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Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway
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Zeitschriftentitel: | Cellular Physiology and Biochemistry |
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Personen und Körperschaften: | , , , , , , , , , |
In: | Cellular Physiology and Biochemistry, 35, 2015, 3, S. 1151-1166 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
S. Karger AG
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Schlagwörter: |
author_facet |
Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming |
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author |
Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming |
spellingShingle |
Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming Cellular Physiology and Biochemistry Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway Physiology |
author_sort |
jin, cheng-wei |
spelling |
Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming 1015-8987 1421-9778 S. Karger AG Physiology http://dx.doi.org/10.1159/000373940 <jats:p>Background/Aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity. Methods: We used vascular smooth muscle cells (VSMCs) to create two cellular senescence models, one for replicative senescence (RS) and one for induced senescence (IS), to test the hypothesis that Gas6 delays senescence. Results: Gas6-treated cells appear relatively younger compared with non-Gas6-treated cells. In particular, Gas6-treated cells displayed decreased staining for SA-β-Gal, fewer G1 phase cells, and decreased levels of p16INK4a and p21Cip1 expression; conversely, Gas6-treated cells displayed more S phase cells and significantly increased proliferation indexes. Furthermore, in both the IS and RS models with Gas6 treatment, the levels of PI3K, p-Akt, and p-FoxO3a decreased following Axl inhibition by R428; similarly, the levels of p-Akt and p-FoxO3a also decreased following PI3K inhibition by LY294002. Conclusion: Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.</jats:p> Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway Cellular Physiology and Biochemistry |
doi_str_mv |
10.1159/000373940 |
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Biologie |
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S. Karger AG, 2015 |
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S. Karger AG, 2015 |
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2015 |
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S. Karger AG |
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Cellular Physiology and Biochemistry |
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title |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_unstemmed |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_full |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_fullStr |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_full_unstemmed |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_short |
Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_sort |
gas6 delays senescence in vascular smooth muscle cells through the pi3k/ akt/foxo signaling pathway |
topic |
Physiology |
url |
http://dx.doi.org/10.1159/000373940 |
publishDate |
2015 |
physical |
1151-1166 |
description |
<jats:p>Background/Aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity. Methods: We used vascular smooth muscle cells (VSMCs) to create two cellular senescence models, one for replicative senescence (RS) and one for induced senescence (IS), to test the hypothesis that Gas6 delays senescence. Results: Gas6-treated cells appear relatively younger compared with non-Gas6-treated cells. In particular, Gas6-treated cells displayed decreased staining for SA-β-Gal, fewer G1 phase cells, and decreased levels of p16INK4a and p21Cip1 expression; conversely, Gas6-treated cells displayed more S phase cells and significantly increased proliferation indexes. Furthermore, in both the IS and RS models with Gas6 treatment, the levels of PI3K, p-Akt, and p-FoxO3a decreased following Axl inhibition by R428; similarly, the levels of p-Akt and p-FoxO3a also decreased following PI3K inhibition by LY294002. Conclusion: Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.</jats:p> |
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author | Jin, Cheng-wei, Wang, Hui, Chen, Yan-qing, Tang, Meng-xiong, Fan, Guan-qi, Wang, Zhi-hao, Li, Li, Zhang, Yun, Zhang, Wei, Zhong, Ming |
author_facet | Jin, Cheng-wei, Wang, Hui, Chen, Yan-qing, Tang, Meng-xiong, Fan, Guan-qi, Wang, Zhi-hao, Li, Li, Zhang, Yun, Zhang, Wei, Zhong, Ming, Jin, Cheng-wei, Wang, Hui, Chen, Yan-qing, Tang, Meng-xiong, Fan, Guan-qi, Wang, Zhi-hao, Li, Li, Zhang, Yun, Zhang, Wei, Zhong, Ming |
author_sort | jin, cheng-wei |
container_issue | 3 |
container_start_page | 1151 |
container_title | Cellular Physiology and Biochemistry |
container_volume | 35 |
description | <jats:p>Background/Aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity. Methods: We used vascular smooth muscle cells (VSMCs) to create two cellular senescence models, one for replicative senescence (RS) and one for induced senescence (IS), to test the hypothesis that Gas6 delays senescence. Results: Gas6-treated cells appear relatively younger compared with non-Gas6-treated cells. In particular, Gas6-treated cells displayed decreased staining for SA-β-Gal, fewer G1 phase cells, and decreased levels of p16INK4a and p21Cip1 expression; conversely, Gas6-treated cells displayed more S phase cells and significantly increased proliferation indexes. Furthermore, in both the IS and RS models with Gas6 treatment, the levels of PI3K, p-Akt, and p-FoxO3a decreased following Axl inhibition by R428; similarly, the levels of p-Akt and p-FoxO3a also decreased following PI3K inhibition by LY294002. Conclusion: Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.</jats:p> |
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imprint | S. Karger AG, 2015 |
imprint_str_mv | S. Karger AG, 2015 |
institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14 |
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physical | 1151-1166 |
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publisher | S. Karger AG |
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series | Cellular Physiology and Biochemistry |
source_id | 49 |
spelling | Jin, Cheng-wei Wang, Hui Chen, Yan-qing Tang, Meng-xiong Fan, Guan-qi Wang, Zhi-hao Li, Li Zhang, Yun Zhang, Wei Zhong, Ming 1015-8987 1421-9778 S. Karger AG Physiology http://dx.doi.org/10.1159/000373940 <jats:p>Background/Aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity. Methods: We used vascular smooth muscle cells (VSMCs) to create two cellular senescence models, one for replicative senescence (RS) and one for induced senescence (IS), to test the hypothesis that Gas6 delays senescence. Results: Gas6-treated cells appear relatively younger compared with non-Gas6-treated cells. In particular, Gas6-treated cells displayed decreased staining for SA-β-Gal, fewer G1 phase cells, and decreased levels of p16INK4a and p21Cip1 expression; conversely, Gas6-treated cells displayed more S phase cells and significantly increased proliferation indexes. Furthermore, in both the IS and RS models with Gas6 treatment, the levels of PI3K, p-Akt, and p-FoxO3a decreased following Axl inhibition by R428; similarly, the levels of p-Akt and p-FoxO3a also decreased following PI3K inhibition by LY294002. Conclusion: Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.</jats:p> Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway Cellular Physiology and Biochemistry |
spellingShingle | Jin, Cheng-wei, Wang, Hui, Chen, Yan-qing, Tang, Meng-xiong, Fan, Guan-qi, Wang, Zhi-hao, Li, Li, Zhang, Yun, Zhang, Wei, Zhong, Ming, Cellular Physiology and Biochemistry, Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway, Physiology |
title | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_full | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_fullStr | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_full_unstemmed | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_short | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
title_sort | gas6 delays senescence in vascular smooth muscle cells through the pi3k/ akt/foxo signaling pathway |
title_unstemmed | Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway |
topic | Physiology |
url | http://dx.doi.org/10.1159/000373940 |