High glucose stimulates cell proliferation and Collagen IV production in rat mesangial cells through inhibiting AMPK-KATP signaling

Zhang, Bei; Shi, Yongquan; Zou, Junjie; Chen, Xiangfang; Tang, Wei; Ye, Fei; Liu, Zhimin

doi:10.1007/s11255-017-1654-3

Cited by 7 publications

(5 citation statements)

References 36 publications

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“…We validated several candidates from this subset and confirmed that many of the downregulated genes are well-known pro-proliferative genes and the upregulated ones are antiproliferative genes (Figure ). There are a number of studies showing the involvement of glucose in the context of cell proliferation, − and we observed that TCF19 is overexpressed upon glucose stimulation . Our data suggest that TCF19 regulates the optimum uptake levels of glucose to maintain a sustainable concentration of glucose in the hepatic cell.…”

Section: Discussionsupporting

confidence: 62%

TCF19 Promotes Cell Proliferation through Binding to the Histone H3K4me3 Mark

et al. 2019

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Transcription factor 19 (TCF19) plays critical roles in type 1 diabetes and the maintenance of pancreatic β cells. Recent studies have also implicated TCF19 in cell proliferation of hepatic carcinoma and non-small cell lung carcinoma; however, the mechanism underlying this regulation remains elusive. At the molecular level, TCF19 contains two modules, the plant homeodomain (PHD) finger and the forkhead-associated (FHA) domain, of unclear function. Here, we show that TCF19 mediates hepatocellular carcinoma HepG2 cell proliferation through its PHD finger that recognizes trimethylated lysine 4 of histone 3 (H3K4me3). W316 of the PHD finger of TCF19 is one of the critical residues eliciting this function. Whole genome microarray analysis and orthogonal cell-based assays identified a large subset of genes involved in cell survival and proliferation that depend on TCF19. Our data suggest that TCF19 acts as a pro-oncogene in hepatocellular carcinoma cells and that its functional PHD finger is critical in cell proliferation.

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Section: Discussionsupporting

confidence: 62%

TCF19 Promotes Cell Proliferation through Binding to the Histone H3K4me3 Mark

et al. 2019

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“…In consistent with these reports, we observed impaired AMPK phosphorylation in diabetic renal tissue as well as in tubular cells incubated with high glucose levels. The impaired AMPK activity in renal tissue positively correlates with mesangial matrix deposition and inefficient tubular reabsorption (Wei et al, 2020; Zhang et al, 2017). Melatonin treatment in STZ‐induced diabetic rats and high‐glucose‐exposed NRK‐52E cells improved AMPK phosphorylation, demonstrating the positive modulatory effect of melatonin on AMPK.…”

Section: Discussionmentioning

confidence: 99%

Melatonin prevents diabetes‐induced nephropathy by modulating the AMPK/SIRT1 axis: Focus on autophagy and mitochondrial dysfunction

Jain

Sherkhane

Kalavala

et al. 2022

Cell Biology International

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Impaired nutrient sensing mechanisms such as AMPK/silent information regulator type 1 (SIRT1) axis and autophagy in renal cells upon chronic diabetic condition accelerate renal injury and upregulating these mechanisms has been reported to prevent renal damage. Melatonin, a neuroendocrine agent, also possess antioxidant and AMPK modulatory effect. In the current study, the protective effect of melatonin against diabetic renal injury was assessed in streptozotocin‐induced diabetic nephropathy model and in in vitro model of high‐glucose‐induced tubular injury. Melatonin (3 and 10 mg/kg) was administered for 28 days after 4 weeks of diabetes induction in Sprague–Dawley rats. For in vitro model, the NRK‐52E cells were co‐incubated with high glucose and melatonin (25 and 50 μM). Melatonin supplementation abrogated the diabetes‐induced renal injury and improved renal function in diabetic rats. Immunoblot analysis of renal tissue lysates revealed improved expression of AMPK, as well as upregulated the expression of nuclear factor erythroid 2‐related factor 2, SIRT1, PGC‐1α, TFAM and enhanced autophagy upon melatonin treatment in diabetic rats. Likewise, melatonin treatment in high glucose exposed NRK‐52E cells improved expression of AMPK, enhanced mitochondrial biogenesis and positively modulated autophagy. However, these effects were repressed upon inhibition of AMPK activity in NRK‐52E cells by treatment of Compound‐C, suggesting that the protective effects of melatonin were mainly mediated through activation of AMPK. These results suggest that melatonin might mediate the renoprotective effect by upregulating the AMPK/SIRT1 axis, enhancing the autophagy and mitochondrial health in DIabetic Nephropathy.

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“…This process inhibits AMPK activation which causes renal hypertrophy and fibrosis in hyperglycemic and hyperlipidemic conditions by regulating several pathways, and has been seen in both in vitro and in vivo experiments. In contrast, activation of AMPK suppressed both renal fibrosis and improved renal function in both in vitro and in vivo experiments [15, 44]. Therefore, AMPK could provide a potential approach to alleviate diabetic renal damage [45].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, TGF-β1, a predominant pathogenic factor, regulates glomerular and tubulointerstitial fibrosis by the phosphorylation and activation of Smad2 and Smad3 as well as the canonical signaling pathway [14]. It is also known that AMP-activated kinase protein (AMPK) acts as a cellular energy homeostasis mediator and contributes to mesangial cell proliferation and fibrosis production [15].…”

Section: Introductionmentioning

confidence: 99%

Coreopsis tinctoria Nutt ameliorates high glucose-induced renal fibrosis and inflammation via the TGF-β1/SMADS/AMPK/NF-κB pathways

Yao

et al. 2019

BMC Complement Altern Med

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BackgroundCoreopsis tinctoria Nutt is an ethnomedicine widely used in Xinjiang, China. It is consumed as a herbal tea by local Uyghur people to treat high blood pressure and diarrhea. Our previous study confirmed that the ethyl acetate extract of Coreopsis tinctoria (AC) had a protective effect on diabetic nephropathy (DN) in an in vivo experiment. Here we aim to elucidate the protective mechanism of AC and marein, the main ingredient in Coreopsis tinctoria on renal fibrosis and inflammation in vitro under high glucose (HG) conditions.MethodsA HG-induced barrier dysfunction model in rat mesangial cells (HBZY-1) was established. The cells were exposed to AC and marein and/or HG for 24 h. Then, the renal protective effects of AC and marein via transforming growth factor-β1 (TGF-β1)/Smads, AMP-activated kinase protein (AMPK), and nuclear factor kappa beta (NF-κB) signaling were assessed.ResultsBoth AC and marein suppressed rat mesangial cell hyperplasia and significantly attenuated the expression of HG-disrupted fibrotic and inflammatory proteins in HBZY-1 cells. It was also confirmed that AC and marein remarkably attenuated HG-induced renal inflammation and fibrosis by regulating the AMPK, TGF-β1/Smads, and NF-κB signaling pathways.ConclusionThese results indicated that AC and marein may delay the progression of DN, at least in part, by suppressing HG-induced renal inflammation and fibrosis. Marein may be one of the bioactive compounds in AC.

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High glucose stimulates cell proliferation and Collagen IV production in rat mesangial cells through inhibiting AMPK-KATP signaling

Abstract: Taken together, activating AMPK-K signaling may protect against HG-induced mesangial cell proliferation and Collagen IV production, and, thereby, provides new insights into the molecular mechanisms underlying early diabetic nephropathy (DN).

Cited by 7 publications

References 36 publications

TCF19 Promotes Cell Proliferation through Binding to the Histone H3K4me3 Mark

TCF19 Promotes Cell Proliferation through Binding to the Histone H3K4me3 Mark

Melatonin prevents diabetes‐induced nephropathy by modulating the AMPK/SIRT1 axis: Focus on autophagy and mitochondrial dysfunction

Coreopsis tinctoria Nutt ameliorates high glucose-induced renal fibrosis and inflammation via the TGF-β1/SMADS/AMPK/NF-κB pathways

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