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Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway

BACKGROUND/AIMS: This study investigated the effects of sitagliptin on migration, proliferation, calcification and apoptosis of vascular smooth muscle cells (VSMCs) under high glucose (HG) conditions. METHODS: VSMCs were isolated from the thoracic aorta of Sprague Dawley rats. The cultured VSMCs wer...

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Autores principales: Shi, Lili, Ji, Ye, Liu, Dandan, Liu, Ying, Xu, Ying, Cao, Yang, Jiang, Xiaoyan, Xu, Changqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652771/
https://www.ncbi.nlm.nih.gov/pubmed/29100378
http://dx.doi.org/10.18632/oncotarget.20417
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author Shi, Lili
Ji, Ye
Liu, Dandan
Liu, Ying
Xu, Ying
Cao, Yang
Jiang, Xiaoyan
Xu, Changqing
author_facet Shi, Lili
Ji, Ye
Liu, Dandan
Liu, Ying
Xu, Ying
Cao, Yang
Jiang, Xiaoyan
Xu, Changqing
author_sort Shi, Lili
collection PubMed
description BACKGROUND/AIMS: This study investigated the effects of sitagliptin on migration, proliferation, calcification and apoptosis of vascular smooth muscle cells (VSMCs) under high glucose (HG) conditions. METHODS: VSMCs were isolated from the thoracic aorta of Sprague Dawley rats. The cultured VSMCs were subjected to control medium, mannitol medium, HG medium (25 mM), pretreatment with 200 nM sitagliptin in control or HG medium, or the ERK1/2 inhibitor PD98059 in HG medium. Cell proliferation, migration, apoptosis and calcification were determined. RESULTS: HG conditions promoted the proliferation, migration, calcification and impairment of apoptosis in VSMCs compared with controls (P<0.05). Pretreatment with sitagliptin effectively attenuated proliferation, migration, calcification of cells and increased apoptosis of HG-cultured VSMCs as compared with the HG group (P<0.05). Culture with HG resulted in the up-regulation of p-ERK1/2 in VSMCs, whereas sitagliptin pretreatment could inhibit HG-induced p-ERK1/2 expression. In addition, the ERK1/2 inhibitor PD98059, inhibited proliferation, migration, calcification and promoted the apoptosis of HG-cultured VSMCs compared with the HG group (P<0.05). CONCLUSION: The effects of sitagliptin on VSMC under high glucose condition were achieved through ERK1/2 signaling pathways.
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spelling pubmed-56527712017-11-02 Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway Shi, Lili Ji, Ye Liu, Dandan Liu, Ying Xu, Ying Cao, Yang Jiang, Xiaoyan Xu, Changqing Oncotarget Research Paper BACKGROUND/AIMS: This study investigated the effects of sitagliptin on migration, proliferation, calcification and apoptosis of vascular smooth muscle cells (VSMCs) under high glucose (HG) conditions. METHODS: VSMCs were isolated from the thoracic aorta of Sprague Dawley rats. The cultured VSMCs were subjected to control medium, mannitol medium, HG medium (25 mM), pretreatment with 200 nM sitagliptin in control or HG medium, or the ERK1/2 inhibitor PD98059 in HG medium. Cell proliferation, migration, apoptosis and calcification were determined. RESULTS: HG conditions promoted the proliferation, migration, calcification and impairment of apoptosis in VSMCs compared with controls (P<0.05). Pretreatment with sitagliptin effectively attenuated proliferation, migration, calcification of cells and increased apoptosis of HG-cultured VSMCs as compared with the HG group (P<0.05). Culture with HG resulted in the up-regulation of p-ERK1/2 in VSMCs, whereas sitagliptin pretreatment could inhibit HG-induced p-ERK1/2 expression. In addition, the ERK1/2 inhibitor PD98059, inhibited proliferation, migration, calcification and promoted the apoptosis of HG-cultured VSMCs compared with the HG group (P<0.05). CONCLUSION: The effects of sitagliptin on VSMC under high glucose condition were achieved through ERK1/2 signaling pathways. Impact Journals LLC 2017-08-24 /pmc/articles/PMC5652771/ /pubmed/29100378 http://dx.doi.org/10.18632/oncotarget.20417 Text en Copyright: © 2017 Shi et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Shi, Lili
Ji, Ye
Liu, Dandan
Liu, Ying
Xu, Ying
Cao, Yang
Jiang, Xiaoyan
Xu, Changqing
Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title_full Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title_fullStr Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title_full_unstemmed Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title_short Sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through ERK1/2 signal pathway
title_sort sitagliptin attenuates high glucose-induced alterations in migration, proliferation, calcification and apoptosis of vascular smooth muscle cells through erk1/2 signal pathway
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652771/
https://www.ncbi.nlm.nih.gov/pubmed/29100378
http://dx.doi.org/10.18632/oncotarget.20417
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