A Functional Comparison of Treatment of Intrinsic Sphincter Deficiency with Muscle-Derived and Adipose Tissue-Derived Stem Cells.

This study investigated the effect of muscle-derived stem cells (MDSCs) and adipose tissue-derived stem cells (ADSCs) in the treatment of stress urinary incontinence (SUI) and their differences in a rat model. MDSCs and ADSC were isolated from rats (n = 10), examined for their properties, and labeled with enhanced green fluorescent protein (EGFP) and ß-galactosidase (ß-gal) gene. Rats received bladder-neck and transurethral sphincter injection of EGFP-labeled MDSCs and ß-gal gene-labeled ADSC and injection of D-Hanks as a control (n = 24 each group). At 0, 15, 30, and 60 days after cells injection, urinary voiding function was assessed by urine dynamics detector. The rats were killed to harvest their urethras for tracking of MDSCs and ADSC. Western blotting and quantitative real-time reverse transcription PCR (qRT-PCR) was performed to detect smooth muscle contents. Urodynamic test showed that MDSCs and ADSC improved the function of urination in rats with intrinsic sphincter deficiency (ISD), and effect of MDSCs-treatment was more pronounced. In addition, histologic analysis showed that the MDSCs and ADSC-treated groups had significantly higher myosin and α-smooth muscle actin (α-SMA) content than the control group. Compared with ADSC-treated groups, the MDSCs-treated groups in myosin and α-SMA content showed the tendency of increase. In summary, MDSCs and ADSCs have obvious effects in the treatment and/or prevention of ISD and transplantation of MDSCs is more effective than ADSC. © 2018 IUBMB Life, 70(10):976-984, 2018.

The effect of a gene associated with retinoid-interferon-induced mortality 19 (GRIM-19) on STAT3-induced gene expression in renal carcinoma.

This study aimed to investigate the exact regulatory mechanisms of retinoid-interferon-induced mortality 19 (GRIM-19) in renal carcinoma. Tumour tissue samples from patients with renal carcinoma (n = 30, there were seven cases of Stage I, eight cases of Stage II, eight cases of Stage III, seven cases of Stage IV) and control subjects were selected from adjacent normal tissue (n = 10). Real-time quantitative PCR and western blotting were used to assess the level of GRIM-19, signal transducer and activator of transcription-3 (STAT3) and its downstream molecules. CD31 was detected by immunohistochemistry. The MTT assay was used to measure cell proliferation. The amount of apoptosis cells was analysed by Flow cytometry. The results showed that expression of GRIM-19 was decreased in renal carcinoma. However, in tumour tissue, STAT3 and its downstream signalling molecules showed the higher expression compared with control. Overexpression of GRIM-19, inhibited tumour growth apoptosis by mediating activators of STAT3 signal. In addition, interferon-ß and all-trans-retinoic acid inhibited the renal carcinoma cell growth and induced apoptosis, and effect of drug combinations was particularly evident. In conclusion, GRIM-19 expression is associated with hyperactivation of STAT3-induced gene expression in renal carcinoma.