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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+Cell+Mol+Med
2017 ; 21
(7
): 1420-1430
Nephropedia Template TP
gab.com Text
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English Wikipedia
Human adipose stromal cell therapy improves survival and reduces renal
inflammation and capillary rarefaction in acute kidney injury
#MMPMID28455887
Collett JA
; Traktuev DO
; Mehrotra P
; Crone A
; Merfeld-Clauss S
; March KL
; Basile DP
J Cell Mol Med
2017[Jul]; 21
(7
): 1420-1430
PMID28455887
show ga
Damage to endothelial cells contributes to acute kidney injury (AKI) by causing
impaired perfusion, while the permanent loss of the capillary network following
AKI has been suggested to promote chronic kidney disease. Therefore, strategies
to protect renal vasculature may impact both short-term recovery and long-term
functional preservation post-AKI. Human adipose stromal cells (hASCs) possess
pro-angiogenic and anti-inflammatory properties and therefore have been tested as
a therapeutic agent to treat ischaemic conditions. This study evaluated hASC
potential to facilitate recovery from AKI with specific attention to capillary
preservation and inflammation. Male Sprague Dawley rats were subjected to
bilateral ischaemia/reperfusion and allowed to recover for either two or seven
days. At the time of reperfusion, hASCs or vehicle was injected into the
suprarenal abdominal aorta. hASC-treated rats had significantly greater survival
compared to vehicle-treated rats (88.7% versus 69.3%). hASC treatment showed
hastened recovery as demonstrated by lower creatinine levels at 48 hrs, while
tubular damage was significantly reduced at 48 hrs. hASC treatment resulted in a
significant decrease in total T cell and Th17 cell infiltration into injured
kidneys at 2 days post-AKI, but an increase in accumulation of regulatory T
cells. By day 7, hASC-treated rats showed significantly attenuated capillary
rarefaction in the cortex (15% versus 5%) and outer medulla (36% versus 18%)
compared to vehicle-treated rats as well as reduced accumulation of interstitial
alpha-smooth muscle actin-positive myofibroblasts. These results suggest for the
first time that hASCs improve recovery from I/R-induced injury by mechanisms that
contribute to decrease in inflammation and preservation of peritubular
capillaries.