Novel Protective Role for Ubiquitin-Specific Protease 18 in Pathological Cardiac Remodeling

Ying, Xiaoying; Zhao, Yichao; Yao, Tianbao; Yuan, Ancai; Xu, Longwei; Gao, Liang; Ding, Song; Ding, Hongwei; Pu, Jun; He, Ben

doi:10.1161/hypertensionaha.116.07562

Cited by 38 publications

(34 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An Alexa Fluor 488 conjugate of WGA was used to visualize cardiomyocyte boundaries, and the size of cardiomyocytes was found to increase with age (Fig 7), consistent with previous reports [1]. This suggested that hypertrophy was an alternative growth method when cardiomyocytes exit proliferation [18]. …”

Section: Resultssupporting

confidence: 87%

Age-Dependent Oxidative DNA Damage Does Not Correlate with Reduced Proliferation of Cardiomyocytes in Humans

Huang

Hong

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

BackgroundPostnatal human cardiomyocyte proliferation declines rapidly with age, which has been suggested to be correlated with increases in oxidative DNA damage in mice and plays an important role in regulating cardiomyocyte proliferation. However, the relationship between oxidative DNA damage and age in humans is unclear.MethodsSixty right ventricular outflow myocardial tissue specimens were obtained from ventricular septal defect infant patients during routine congenital cardiac surgery. These specimens were divided into three groups based on age: group A (age 0–6 months), group B (age, 7–12 months), and group C (>12 months). Each tissue specimen was subjected to DNA extraction, RNA extraction, and immunofluorescence.ResultsImmunofluorescence and qRT-PCR analysis revealed that DNA damage markers—mitochondrial DNA copy number, oxoguanine 8, and phosphorylated ataxia telangiectasia mutated—were highest in Group B. However immunofluorescence and qRT-PCR demonstrated that two cell proliferation markers, Ki67 and cyclin D2, were decreased with age. In addition, wheat germ agglutinin-staining indicated that the average size of cardiomyocytes increased with age.ConclusionsOxidative DNA damage of cardiomyocytes was not correlated positively with age in human beings. Oxidative DNA damage is unable to fully explain the reduced proliferation of human cardiomyocytes.

show abstract

Section: Resultssupporting

confidence: 87%

Age-Dependent Oxidative DNA Damage Does Not Correlate with Reduced Proliferation of Cardiomyocytes in Humans

Huang

Hong

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…In hearts of patients with dilated cardiomyopathy, USP18 expression was significantly higher than in hearts from healthy donors. Moreover, in murine hearts exposed to increased afterload, augmented expression of USP18 in cardiomyocytes was related to less pronounced myocardial fibrosis, reduced left ventricular wall hypertrophy and delayed onset of heart failure (Ying et al, 2016). In contrast, USP18deficient mice presented advanced cardiac remodelling (Ying et al, 2016).…”

Section: Cardiac Remodellingmentioning

confidence: 98%

“…Ying and others (Ying et al, 2016) had shed a new light on activity of USP18 and extended its action to the cardiovascular system. Their study demonstrated that USP18 inhibits cardiac remodelling and protects from the development of heart failure.…”

Section: Cardiac Remodellingmentioning

confidence: 99%

“…These diverse functions make USP18 an interesting object for research and many studies describing this unique molecule have been published recently. Among others, its contribution to cell signalling, response to viral and bacterial infections, development of several malignancies and development of autoimmune diseases have been described (Liu et al, 1999;Ritchie et al, 2004;Hoeller et al, 2006;Catic et al, 2007;Duex & Sorkin, 2009;François-Newton et al, 2011;Murray et al, 2011;Burkart et al, 2012;Guo et al, 2012;Yim et al, 2012;Coit et al, 2013;Honke et al, 2013;Hong et al, 2014;Zhang et al, 2015;Honke et al, 2016;Ying et al, 2016;An et al, 2017;Arimoto et al, 2017;Basters et al, 2017;Mustachio et al, 2017;Basters et al, 2018;Shaabani et al, 2018;Gu et al, 2019). USP18 was also found to serve as an inhibitor of cardiac remodelling (Ying et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Versatility of USP18 in physiology and pathophysiology

Dziamałek-Macioszczyk

Harazny

Stompór

2019

Acta Biochim Pol

View full text Add to dashboard Cite

Ubiquitin-specific peptidase 18 (USP18) is a multifunctional protein and its roles are still being investigated. This enzyme removes ubiquitin-like molecules from their substrates and the only known interferon-stimulated gene 15 (ISG15) specific protease. Apart from its enzymatic function, it also inhibits interferon type I and III signalling pathways. USP18 is known to regulate multiple processes, such as: cell cycle, cell signalling and response to viral and bacterial infections. Moreover, it contributes to the development of several autoimmune diseases and carcinogenesis, and recently was described as a cardiac remodelling inhibitor. This review summarizes the current knowledge on USP18 functions, highlighting its contribution to the development of heart failure, given the fact that this disease's etiology is now considered to be inflammatory in nature.

show abstract

“…In experimental study, the overexpression of A20 attenuated the hypertrophic stimulant such as phenylephrine-induced development of pathological hypertrophy. 92 97 A molecular study found that USP18 inactivates TAK1 by deubiquitinating K63-linked polyubiquitination and it subsequently suppresses the downstream NF-jB and JNK1/2 signalling pathways, which plays critical role in NAFLD progression. 98 USP14 also contributes to suppress the development of cardiac hypertrophy by increasing phosphorylation of GSK-3b (Table 2).…”

mentioning

confidence: 99%

The role of K63‐linked polyubiquitination in cardiac hypertrophy

Ponnusamy

Xin

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

Ubiquitination, also known as ubiquitylation, is a vital post‐translational modification of proteins that play a crucial role in the multiple biological processes including cell growth, proliferation and apoptosis. K63‐linked ubiquitination is one of the vital post‐translational modifications of proteins that are involved in the activation of protein kinases and protein trafficking during cell survival and proliferation. It also contributes to the development of various disorders including cancer, neurodegeneration and cardiac hypertrophy. In this review, we summarize the role of K63‐linked ubiquitination signalling in protein kinase activation and its implications in cardiac hypertrophy. We have also provided our perspectives on therapeutically targeting K63‐linked ubiquitination in downstream effector molecules of growth factor receptors for the treatment of cardiac hypertrophy.

show abstract

Novel Protective Role for Ubiquitin-Specific Protease 18 in Pathological Cardiac Remodeling

Cited by 38 publications

References 44 publications

Age-Dependent Oxidative DNA Damage Does Not Correlate with Reduced Proliferation of Cardiomyocytes in Humans

Age-Dependent Oxidative DNA Damage Does Not Correlate with Reduced Proliferation of Cardiomyocytes in Humans

Versatility of USP18 in physiology and pathophysiology

The role of K63‐linked polyubiquitination in cardiac hypertrophy

Contact Info

Product

Resources

About