The Effect of Placental Mesenchymal Stem Cells on The Protection of Chronic Renal Failure: The Role of Adiponectin

Abstract

Chronic glomerular and tubulointerstitial fibrosis represents a major pathological process leading to end-stage renal failure. Mesenchymal stem cell (MSC) therapy has emerged as a promising approach for renal tissue repair. The identification of molecular markers associated with disease progression may contribute to the evaluation of therapeutic responses. Adiponectin has been suggested as a potential indicator in chronic kidney injury. The present study aimed to investigate adiponectin-related molecular changes following MSC therapy in a rat model of chronic renal injury. Mesenchymal stem cells were isolated from the amniotic membrane of term placentas. Chronic renal injury was induced in rats by subtotal (5/6) nephrectomy. MSCs were administered via the tail vein, and animals were evaluated at 15 and 30 days after transplantation. Protein and mRNA expression levels of adiponectin, adiponectin receptor 1, fibronectin, and phosphorylated AMP-activated protein kinase (AMPK) were assessed using Western blotting and real-time PCR. Serum and urinary adiponectin levels, as well as urinary albumin levels, were measured by rat-specific ELISA kits. Compared to control animals, nephrectomized rats exhibited increased expression levels of adiponectin, adiponectin receptor 1, fibronectin, and phosphorylated AMPK. Following MSC administration, these molecular alterations showed a declining trend. In parallel, urinary albumin levels were reduced in MSC-treated groups. The findings suggest that MSC therapy is associated with modulation of adiponectin-related molecular pathways in chronic renal injury. Adiponectin-associated changes may provide preliminary insight into molecular responses during disease progression; however, further studies are required to clarify its utility as a definitive biomarker.