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Ying Wang Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Xiao-Hui Wang Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Deng-Xuan Fan Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Yuan Zhang Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Ming-Qing Li Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Hai-Xia Wu Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Li-Ping Jin Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China
Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Department of Reproductive Medicine, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China

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Mammalian proprotein convertases (PCs) play an important role in folliculogenesis, as they proteolytically activate a variety of substrates such as the transforming growth factor beta (TGFβ) superfamily. PC subtilism/kexin 6 (PCSK6) is a member of the PC family and is ubiquitously expressed and implicated in many physiological and pathological processes. However, in human granulosa cells, the expression of the PC family members, their hormonal regulation, and the function of PCs are not clear. In this study, we found that PCSK6 is the most highly expressed PC family member in granulosa cells. LH increased PCSK6 mRNA level and PCSK6 played an anti-apoptosis function in KGN cells. Knockdown of PCSK6 not only increased the secretion of activin A and TGFβ2 but also decreased the secretion of follistatin, estrogen, and the mRNA levels of FSH receptor (FSHR) and P450AROM (CYP19A1). We also found that, in the KGN human granulosa cell line, TGFβ2 and activin A could promote the apoptosis of KGN cells and LH could regulate the follistatin level. These data indicate that PCSK6, which is regulated by LH, is highly expressed in human primary granulosa cells of pre-ovulatory follicles and plays important roles in regulating a series of downstream molecules and apoptosis of KGN cells.

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Tian Shuang Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
School of Human Kinetics, Faculty of Health, Laurentian University, Ontario, Canada
Department of Biology, Laurentian University, Ontario, Canada

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Ming Fu Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
School of Human Kinetics, Faculty of Health, Laurentian University, Ontario, Canada
Health Sciences North Research Institute, Sudbury, Ontario, Canada

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Guangdong Yang Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
Department of Chemistry and Biochemistry, Laurentian University, Ontario, Canada

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Ying Huang Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
School of Human Kinetics, Faculty of Health, Laurentian University, Ontario, Canada

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Zhongming Qian Nantong University, Nantong, Jiangsu, China

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Lingyun Wu Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
School of Human Kinetics, Faculty of Health, Laurentian University, Ontario, Canada
Health Sciences North Research Institute, Sudbury, Ontario, Canada

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Rui Wang Cardiovascular and Metabolic Research Unit, Laurentian University, Ontario, Canada
Department of Biology, Laurentian University, Ontario, Canada
Department of Biology, York University, Toronto, Ontario, Canada

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Both estrogen and hydrogen sulfide (H2S) inhibit the proliferation of vascular smooth muscle cells (SMCs) and development of atherosclerosis. In the absence of endogenous H2S as occurred in CSE-knockout (KO) mouse, however, estrogen stimulates the proliferation of vascular SMCs. The underlying mechanisms for this seemingly controversial vascular effect of estrogen are unclear. In the present study, we demonstrated that the stimulatory effect of estrogen on the proliferation of CSE-KO SMCs was suppressed by the inhibitor of insulin-like growth factor-1 receptor (IGF-1R) or knockdown of IGF-1R protein expression. Estrogen downregulated the expression of insulin-like growth factor-1 (IGF-1) and IGF-1R in aortic tissues or aortic SMCs isolated from WT and CSE-KO mice. Furthermore, endogenous H2S downregulated IGF-1R, but upregulated estrogen receptor (ER)-α, in aortic tissues or SMCs. ER-α and IGF-1R were co-located in SMCs and co-immunoprecipitated, which was decreased by H2S. Finally, both endogenous and exogenous H2S induced the S-sulfhydration of IGF-1R, but not ER-α, in WT-SMCs and CSE-KO SMCs, which underlies the decreased formation of IGF-1R/ER-α hybrid in the presence of H2S. Thus, the absence of H2S favors the interaction of estrogen with IGF-1R/ER-α hybrid to stimulate SMCs proliferation. The appreciation of a critical role of H2S in preventing estrogen-induced SMCs proliferation will help better understand the regulation of complex vascular effects of estrogen and sex-related cardiovascular diseases.

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Weixia Han Department of Pathology, Hebei Medical University, Shijiazhuang, China
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang, China

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Chen Wang Department of Pathology, Second Hospital, Shanxi Medical University, Taiyuan, China

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Zhifen Yang Department of Pathology, Hebei Medical University, Shijiazhuang, China

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Lin Mu Department of Pathology, Hebei Medical University, Shijiazhuang, China

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Ming Wu Department of Pathology, Hebei Medical University, Shijiazhuang, China

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Nan Chen Department of Pathology, Hebei Medical University, Shijiazhuang, China

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Chunyang Du Department of Pathology, Hebei Medical University, Shijiazhuang, China

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Huijun Duan Department of Pathology, Hebei Medical University, Shijiazhuang, China
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang, China

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Yonghong Shi Department of Pathology, Hebei Medical University, Shijiazhuang, China
Hebei Key Laboratory of Kidney Diseases, Shijiazhuang, China

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Renal fibrosis is the major pathological characteristic of diabetic nephropathy (DN). Reportedly, increased SIRT1 expression played a renal protective role in animal models of DN. This study was designed to elucidate the molecular mechanisms underlying the protective effects of SRT1720, an SIRT1 activator, against diabetes-induced renal fibrosis. Type 2 diabetic mice (db/db) were treated with SRT1720 (50 mg/kg/day) by gavage for 10 weeks. Renal proximal tubular epithelial cells (HK-2 cells) were treated with high glucose (HG, 30 mM) in the presence or absence of SRT1720 (2.5 µM) for 48 h. We observed that impaired SIRT1 expression and activity were restored by SRT1720 administration in db/db mice as well as in HG-treated HK-2 cells. Moreover, SRT1720 administration improved the renal function, attenuated glomerular hypertrophy, mesangial expansion, glomerulosclerosis and interstitial fibrosis and inhibited TGFB1 and CTGF expressions and nuclear factor κB (NF-KB) activation in db/db mice. Similarly, HG-induced epithelial-to-mesenchymal transformation (EMT) and collagen IV and fibronectin expressions were inhibited in SRT1720-treated HK-2 cells. Mechanistic studies demonstrated that SRT1720 suppressed HIF1A, GLUT1 and SNAIL expressions both in vivo and in vitro. Furthermore, HIF1A or GLUT1 knockdown effectively abrogated HG-induced EMT and collagen IV and fibronectin expressions in HK-2 cells. These findings suggest that SRT1720 prevented diabetes-induced renal fibrosis via the SIRT1/HIF1A/GLUT1/SNAIL pathway.

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Shang-Wu Shih Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan
Department of Life Science, National Taiwan University, Taipei, Taiwan

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Jia-Jiun Yan Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan

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Yi-Hsing Wang Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan

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Yi-Ling Tsou Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan

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Ling Chiu Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan
Department of Life Science, National Taiwan University, Taipei, Taiwan

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Yung-Che Tseng Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan

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Ming-Yi Chou Department of Life Science, National Taiwan University, Taipei, Taiwan

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Pung-Pung Hwang Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan
Department of Life Science, National Taiwan University, Taipei, Taiwan

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Estrogen-related receptors (ERRs) are known to function in mammalian kidney as key regulators of ion transport-related genes; however, a comprehensive understanding of the physiological functions of ERRs in vertebrate body fluid ionic homeostasis is still elusive. Here, we used medaka (Oryzias melastigma), a euryhaline teleost, to investigate how ERRs are involved in ion regulation. After transferring medaka from hypertonic seawater to hypotonic freshwater (FW), the mRNA expression levels of errγ2 were highly upregulated, suggesting that Errγ2 may play a crucial role in ion uptake. In situ hybridization showed that errγ2 was specifically expressed in ionocytes, the cells responsible for Na+/Cl transport. In normal FW, ERRγ2 morpholino knockdown caused reductions in the mRNA expression of Na+/Cl cotransporter (Ncc), the number of Ncc ionocytes, Na+/Cl influxes of ionocytes, and whole-body Na+/Cl contents. In FW with low Na+ and low Cl, the expression levels of mRNA for Na+/H+ exchanger 3 (Nhe3) and Ncc were both decreased in Errγ2 morphants. Treating embryos with DY131, an agonist of Errγ, increased the whole-body Na+/Cl contents and ncc mRNA expression in Errγ2 morphants. As such, medaka Errγ2 may control Na+/Cl uptake by regulating ncc and/or nhe3 mRNA expression and ionocyte number, and these regulatory actions may be subtly adjusted depending on internal and external ion concentrations. These findings not only provide new insights into the underpinning mechanism of actions of ERRs, but also enhance our understanding of their roles in body fluid ionic homeostasis for adaptation to changing environments during vertebrate evolution.

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Mingjuan Deng Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China

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Fang Qu Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Beijing Laboratory for Food Quality and Safety, China Agricultural University, Beijing, China

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Long Chen Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Research Center for Probiotics, China Agricultural University, Beijing, China

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Chang Liu Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Beijing Laboratory for Food Quality and Safety, China Agricultural University, Beijing, China

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Ming Zhang School of Food and Chemical Engineering, Beijing Technology and Business University, Beijing, China

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Fazheng Ren Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Beijing Laboratory for Food Quality and Safety, China Agricultural University, Beijing, China
Research Center for Probiotics, China Agricultural University, Beijing, China

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Huiyuan Guo Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Research Center for Probiotics, China Agricultural University, Beijing, China

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Hao Zhang Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Beijing Laboratory for Food Quality and Safety, China Agricultural University, Beijing, China

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Shaoyang Ge Research Center for Probiotics, China Agricultural University, Beijing, China
Hebei Engineering Research Center of Animal Product, Sanhe, China

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Chaodong Wu Department of Nutrition, Texas A&M University, College Station, Texas, USA

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Liang Zhao Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Key Laboratory of Precision Nutrition and Food Quality, Ministry of Education, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China
Research Center for Probiotics, China Agricultural University, Beijing, China

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This study aimed to assess the effects of three major SCFAs (acetate, propionate, and butyrate) on NASH phenotype in mice. C57BL/6 mice were fed a methionine- and choline-deficient (MCD) diet and treated with sodium acetate, sodium propionate, or sodium butyrate during the 6-week feeding period. SCFA treatment significantly reduced serum levels of alanine aminotransferase and aspartate transaminase, the numbers of lipid droplets, and the levels of triglycerides and cholesterols in livers of the mice compared with control treatment. SCFAs also reduced MCD-induced hepatic aggregation of macrophages and proinflammatory responses. Among the three SCFAs, sodium acetate (NaA) revealed the best efficacy at alleviating MCD-induced hepatic steatosis and inflammation. Additionally, NaA increased AMP-activated protein kinase activation in the liver and induced the expression of fatty acid oxidation gene in both the liver and cultured hepatocytes. In vitro, NaA decreased MCD-mimicking media-induced proinflammatory responses in macrophages to a greater extent than in hepatocytes. These results indicated that NaA alleviates steatosis in a manner involving AMPK activation. Also, NaA alleviation of hepatic inflammation appears to be due to, in large part, suppression of macrophage proinflammatory activation. SCFAs may represent as a novel and viable approach for alleviating NASH.

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