemic AKI, we provide evidence that incorporation of BMCs in
vascular components (such as endothelial and smooth muscle cells) becomes evident
within four days after renal ischemia and reperfusion, associated with an
increase in stromal cell-derived factor-1 (SDF1) in endothelium and that in
CXCR4/SDF1-receptor in BMCs. Notably, anti-CXCR4 antibody decreased the numbers
of infiltrated BMCs and BMC-derived endothelium-like cells, but not of
BMC-derived smooth muscle cell-like cells. These results suggest that
reconstitution of renal endothelium post-ischemia partially depends on a
paracrine loop of SDF1-CXCR4 between resident endothelium and BMCs. Such a
chemokine ligand-receptor system may be attributable for selecting a cellular
lineage (s), required for renal vascular protection, repair and homeostasis, even
in an earlier phase of AKI.