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Tytuł:
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Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy.
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Autorzy:
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Zong DD; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.
Liu XM; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.
Li JH; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.
Ouyang RY; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.
Long YJ; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China.
Chen P; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. .; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China. .; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China. .
Chen Y; Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. .; Research Unit of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China. .; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, 410011, Hunan, China. .
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Źródło:
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Respiratory research [Respir Res] 2021 Jan 19; Vol. 22 (1), pp. 22. Date of Electronic Publication: 2021 Jan 19.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: 2001- : London : BioMed Central Ltd.
Original Publication: London : Current Science Ltd., c2000-
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MeSH Terms:
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Apoptosis/*physiology
Autophagy/*physiology
Human Umbilical Vein Endothelial Cells/*metabolism
Receptor, Notch1/*metabolism
Resveratrol/*pharmacology
Smoke/*adverse effects
Antioxidants/pharmacology ; Apoptosis/drug effects ; Autophagy/drug effects ; Cigarette Smoking/adverse effects ; Cigarette Smoking/metabolism ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Human Umbilical Vein Endothelial Cells/drug effects ; Humans ; Signal Transduction/drug effects ; Signal Transduction/physiology
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References:
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Grant Information:
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81900042 National Natural Science Foundation of China; 2018JJ3763 Natural Science Foundation of Hunan Province; 2012-650 National Key Clinical Specialty Construction Projects of China
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Contributed Indexing:
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Keywords: Apoptosis; Autophagy; Endothelial cells; Notch1 signaling; Resveratrol
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Substance Nomenclature:
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0 (Antioxidants)
0 (NOTCH1 protein, human)
0 (Receptor, Notch1)
0 (Smoke)
Q369O8926L (Resveratrol)
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Entry Date(s):
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Date Created: 20210120 Date Completed: 20210129 Latest Revision: 20210129
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Update Code:
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20240105
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PubMed Central ID:
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PMC7816466
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DOI:
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10.1186/s12931-021-01620-3
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PMID:
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33468121
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Background: Increasing evidence shows that endothelial apoptosis contributes to cigarette smoke (CS)-induced disease progression, such as chronic obstructive pulmonary disease (COPD). Our previous studies have validated Notch1 as an anti-apoptotic signaling in CS-induced endothelial apoptosis. Resveratrol (RESV) is a naturally occurring polyphenol that exhibits an anti-apoptotic activity in endothelial cells that exposed to many kinds of destructive stimulus. However, the effects of resveratrol on Notch1 signaling in CS-induced endothelial apoptosis have not yet been fully elucidated. Therefore, the aim of this study was to examine whether RESV can protect endothelial cells from CS-induced apoptosis via regulating Notch1 signaling.
Methods: Human umbilical vein endothelial cells (HUVECs) were pretreated with RESV for 2 h, followed by cotreatment with 2.5%CSE for 24 h to explore the role of RESV in CSE induced endothelial apoptosis. 3-methyladenine (3-MA) or rapamycin was used to alter autophagic levels. Lentivirus Notch1 intracellular domain (LV-N1ICD), γ-secretase inhibitor (DAPT) and Notch1 siRNA were used to change Notch1 expression. The expression of Notch1, autophagic and apoptotic markers were examined by Western blot and the apoptosis rate was detected by Flow cytometry analysis.
Results: Our results showed that activating autophagy reduced CSE-induced endothelial apoptosis, while blocking autophagy promoted cell apoptosis in HUVECs. RESV pretreatment attenuated the CSE-induced endothelial apoptosis and activated Notch1 signaling. RESV pretreatment also increased LC3b-II and Beclin1 production, decreased p62 and mTOR expression. 3-MA treatment inhibited autophagy and aggravated CSE induced apoptosis, while rapamycin promoted autophagy, led to a decrease in cell apoptosis. LV-N1ICD transfection upregulated autophagy and reduced apoptosis. However, this protective effect was abolished by 3-MA treatment. In cells treated with DAPT or Notch1 siRNA, autophagy was decreased, while apoptosis was increased. RESV partly rescued the DAPT or Notch1 siRNA induced apoptosis by activating Notch1 signaling.
Conclusion: In HUVECs, RESV attenuates CSE induced endothelial apoptosis by inducing autophagy in a Notch1-dependent manner.
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