Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Am+Soc+Nephrol 2015 ; 26 (9): 2139-51 Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Heme Oxygenase-1 Regulates Myeloid Cell Trafficking in AKI #MMPMID25677389
Hull TD; Kamal AI; Boddu R; Bolisetty S; Guo L; Tisher CC; Rangarajan S; Chen B; Curtis LM; George JF; Agarwal A
J Am Soc Nephrol 2015[Sep]; 26 (9): 2139-51 PMID25677389show ga
Renal ischemia-reperfusion injury is mediated by a complex cascade of events, including the immune response, that occur secondary to injury to renal epithelial cells. We tested the hypothesis that heme oxygenase-1 (HO-1) expression, which is protective in ischemia-reperfusion injury, regulates trafficking of myeloid-derived immune cells in the kidney. Age-matched male wild-type (HO-1+/+), HO-1?knockout (HO-1?/?), and humanized HO-1?overexpressing (HBAC) mice underwent bilateral renal ischemia for 10 minutes. Ischemia-reperfusion injury resulted in significantly worse renal structure and function and increased mortality in HO-1?/? mice. In addition, there were more macrophages (CD45+ CD11bhiF4/80lo) and neutrophils (CD45+ CD11bhi MHCII? Gr-1hi) in HO-1?/? kidneys than in sham and HO-1+/+ control kidneys subjected to ischemia-reperfusion. However, ischemic injury resulted in a significant decrease in the intrarenal resident dendritic cell (DC; CD45+MHCII+CD11bloF4/80hi) population in HO-1?/? kidneys compared with controls. Syngeneic transplant experiments utilizing green fluorescent protein?positive HO-1+/+ or HO-1?/? donor kidneys and green fluorescent protein?negative HO-1+/+ recipients confirmed increased migration of the resident DC population from HO-1?/? donor kidneys, compared to HO-1+/+ donor kidneys, to the peripheral lymphoid organs. This effect on renal DC migration was corroborated in myeloid-specific HO-1?/? mice subjected to bilateral ischemia. These mice also displayed impaired renal recovery and increased fibrosis at day 7 after injury. These results highlight an important role for HO-1 in orchestrating the trafficking of myeloid cells in AKI, which may represent a key pathway for therapeutic intervention.
free
free
free
J+Am+Soc+Nephrol 2015 ; 26 (9): 2139-51
