title: Therapeutic effects of human amniotic fluid-derived stem cells on renal interstitial fibrosis in a murine model of unilateral ureteral obstruction.
abstract: Interstitial fibrosis is regarded as the main pathway for the progression of chronic kidney disease (CKD) and is often associated with severe renal dysfunction. Stem cell-based therapies may provide alternative approaches for the treatment of CKD. Human amniotic fluid-derived stem cells (hAFSCs) are a novel stem cell population, which exhibit both embryonic and mesenchymal stem cell characteristics. Herein, the present study investigated whether the transplantation of hAFSCs into renal tissues could improve renal interstitial fibrosis in a murine model of unilateral ureteral obstruction (UUO). We showed that hAFSCs provided a protective effect and alleviated interstitial fibrosis as reflected by an increase in microvascular density; additionally, hAFSCs treatment beneficially modulated protein levels of vascular endothelial growth factor (VEGF), hypoxia inducible factor-1α (HIF-1α) and transforming growth factor-β1 (TGF-β1). Therefore, we hypothesize that hAFSCs could represent an alternative, readily available source of stem cells that can be applied for the treatment of renal interstitial fibrosis.
authors.affiliation: Department of Nephrology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, PR China. sundong126@yahoo.com
authors.forename: Dong
authors.initials: D
authors.lastname: Sun
authors.forename: Lin
authors.initials: L
authors.lastname: Bu
authors.forename: Caixia
authors.initials: C
authors.lastname: Liu
authors.forename: Zhongcheng
authors.initials: Z
authors.lastname: Yin
authors.forename: Xudong
authors.initials: X
authors.lastname: Zhou
authors.forename: Xiaoju
authors.initials: X
authors.lastname: Li
authors.forename: Aiguo
authors.initials: A
authors.lastname: Xiao
mesh_terms: D000653:Amniotic Fluid / Q000166:cytology*; D000818:Animals; D017209:Apoptosis; D015820:Cadherins / Q000378:metabolism; D002196:Capillaries / Q000473:pathology; D049109:Cell Proliferation; D048430:Cell Shape; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D024042:Collagen Type I / Q000378:metabolism; D004195:Disease Models, Animal; D005355:Fibrosis; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000378:metabolism; D007674:Kidney Diseases / Q000150:complications* / Q000473:pathology / Q000628:therapy*; D007684:Kidney Tubules / Q000098:blood supply / Q000473:pathology; D051379:Mice; D010641:Phenotype; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000166:cytology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014517:Ureteral Obstruction / Q000150:complications* / Q000473:pathology / Q000628:therapy*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D015820:Cadherins; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D024042:Collagen Type I; C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D019394:Ki-67 Antigen; D018809:Proliferating Cell Nuclear Antigen; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A