Год публикации:
Все года
2018
2019
2020
Название |
Дата публикации |
Коллектив авторов |
Журнал |
DOI |
Индекс цитирования |
Ссылка на источник |
T-cadherin promotes autophagy and survival in vascular smooth muscle cells through MEK1/2/Erk1/2 axis activation
|
|
Леш Клаус-Петер Юлиус
Свистунов А.А
Несвижский Юрий Владимирович
|
Cellular Signalling |
|
|
Autophagy is an evolutionary conserved intracellular catabolic process of vital importance to cell and tissue homeostasis. Autophagy is implicated in the pathogenesis of atherosclerosis but participating cells, molecular mechanisms and functional outcomes have not been fully elucidated. T-cadherin, an atypical glycosylphosphatidylinositol-anchored member of the cadherin superfamily of adhesion molecules, is upregulated on smooth muscle cells (SMCs)1
in atherosclerotic lesions. Here, using rat and murine aortic SMCs as
experimental models, we surveyed the ability of T-cadherin to regulate
autophagy in SMCs during serum-starvation stress. Ectopic upregulation
of T-cadherin in SMCs resulted in augmented autophagy characterized by
increased autophagic flux, LC3-II abundance and autophagosome formation.
Analysis of signal transduction pathway effectors and use of specific
pharmacological inhibitors demonstrated that T-cadherin-associated
enhancement of the autophagic response to serum-deprivation was
dependent on MEK1/2/Erk1/2 activation and independent of
PI3K/Akt/mTORC1, reactive oxygen species or endoplasmic reticulum
stress. T-cadherin upregulation on SMCs conferred a survival advantage
during prolonged serum-starvation which was sensitive to inhibition of
MEK1/2/Erk1/2 by PD98059 or UO126 and to blockade of autophagy by
chloroquine. Loss of T-cadherin expression in SMCs diminished autophagy
responsiveness and compromised survival under conditions of
serum-starvation. Overall our findings have identified T-cadherin as a
novel positive regulator of autophagy and survival in SMCs.
Читать
тезис
Публикация |
T-cadherin promotes autophagy and survival in vascular smooth muscle cells through MEK1/2/Erk1/2 axis activation
|
|
Леш Клаус-Петер Юлиус (Заведующий лабораторией психиатрической нейробиологии)
Свистунов А.А (Первый проректор)
Несвижский Юрий Владимирович (Профессор)
|
Cellular Signalling |
|
|
Autophagy is an evolutionary conserved intracellular catabolic process of vital importance to cell and tissue homeostasis. Autophagy is implicated in the pathogenesis of atherosclerosis but participating cells, molecular mechanisms and functional outcomes have not been fully elucidated. T-cadherin, an atypical glycosylphosphatidylinositol-anchored member of the cadherin superfamily of adhesion molecules, is upregulated on smooth muscle cells (SMCs)1
in atherosclerotic lesions. Here, using rat and murine aortic SMCs as
experimental models, we surveyed the ability of T-cadherin to regulate
autophagy in SMCs during serum-starvation stress. Ectopic upregulation
of T-cadherin in SMCs resulted in augmented autophagy characterized by
increased autophagic flux, LC3-II abundance and autophagosome formation.
Analysis of signal transduction pathway effectors and use of specific
pharmacological inhibitors demonstrated that T-cadherin-associated
enhancement of the autophagic response to serum-deprivation was
dependent on MEK1/2/Erk1/2 activation and independent of
PI3K/Akt/mTORC1, reactive oxygen species or endoplasmic reticulum
stress. T-cadherin upregulation on SMCs conferred a survival advantage
during prolonged serum-starvation which was sensitive to inhibition of
MEK1/2/Erk1/2 by PD98059 or UO126 and to blockade of autophagy by
chloroquine. Loss of T-cadherin expression in SMCs diminished autophagy
responsiveness and compromised survival under conditions of
serum-starvation. Overall our findings have identified T-cadherin as a
novel positive regulator of autophagy and survival in SMCs.
Читать
тезис
Публикация |