1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

Yang, Lina; Wu, Lan; Du, Shuyan; Hu, Ye; Fan, Yi; Ma, Jun

doi:10.3892/mmr.2016.5323

Cited by 17 publications

(20 citation statements)

References 26 publications

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“…Tumour cells with higher ROS levels are more likely to be killed than normal cells with lower ROS levels, as elevated levels of ROS can activate multiple signalling pathways that induce apoptosis such as mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor-kappa B (NF-jB) signalling pathways [7]. Accordingly, targeting relevant signalling pathways, especially ROS-related pathways, may have potential for lung cancer treatment [8]. Some quinolizidine alkaloids have been reported to exert pro-oxidant actions, which may be an important mechanism for their anticancer and apoptosisinducing properties [9].…”

Section: Introductionmentioning

confidence: 99%

Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Section: Introductionmentioning

confidence: 99%

Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Peritoneal dialysis (PD) is a primary treatment of end-stage renal disease (ESRD). High glucose (HG) damages the structure and function of the peritoneal membrane, which leads to peritoneal fibrosis and ultrafiltration failure via inflammation, apoptosis, oxidative stress and epithelial-mesenchymal transition (EMT) (1)(2)(3). Recent studies have also revealed that HG regulates autophagy in certain diseases (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Effect of 1,25(OH)2D3 on high glucose-induced autophagy inhibition in peritoneum

Yang¹,

Fan²,

Zhang³

et al. 2017

Molecular Medicine Reports

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High glucose (HG) may damage the structure and function of the peritoneal membrane, and is considered to be one of the most important factors that leads to peritoneal fibrosis and ultrafiltration failure. Recently, 1,25(OH)2D3, the active form of vitamin D, was demonstrated to protect against epithelial‑mesenchymal transition and fibrosis in peritoneal mesothelium and other organs. Accumulating evidence has suggested that autophagy serves a protective role in certain diseases by regulating cell survival. The present study examined whether 1,25(OH)2D3 has an effect on autophagy in peritoneal mesothelial cells. The protein level of Beclin, anti‑ubiquitin‑binding protein p62 (p62), microtubule‑associated proteins 1A/1B light chain 3B (LC3-II), mechanistic target of rapamycin (mTOR) and phosphorylated mTOR were evaluated by western blot analysis. Autophagosomes were detected under transmission electron microscopy. It was revealed that exposure to HG inhibited autophagy in peritoneal mesothelial cells. However, 1,25(OH)2D3 alleviated autophagy inhibition induced by HG in human peritoneal mesothelial cells, which activated expression of autophagy‑associated genes encoding Beclin‑1 and LC3-II downregulated the expression of p62 via mTOR signaling pathway. In a mouse model of HG‑treated peritoneal mesothelium, autophagy inhibition was observed in peritoneum, 1,25(OH)2D3 attenuated HG‑induced autophagy inhibition in peritoneal mesothelium via the mTOR signaling pathway. These findings suggested that 1,25(OH)2D3 may be a potential therapy for peritoneal injury.

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“…MicroRNA-15a-5p suppressed PMC EMT (76) and microRNA-21 promoted PMC EMT (77). VDR, PPARγ and PPARβ/δ are also involved in the regulation of PMC activity and homeostasis during peritoneal dialysis (41)(42)(43)(44)(45)(46)(47). As RXRα is a dimerization partner for VDR and PPAR, the role of RXRα in PMC homeostasis during PD was investigated.…”

Section: Discussionmentioning

confidence: 99%

“…RXRα can form heterodimers with other nuclear receptors, including peroxisome proliferator activated receptor (PPAR), vitamin D receptor (VDR) and thyroid hormone receptors, resulting in the involvement of RXRα in multiple signaling pathways (35)(36)(37)(38)(39)(40). Previous studies have shown that vitamin D/VDR can inhibit peritoneal fibrosis and functional deterioration induced by chlorhexidine gluconate by inhibiting PMC EMT (41)(42)(43). Telmisartan inhibits peritoneal fibrosis through PPAR-γ activation (44).…”

Section: Effect Of Astragaloside IV and The Role Of Nuclear Receptor mentioning

confidence: 99%

Effect of astragaloside IV and the role of nuclear receptor RXRα in human peritoneal mesothelial cells in high glucose‑based peritoneal dialysis fluids

et al. 2019

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Peritoneal fibrosis is a serious complication that can occur during peritoneal dialysis (PD), which is primarily caused by damage to peritoneal mesothelial cells (PMCs). The onset of peritoneal fibrosis is delayed or inhibited by promoting PMC survival and inhibiting PMC epithelial-to-mesenchymal transition (EMT). In the present study, the effect of astragaloside IV and the role of the nuclear receptor retinoid X receptor-α (RXRα) in PMCs in high glucose-based PD fluids was investigated. Human PMC HMrSV5 cells were transfected with RXRα short hairpin RNA (shRNA), or an empty vector, and then treated with PD fluids and astragaloside IV. Cell viability, apoptosis and EMT were examined using the Cell Counting Kit-8 assay and flow cytometry, and by determining the levels of caspase-3, E-cadherin and α-smooth muscle actin (α-SMA) via western blot analysis. Cell viability and apoptosis were increased, as were the levels of E-cadherin in HMrSV5 cells following treatment with PD fluid. The protein levels of α-SMA and caspase-3 were increased by treatment with PD fluid. Exposure to astragaloside IV inhibited these changes; however, astragaloside IV did not change cell viability, apoptosis, E-cadherin or α-SMA levels in HMrSV5 cells under normal conditions. Transfection of HMrSV5 cells with RXRα shRNA resulted in decreased viability and E-cadherin expression, and increased apoptosis and α-SMA levels, in HMrSV5 cells treated with PD fluids and co-treated with astragaloside IV or vehicle. These results suggested that astragaloside IV increased cell viability, and inhibited apoptosis and EMT in PMCs in PD fluids, but did not affect these properties of PMCs under normal condition. Thus, the present study suggested that RXRα is involved in maintaining viability, inhibiting apoptosis and reducing EMT of PMCs in PD fluid.

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1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

Cited by 17 publications

References 26 publications

Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways

Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways

Effect of 1,25(OH)2D3 on high glucose-induced autophagy inhibition in peritoneum

Effect of astragaloside IV and the role of nuclear receptor RXRα in human peritoneal mesothelial cells in high glucose‑based peritoneal dialysis fluids

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