Retracted: miR‐124a enhances therapeutic effects of bone marrow stromal cells transplant on diabetic nephropathy‐related epithelial‐to‐mesenchymal transition and fibrosis

Abstract

Background Epithelial‐to‐mesenchymal transition (EMT) has been gradually considered as one of the major pathways that causes the production of interstitial myofibroblasts in diseased kidneys. Materials and Methods The study was done to investigate the effect of a bone marrow stromal cell (BMSCs) transplant on rat podocytes and diabetic nephropathy (DN) rats in high‐glucose concentration, and to explore the effect of miR‐124a on BMSC therapy. High glucose–injured podocytes and streptozotocin‐induced DN rats have been respectively used as injury models in in vitro and in vivo studies. Podocyte viability was measured using the Cell Counting Kit‐8 assay. Renal pathological examination was observed by HE staining and Masson staining. The messenger RNA and protein levels were determined via real‐time polymerase chain reaction and Western blotting, respectively. Results By mediating the activation of caveolin‐1 (cav‐1) and β‐catenin and affecting the expression levels of EMT biomarkers including p‐cadherin, synaptopodin, fibroblast‐specific protein‐1, α‐smooth muscle actin and snail, our in vitro study confirmed that miR‐124a played a significant role in the treatment of high glucose–induced podocyte injury by BMSCs. The therapeutic effects of the BMSC transplant on DN rats were also proved to be further enhanced by miR‐124a overexpression in BMSCs, and such a phenomenon was accompanied by the improvement of renal fibrosis and mitigation of DN‐related kidney impairment. Regulation of fibronectin, collagen1, and EMT‐related proteins was closely implicated with the mechanism, and the activation of cav‐1 and β‐catenin was also possibly involved. Conclusion The study demonstrated the pivotal effect of miR‐124a on BMSC therapy for DN rats via mitigating EMT and fibrosis. Our results provide a novel insight into how therapeutic effects of BMSCs can be improved at the posttranscriptional level.

Stem/progenitor cell in kidney: characteristics, homing, coordination, and maintenance

“…HSC transplantation is effective in autoimmune disease [27][28][29], and also greatly improves renal function in autoimmune nephropathy such as IgA nephropathy [30,31], focal segmental glomerulosclerosis (FSGS) [32], and crescentic glomerulonephritis [33], by eradicating autoreactive immune cells and regenerating a naive, selftolerant immune system [34]. A large body of evidences indicate a great of potential therapeutic effects of BMSCs on AKI [35][36][37], CKD [37,38], FSGS [39,40], diabetic nephropathy [41][42][43], renovascular disease [44], lupus nephritis [45,46], polycystic kidney disease [47], and others [48][49][50][51]. Studies have also shown that EPCs contribute to endothelial repair in IRI-induced kidney [52,53] and restore the microvasculature, hemodynamics, and renal function in the stenotic kidney [54][55][56].…”

A novel lncRNA LNC_000052 leads to the dysfunction of osteoporotic BMSCs via the miR-96-5p–PIK3R1 axis

“…To examine the therapeutic effects of RNA-modified BMSCs, OVX rats were intravenously injected with BMSCs. This method has been widely applied both in the lab and in clinical trails benefiting from BMSCs’ homing capacity to injured tissues 6 , 45 . However, the migration and homing of BMSCs are affected by various factors, such as chemokines, mechanical stress, microgravity, and the first-pass retention in some tissues 4 , 46 .…”

Ginsenoside Rg1 Alleviates Podocyte Injury Induced by Hyperlipidemia via Targeting the mTOR/NF‐κB/NLRP3 Axis

“…The suitably treated cells were then incubated for an additional 2 h with cell-counting kit-8 (CCK-8, KeyGEN BioTECH, Nanjing, China) solution (10 µ L/well), and the optical density of each well was measured at 450 nm. A decrease in cell viability to 30–40% was indicative of podocyte injury [ 29 , 30 ].…”