We have located links that may give you full text access.
Death-Associated Protein Kinase 1 Promotes Alveolar Epithelial Cell Apoptosis and Ventilator-Induced Lung Injury Through P53 Pathway.
Shock 2021 July 9
OBJECTIVES: Mechanical stretch induced alveolar epithelial cell (AEC) apoptosis participates in the onset of ventilator induced lung injury (VILI). In this study, we explored whether death associated protein kinase 1 (DAPK1) mediated cyclic stretch (CS) induced AEC apoptosis and VILI though P53 pathway.
MATERIALS AND METHODS: AEC apoptosis was induced by CS using the FX-5000T Flexercell Tension Plus system. C57BL/6 mouse received high tidal volume ventilation to build VILI model. DAPK1 inhibitor, P53 inhibitor or DAPK1 plasmid was used to regulate the expression of DAPK1 and P53, respectively. Flow cytometery was performed to assay cell apoptosis and the changes of mitochondrial membrane potential (MMP); Immunoblotting was adopted to analyse related protein expression; The binding of related proteins was detected by coimmunoprecipitation; AEC apoptosis in vivo was determined by immunohistochemistry assay.
RESULTS: CS promoted AEC apoptosis, increased DAPK1 and P53 expression and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1. Moreover, DAPK1 plasmid transfection also promoted the expression of Bax and the change of MMP, but decreased the level of Bcl-2. Inhibition of DAPK1 or P53 in vivo alleviated high tidal volume ventilation induced AEC apoptosis and lung injury.
CONCLUSIONS: DAPK1 contributes to AEC apoptosis and the onset of VILI though P53 and its intrinsic pro-apoptotic pathway. Inhibition of DAPK1 or P53 alleviates high tidal volume ventilation induced lung injury and AEC apoptosis.
MATERIALS AND METHODS: AEC apoptosis was induced by CS using the FX-5000T Flexercell Tension Plus system. C57BL/6 mouse received high tidal volume ventilation to build VILI model. DAPK1 inhibitor, P53 inhibitor or DAPK1 plasmid was used to regulate the expression of DAPK1 and P53, respectively. Flow cytometery was performed to assay cell apoptosis and the changes of mitochondrial membrane potential (MMP); Immunoblotting was adopted to analyse related protein expression; The binding of related proteins was detected by coimmunoprecipitation; AEC apoptosis in vivo was determined by immunohistochemistry assay.
RESULTS: CS promoted AEC apoptosis, increased DAPK1 and P53 expression and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1. Moreover, DAPK1 plasmid transfection also promoted the expression of Bax and the change of MMP, but decreased the level of Bcl-2. Inhibition of DAPK1 or P53 in vivo alleviated high tidal volume ventilation induced AEC apoptosis and lung injury.
CONCLUSIONS: DAPK1 contributes to AEC apoptosis and the onset of VILI though P53 and its intrinsic pro-apoptotic pathway. Inhibition of DAPK1 or P53 alleviates high tidal volume ventilation induced lung injury and AEC apoptosis.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
Perioperative echocardiographic strain analysis: what anesthesiologists should know.Canadian Journal of Anaesthesia 2024 April 11
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app