CKIP-1 plays an important role in the regulation of cardiac remodeling induced by simulated microgravity

Author(s):  
Yingxian Li
2018 ◽  
Vol 9 ◽  
Author(s):  
Shukuan Ling ◽  
Yuheng Li ◽  
Guohui Zhong ◽  
Yongjun Zheng ◽  
Qing Xu ◽  
...  

2021 ◽  
Author(s):  
Guohui Zhong ◽  
Dingsheng Zhao ◽  
Jianwei Li ◽  
Zifan Liu ◽  
Junjie Pan ◽  
...  

Cardiac muscle is extremely sensitive to changes in loading conditions, the microgravity during space flight can cause cardiac remodeling and function decline. At present, the mechanism of microgravity-induced cardiac remodeling remains to be revealed. WW domain-containing E3 ubiquitin protein ligase 1 (WWP1) is an important activator of pressure-overload induced cardiac remodeling by stabilizing disheveled segment polarity proteins 2 (DVL2) and activating CaMKII/HDAC4/MEF2C axis. However, the role of WWP1 in the cardiac remodeling induced by microgravity is unknown. The purpose of this study was to determine whether WWP1 was also involved in the regulation of cardiac remodeling caused by microgravity. Firstly, we detected the expression of WWP1 and DVL2 in the heart from mice and monkeys after simulated microgravity using western blotting and Immunohistochemistry. Secondly, WWP1 knockout (KO) and wild type mice were subjected to hindlimb unloading (HU) to simulate microgravity effect. We assessed the cardiac remodeling in morphology and function through histological analysis and echocardiography. Finally, we detected the phosphorylation level of CaMKII and HDAC4 in the heart from WT and WWP1 KO mice after HU. The results revealed the increased expression of WWP1 and DVL2 in the heart both from mice and monkey after simulated microgravity. WWP1 deficiency protected against simulated microgravity-induced cardiac atrophy and function decline. Histological analysis demonstrated WWP1 KO inhibited the decreases in the size of individual cardiomyocytes of mice after hindlimb unloading. WWP1 KO can inhibit the activation of DVL2/CaMKII/HDAC4 pathway in heart of mice induced by simulated microgravity. These results demonstrated WWP1 as a potential therapeutic target for cardiac remodeling and function decline induced by simulated microgravity. Keywords: WWP1, simulated microgravity, cardiac remodeling, DVL2, HDAC4.


Phytomedicine ◽  
2019 ◽  
Vol 56 ◽  
pp. 83-93 ◽  
Author(s):  
Huiyuan Sun ◽  
Shukuan Ling ◽  
Dingsheng Zhao ◽  
Yang Li ◽  
Guohui Zhong ◽  
...  

Author(s):  
Guohui Zhong ◽  
Dingsheng Zhao ◽  
Jianwei Li ◽  
Zifan Liu ◽  
Junjie Pan ◽  
...  

Cardiac muscle is extremely sensitive to changes in loading conditions; the microgravity during space flight can cause cardiac remodeling and function decline. At present, the mechanism of microgravity-induced cardiac remodeling remains to be revealed. WW domain-containing E3 ubiquitin protein ligase 1 (WWP1) is an important activator of pressure overload-induced cardiac remodeling by stabilizing disheveled segment polarity proteins 2 (DVL2) and activating the calcium-calmodulin-dependent protein kinase II (CaMKII)/histone deacetylase 4 (HDAC4)/myocyte-specific enhancer factor 2C (MEF2C) axis. However, the role of WWP1 in cardiac remodeling induced by microgravity is unknown. The purpose of this study was to determine whether WWP1 was also involved in the regulation of cardiac remodeling caused by microgravity. Firstly, we detected the expression of WWP1 and DVL2 in the heart from mice and monkeys after simulated microgravity using western blotting and immunohistochemistry. Secondly, WWP1 knockout (KO) and wild-type (WT) mice were subjected to tail suspension (TS) to simulate microgravity effect. We assessed the cardiac remodeling in morphology and function through a histological analysis and echocardiography. Finally, we detected the phosphorylation levels of CaMKII and HDAC4 in the hearts from WT and WWP1 KO mice after TS. The results revealed the increased expression of WWP1 and DVL2 in the hearts both from mice and monkeys after simulated microgravity. WWP1 deficiency alleviated simulated microgravity-induced cardiac atrophy and function decline. The histological analysis demonstrated WWP1 KO inhibited the decreases in the size of individual cardiomyocytes of mice after tail suspension. WWP1 KO can inhibit the activation of the DVL2/CaMKII/HDAC4 pathway in the hearts of mice induced by simulated microgravity. These results demonstrated WWP1 as a potential therapeutic target for cardiac remodeling and function decline induced by simulated microgravity.


2015 ◽  
Vol 66 (16) ◽  
pp. C88
Author(s):  
Guohui Zhong ◽  
Shukuan Ling ◽  
Hongxing Li ◽  
Yuheng Li ◽  
Weijia Sun ◽  
...  

2018 ◽  
Author(s):  
A Dieckerhoff ◽  
J Möllmann ◽  
M Schwarz ◽  
E Liehn ◽  
S Diebold ◽  
...  

2017 ◽  
Vol 2 (2) ◽  
pp. 69-74
Author(s):  
Mohammad Aminullah ◽  
Fahmida Akter Rima ◽  
Asraful Hoque ◽  
Mokhlesur Rahman Sazal ◽  
Prodip Biswas ◽  
...  

Background: Cardiac remodeling is important issue after surgical closure of ventricular septal defect.Objective: The purpose of the present study was to evaluate cardiac remodeling by echocardiography by measuring the ejection fraction, fractional shortening, left ventricular internal diameter during diastole (LVIDd) and left ventricular internal diameter during systole (LVIDs) after surgical closure of ventricular septal defect in different age group. Methodology: This prospective cohort studies was conducted in the Department of Cardiac Surgery at National Institute of Cardiovascular Disease (NICVD), Dhaka. Patient with surgical closure of VSD were enrolled into this study purposively and were divided into 3 groups according to the age. In group A (n=10), patients were within the age group of 2.0 to 6.0 years; age of group B (n=8) patients were 6.1-18.0 years and the group C (n=6) aged range was 18.1-42.0 years. Echocardiographic variables such as ejection fraction, fractional shortening, LVIDd, LVIDs were taken preoperatively and at 1st and 3rd month of postoperative values. Result: A total number of 24 patients was recruited for this study. The mean ages of all groups were 12.60±12.09. After 1 month ejection fraction were decreased by 5.97%, 6.71% and 5.66% in group A, group B and group C respectively. After 3 months ejection fraction were increased by 6.13%, 5.13% and 5.14% in group A, group B and group C respectively. After 1 month fractional shortening were decreased by 13.55%, 9.30% and 9.09% in group A, group B and group C respectively. After 3 months fractional shortening were increased by 7.23%, 7.35% and 4.55% in group A, group B and group C respectively. After 1 month LVIDd were increased by 1.97%, 1.91% and 1.32% in group A, group B and group C respectively. After 3 months LVIDd were decreased by 10.84%, 9.89% and 7.34% in group A, group B and group C respectively. After 1 month LVIDs were increased by 2.19%, 2.86% and 1.98% in group A, group B and group C respectively. After 3 months LVIDs were decreased by 11.68%, 10.97% and 8.87% in group A, group B and group C respectively.Conclusion: Cardiac remodeling occurred after surgical closure of ventricular septal defect and remodeling were more significant in younger age group. Journal of National Institute of Neurosciences Bangladesh, 2016;2(2):69-74


1993 ◽  
Author(s):  
Jeanne Becker ◽  
Thomas Goodwin ◽  
Tacey Prewett ◽  
Glenn Spaulding

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