TY - JOUR
T1 - Beneficial effects of systemically administered human muse cells in adriamycin nephropathy
AU - Uchida, Nao
AU - Kushida, Yoshihiro
AU - Kitada, Masaaki
AU - Wakao, Shohei
AU - Kumagai, Naonori
AU - Kuroda, Yasumasa
AU - Kondo, Yoshiaki
AU - Hirohara, Yukari
AU - Kure, Shigeo
AU - Chazenbalk, Gregorio
AU - Dezawa, Mari
N1 - Publisher Copyright:
© 2017 by the American Society of Nephrology.
PY - 2017/10
Y1 - 2017/10
N2 - Multilineage-differentiating stress-enduring (Muse) cells are nontumorigenic endogenous pluripotent-like stem cells that can be collected from various organs. Intravenously administered Muse cells have been shown to spontaneously migrate to damaged tissue and replenish lost cells, but the effect in FSGS is unknown.We systemically administered human bonemarrow-derivedMuse cells without concurrent administration of immunosuppressants to severe combined immune-deficient (SCID) and BALB/c mouse models with adriamycin-induced FSGS (FSGSSCID and FSGS-BALB/c, respectively). In FSGS-SCID mice, human Muse cells preferentially integrated into the damaged glomeruli and spontaneously differentiated into cells expressing markers of podocytes (podocin; 31%), mesangial cells (megsin; 13%), and endothelial cells (CD31; 41%) without fusing to the host cells; attenuated glomerular sclerosis and interstitial fibrosis; and induced the recovery of creatinine clearance at 7 weeks. Human Muse cells induced similar effects in FSGS-BALB/c mice at 5 weeks, despite xenotransplant without concurrent immunosuppressant administration, and led to improvement in urine protein, creatinine clearance, and plasma creatinine levels more impressive than that in the FSGS-SCID mice at 5 weeks. However, functional recovery in FSGS-BALB/c mice was impaired at 7 weeks due to immunorejection, suggesting the importance of Muse cell survival asglomerular cells in theFSGSkidney for tissue repair andfunctional recovery. In conclusion,Musecells are unique reparative stem cells that preferentially home to damaged glomeruli and spontaneously differentiate into glomerular cells after systemic administration. Introductionofgenes toinducedifferentiation is not requiredbefore Muse cell administration; thus, Muse cells may be a feasible therapeutic strategy in FSGS.
AB - Multilineage-differentiating stress-enduring (Muse) cells are nontumorigenic endogenous pluripotent-like stem cells that can be collected from various organs. Intravenously administered Muse cells have been shown to spontaneously migrate to damaged tissue and replenish lost cells, but the effect in FSGS is unknown.We systemically administered human bonemarrow-derivedMuse cells without concurrent administration of immunosuppressants to severe combined immune-deficient (SCID) and BALB/c mouse models with adriamycin-induced FSGS (FSGSSCID and FSGS-BALB/c, respectively). In FSGS-SCID mice, human Muse cells preferentially integrated into the damaged glomeruli and spontaneously differentiated into cells expressing markers of podocytes (podocin; 31%), mesangial cells (megsin; 13%), and endothelial cells (CD31; 41%) without fusing to the host cells; attenuated glomerular sclerosis and interstitial fibrosis; and induced the recovery of creatinine clearance at 7 weeks. Human Muse cells induced similar effects in FSGS-BALB/c mice at 5 weeks, despite xenotransplant without concurrent immunosuppressant administration, and led to improvement in urine protein, creatinine clearance, and plasma creatinine levels more impressive than that in the FSGS-SCID mice at 5 weeks. However, functional recovery in FSGS-BALB/c mice was impaired at 7 weeks due to immunorejection, suggesting the importance of Muse cell survival asglomerular cells in theFSGSkidney for tissue repair andfunctional recovery. In conclusion,Musecells are unique reparative stem cells that preferentially home to damaged glomeruli and spontaneously differentiate into glomerular cells after systemic administration. Introductionofgenes toinducedifferentiation is not requiredbefore Muse cell administration; thus, Muse cells may be a feasible therapeutic strategy in FSGS.
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U2 - 10.1681/ASN.2016070775
DO - 10.1681/ASN.2016070775
M3 - Article
C2 - 28674043
AN - SCOPUS:85030478810
SN - 1046-6673
VL - 28
SP - 2946
EP - 2960
JO - Journal of the American Society of Nephrology
JF - Journal of the American Society of Nephrology
IS - 10
ER -