Int J Med Sci
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Autosomal dominant tubulointerstitial kidney disease due to UMOD mutations (ADTKD-UMOD) results in chronic interstitial nephritis, which gradually develops into end-stage renal disease. It is believed that the accumulation of mutant uromodulin causes the endoplasmic reticulum (ER) stress, then leads to the kidney damage. But the underlying mechanism remains unclear. ⋯ Moreover in vitro experiments, ER stress induced by tunicamycin (TM) not only significantly increased the expression of GRP78 and CHOP, but also caused the epithelial to myofibroblast transformation (EMT) of renal tubular epithelial cells, evidenced by decreased expression of E-cadherin and increased expression of vimentin, and extracellular matrix (ECM) deposition, evidenced by increased expression of fibronectin (FN). CHOP knockdown could restore the upregulation of vimentin and FN induced by TM. Thus, specific activation of CHOP in renal tubular epithelial cells induced by UMOD protein might be the key reason of renal interstitial fibrosis in ADTKD-UMOD patients.
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Objective: The study aims to evaluate long-term ovarian reserve change by serum anti-Mullerian hormone (AMH) level and determine the factors that affect the changes after laparoscopic endometrioma cystectomy. Methods: In a prospective longitudinal study, 104 patients with unilateral (n=77) and bilateral (n=27) endometrioma underwent laparoscopic endometrioma cystectomy. AMH levels were measured preoperatively and at 1, 3, 6, and 12 months postoperatively. ⋯ Although most factors were associated with AMH level changes in monovariant linear regression, multivariant linear regression analysis showed only three factors that reached the statistical significance, including bilateral endometriomas, mean size of the endometrioma, and preoperative AMH levels. Conclusions: Serum AMH levels decline significantly after laparoscopic cystectomy of endometriomas but recovered at 12 months compared with the first 6 months with unilateral endometrioma. Bilateral endometriomas, size of the cyst, and preoperative AMH levels might independently affect AMH levels at 12 months after surgery.
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Pre-eclampsia is a severe pregnant complication, mainly characterized by insufficient trophoblast invasion, impaired uterine spiral artery remodeling, placental hypoxia and ischemia, and endothelial dysfunction. However, the potential mechanisms of pre-eclampsia remain unclear. SIRT1 is a NAD+-dependent deacetylase, involving in multiple biological processes, including energy metabolism, oxidative stress, inflammatory response, and cellular autophagy. ⋯ Additionally, resveratrol, a SIRT1 agonist, attenuates vascular endothelial injury and placental dysfunction, and exerts protective effect on decreasing blood pressure. In this review, we provide new insights into the development of pre-eclampsia, which can establish a theoretical basis for prevention and treatment for pre-eclampsia. Besides, we also propose questions that still need to be further addressed in order to elucidate the comprehensive molecular mechanisms of pre-eclampsia in the future.
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Mitogen-inducible gene 6 (Mig-6) is a tumor suppressor gene that plays an important role in many types of cancers by interacting with EGFR. However, its molecular mechanism in hepatocellular carcinoma (HCC) and its relationship with miRNAs need to be elucidated. Therefore, this study aimed to explore whether Mig-6 could promote apoptosis and the inhibition of autophagy via its downstream miRNA in HCC cell lines. ⋯ It affected the apoptosis and autophagy of HCC cells, at least partly by regulating the expression of TGF-β2. Additionally, the relationship between Mig-6 and transforming growth factor TGF-β2 was explored in depth for the first time. These findings revealed an important role of Mig-6 in the apoptosis and autophagy of HCC cells by regulating miR-193a-3p, providing a novel insight into the therapeutic target in HCC.
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Ageing is one of the major risk factors of human diseases, including cancer, diabetes, and cardiovascular disease. Mulberry exhibits a wide range of functions, such as anti-oxidant, anti-inflammation, and anti-diabetes. In this study, we investigated the role of mulberry polyphenol extract (MPE) in K-Ras-induced senescence of smooth muscle cells. ⋯ MPE repressed K-Ras-induced G0/G1 arrest, whereas L-NAME and AMPK inhibitor blocked the effects of MPE. Our results indicated that MPE recovered the K-Ras-induced senescence of vascular smooth muscle cells through iNOS and AMPK-dependent pathway. Our findings suggested that MPE may prevent ageing-induced atherosclerosis.