Vasopressin activates Akt/mTOR pathway in smooth muscle cells cultured in high glucose concentration

Montes, Daniela K.; Brenet, Marianne; Muñoz, Vanessa C.; Burgos, Patricia V.; Villanueva, Carolina I.; Figueroa, Carlos D.; González, Carlos B.

doi:10.1016/j.bbrc.2013.10.169

Cited by 11 publications

(7 citation statements)

References 32 publications

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“…The high extracellular glucose concentration might lead to alterations of the mechanisms regulating signalling pathways involved in cell proliferation. However, it was not found changes in Akt nor mTOR phosphorylation when cells were exposed to high extracellular glucose concentration (Montes et al., ). Studies also suggested that there was a requirement for activation of both ERK1/ERK2 and mTOR/p70S6K signal pathways for a full commitment to 15 m m glucose‐induced pancreatic beta‐cell mitogenesis (Hugl et al., ; Lingohr et al., ).…”

Section: Discussionmentioning

confidence: 99%

Inhibition ofPI3K‐Akt‐mTORsignal pathway dismissed the stimulation of glucose on goose liver cell growth

Wei

Han

et al. 2016

Animal Physiology Nutrition

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In the formation of goose fatty liver induced by a high-carbohydrate diet, it is characterized by the quick cell growth of liver. The carbohydrate is mostly digested and absorbed in the small intestine by the form of glucose. Recent studies have suggested a crucial role for PI3K-Akt-mTOR pathway in regulating cell proliferation, and then we speculate that PI3K-Akt-mTOR pathway may mediate glucose-induced liver cell proliferation. Goose primary hepatocytes were isolated and incubated in either no addition as a control or glucose or PI3K-Akt-mTOR pathway inhibitors or cotreatment with glucose and PI3K-Akt-mTOR pathway inhibitors. The results firstly showed that 35 mmol/l glucose stimulated the mRNA level and protein content of factors involved in PI3K-Akt-mTOR signal pathway in goose primary hepatocytes. Secondly, 35 mmol/l glucose evidently changed the cell cycle PI index and protein expression of cyclin D1. Meanwhile, the upregulation of 35 mmol/l glucose on the DNA synthesis rate, cell cycle PI index, the mRNA expression, protein content and protein expression of factors involved in the cell proliferation was decreased significantly by the inhibitors of PI3K-Akt-mTOR pathway, LY294002, rapamycin or NVP-BEZ235. In summary, glucose could stimulate the cell proliferation, and the PI3K-Akt-mTOR pathway inhibitors could dismiss glucose-induced the upregulation of cell proliferation in goose primary hepatocyte.

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Section: Discussionmentioning

confidence: 99%

Inhibition ofPI3K‐Akt‐mTORsignal pathway dismissed the stimulation of glucose on goose liver cell growth

Wei

Han

et al. 2016

Animal Physiology Nutrition

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“…The preliminary study indicated that activated Akt/mTOR is an important mediator in MSC aging ( 22 ). Notably, it has additionally been reported that high glucose activates the PI3K/Akt signaling pathway in podocytes ( 23 ), vascular smooth muscle cells ( 24 ) and vascular endothelial cells ( 25 ). Therefore, the present study aimed to investigate if HG induces MSC aging via the Akt/mTOR pathway.…”

Section: Introductionmentioning

confidence: 99%

High glucose induces the aging of mesenchymal stem cells via Akt/mTOR signaling

Zhang

Chen

et al. 2017

Molecular Medicine Reports

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It has previously been demonstrated that glucose is important in the process of stem cell aging. However, the mechanisms of cell senescence induced by high glucose (HG) remain to be elucidated. The preliminary study indicated that D-galactose induced mesenchymal stem cell (MSCs) aging. The present study demonstrated, following treatment with 11.0 or 22.0 mM HG for 14 days, that HG significantly promoted MSCs aging and the expression levels of phosphorylated (p-)phosphatidylinositol 3-kinase/protein kinase B (Akt) and p-mammalian target of rapamycin signaling (mTOR) in the HG groups were increased compared with the control group. However, following Akt inhibition with 1.0 or 10.0 nM MK-2206, which is an Akt-specific small molecule inhibitor, the senescence-cell value in the HG group was significantly decreased compared with the control group. These results indicated that HG induced MSCs senescence and this effect was primarily mediated via the Akt/mTOR signaling pathway.

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“…It has been reported that high glucose can activate the PI3K/Akt signaling pathway in podocytes [ 15 ], vascular smooth muscle cells [ 16 ], vascular endothelial cells [ 17 ], and human pancreatic cancer cells [ 18 ] and that it can induce the expression of extracellular matrix molecules in human renal proximal tubular cells [ 19 ]. In this study, we investigate the high glucose-induced expression of extracellular matrix molecules (such as fibronectin, collagen IV, and laminin), the phosphorylation of Akt, and the mechanism involved in the high glucose-induced expression of fibronectin, collagen IV, and laminin in RPE cells.…”

Section: Introductionmentioning

confidence: 99%

The PI3K/Akt Signaling Pathway Mediates the High Glucose-Induced Expression of Extracellular Matrix Molecules in Human Retinal Pigment Epithelial Cells

Dong

Zhang

et al. 2015

Journal of Diabetes Research

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Prolonged hyperglycemia is an important risk factor of the pathogenesis of diabetic retinopathy (DR). Extracellular matrix molecules, such as fibronectin, collagen IV, and laminin, are associated with fibrotic membranes. In this study, we investigated the expression of fibronectin, collagen IV, and laminin in RPE cells under high glucose conditions. Furthermore, we also detected the phosphorylation of protein kinase B (Akt) under high glucose conditions in RPE cells. Our results showed that high glucose upregulated fibronectin, collagen IV, and laminin expression, and activated Akt in RPE cells. We also found that pretreatment with LY294002 (an inhibitor of phosphatidylinositol 3-kinase) abolished high glucose-induced expression of fibronectin, collagen IV, and laminin in RPE cells. Thus, high glucose induced the expression of fibronectin, collagen IV, and laminin through PI3K/Akt signaling pathway in RPE cells, and the PI3K/Akt signaling pathway may contribute to the formation of fibrotic membrane during the development of DR.

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Vasopressin activates Akt/mTOR pathway in smooth muscle cells cultured in high glucose concentration

Cited by 11 publications

References 32 publications

Inhibition ofPI3K‐Akt‐mTORsignal pathway dismissed the stimulation of glucose on goose liver cell growth

Inhibition ofPI3K‐Akt‐mTORsignal pathway dismissed the stimulation of glucose on goose liver cell growth

High glucose induces the aging of mesenchymal stem cells via Akt/mTOR signaling

The PI3K/Akt Signaling Pathway Mediates the High Glucose-Induced Expression of Extracellular Matrix Molecules in Human Retinal Pigment Epithelial Cells

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