Endothelial to mesenchymal transition contributes to nicotine-induced atherosclerosis
Qin W., Zhang L., Li Z., Xiao D., Zhang Y., Zhang H., Mokembo J. N., Monayo S. M., Jha N. K., Kopy'lov F. Yu., Shhekochikhin D. Yu.
Theranostics
Vol.10, Issue12, P. 5276-5289
Опубликовано: 2020
Тип ресурса: Статья
Аннотация:
Rationale: Nicotine exposure via cigarette smoking is strongly associated with atherosclerosis. However, the underlying mechanisms remain poorly understood. The current study aimed to identify whether endothelial to mesenchymal transition (EndMT) contributes to nicotine-induced atherosclerosis. Methods: ApoE-/- mice were administered nicotine in their drinking water for 12 weeks. The effects of nicotine on EndMT were determined by immunostaining on aortic root and RNA analysis in aortic intima. In vitro nicotine-treated cell model was established on human aortic endothelial cells (HAECs). The effects of nicotine on the expression of EndMT-related markers, ERK1/2 and Snail were quantified by real-time PCR, western blot and immunofluorescent staining. Results: Nicotine treatment resulted in larger atherosclerotic plaques in ApoE-/- mice. The vascular endothelial cells from nicotine-treated mice showed mesenchymal phenotype, indicating EndMT. Moreover, nicotine-induced EndMT process was a
Ключевые слова:
Atherosclerosis; EndMT; Nicotine; Snail; α7nAChR
alpha smooth muscle actin; bungarotoxin receptor; cholinergic receptor blocking agent; mitogen activated protein kinase 1; mitogen activated protein kinase 3; nicotine; nicotinic receptor; platelet endothelial cell adhesion molecule 1; small interfering RNA; transcription factor Snail; vascular endothelial cadherin; animal experiment; animal model; animal tissue; aortic endothelial cell; aortic root; apolipoprotein E knockout mouse; Article; atherosclerosis; atherosclerotic plaque; cardiovascular risk; cell membrane permeability; cell structure; cell transformation; controlled study; cytoskeleton; disease course; drug effect; endothelial dysfunction; endothelial to mesenchymal transition; enzyme activation; gene silencing; human; human cell; immunohistochemistry; in vitro study; in vivo study; intracellular signaling; male; MAPK signaling; mouse; mRNA expression level; nonhuman; phenotype; protein expression; real time polymerase chain reaction; RNA analysis; smoking habit; upregulatio
Язык текста: Английский
ISSN: 1838-7640
Qin W.
Zhang L.
Li Z.
Xiao D.
Zhang Y.
Zhang H.
Mokembo J. N.
Monayo S. M.
Jha N. K.
Kopy'lov F. Yu. Filipp Yuryevich 1976-
Shhekochikhin D. Yu. Dmitrij Yuryevich 1985-
Zhang Y.
Qин W.
Жанг Л.
Ли З.
Хиао Д.
Жанг Y.
Жанг Х.
Мокембо Й. Н.
Монайо С. М.
Йха Н. К.
Копылов Ф. Ю. Филипп Юрьевич 1976-
Щекочихин Д. Ю. Дмитрий Юрьевич 1985-
Жанг Y.
Endothelial to mesenchymal transition contributes to nicotine-induced atherosclerosis
Текст визуальный непосредственный
Theranostics
Vol.10, Issue12 P. 5276-5289
2020
Статья
Atherosclerosis EndMT Nicotine Snail α7nAChR
alpha smooth muscle actin bungarotoxin receptor cholinergic receptor blocking agent mitogen activated protein kinase 1 mitogen activated protein kinase 3 nicotine nicotinic receptor platelet endothelial cell adhesion molecule 1 small interfering RNA transcription factor Snail vascular endothelial cadherin animal experiment animal model animal tissue aortic endothelial cell aortic root apolipoprotein E knockout mouse Article atherosclerosis atherosclerotic plaque cardiovascular risk cell membrane permeability cell structure cell transformation controlled study cytoskeleton disease course drug effect endothelial dysfunction endothelial to mesenchymal transition enzyme activation gene silencing human human cell immunohistochemistry in vitro study in vivo study intracellular signaling male MAPK signaling mouse mRNA expression level nonhuman phenotype protein expression real time polymerase chain reaction RNA analysis smoking habit upregulatio
Rationale: Nicotine exposure via cigarette smoking is strongly associated with atherosclerosis. However, the underlying mechanisms remain poorly understood. The current study aimed to identify whether endothelial to mesenchymal transition (EndMT) contributes to nicotine-induced atherosclerosis. Methods: ApoE-/- mice were administered nicotine in their drinking water for 12 weeks. The effects of nicotine on EndMT were determined by immunostaining on aortic root and RNA analysis in aortic intima. In vitro nicotine-treated cell model was established on human aortic endothelial cells (HAECs). The effects of nicotine on the expression of EndMT-related markers, ERK1/2 and Snail were quantified by real-time PCR, western blot and immunofluorescent staining. Results: Nicotine treatment resulted in larger atherosclerotic plaques in ApoE-/- mice. The vascular endothelial cells from nicotine-treated mice showed mesenchymal phenotype, indicating EndMT. Moreover, nicotine-induced EndMT process was a