miR‐1/miR‐206 regulate Hsp60 expression contributing to glucose‐mediated apoptosis in cardiomyocytes

Shan, Zhi; Lin, Qiaoli; Deng, Chunyu; Zhu, Ji-Xiao; Mai, Liping; Liu, Juli; Fu, Yong-Heng; Li, Xiaoying; Li, Yang-Xin; Zhang, Youyi; Lin, Shu; Yu, Xiang

doi:10.1016/j.febslet.2010.07.027

Cited by 182 publications

(140 citation statements)

References 39 publications

Supporting

Mentioning

135

Contrasting

Order By: Relevance

“…miR-1 has a single target site in the 3'-untranslated region of HSP60 mRNA, thus determining post-transcriptional repression of HSP60 synthesis in rat ventricular CMC [34]. Similar effects have also been demonstrated for miR-206 [34]. This miR-induced reduction of HSP60 can trigger CMC apoptosis.…”

Section: Hsp60 Has Anti-apoptotic Effects In Cardio-myocytessupporting

confidence: 60%

“…In these conditions, the levels of HSP60 protein and mRNA were found increased (from 2 to 5-fold) [11,12]. These data were confirmed in another study that showed a cHSP60 decrease, while mitochondrial HSP60 increased in CMC from both dilated cardiomyopathy and ischemic hearts [34]. In patients with dilated cardiomyopathy HSP60 was found not only in CMC but also in connective tissue [12].…”

Section: Hsp60 and The Pathogenesis Of Heart Failure (Hf) And Hypertesupporting

confidence: 56%

“…For example, miR-1 has been found to be pro-apoptotic [33]. miR-1 has a single target site in the 3'-untranslated region of HSP60 mRNA, thus determining post-transcriptional repression of HSP60 synthesis in rat ventricular CMC [34]. Similar effects have also been demonstrated for miR-206 [34].…”

Section: Hsp60 Has Anti-apoptotic Effects In Cardio-myocytesmentioning

confidence: 66%

See 2 more Smart Citations

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60, the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

show abstract

Section: Hsp60 Has Anti-apoptotic Effects In Cardio-myocytessupporting

confidence: 60%

Section: Hsp60 and The Pathogenesis Of Heart Failure (Hf) And Hypertesupporting

confidence: 56%

See 1 more Smart Citation

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

View full text Add to dashboard Cite

show abstract

“…In particular, the MyomiR, miR1, has been previously shown to regulate myoblast differentiation, apoptosis, and load-induced skeletal muscle hypertrophy (19,21,35). Herein, we have elucidated a novel function for miR1 in promoting the skeletal muscle atrophy associated with Dex and Mstn treatment (Fig.…”

Section: Discussionmentioning

confidence: 84%

Muscle-specific MicroRNA1 (miR1) Targets Heat Shock Protein 70 (HSP70) during Dexamethasone-mediated Atrophy*

Kukreti

Kottaiswamy

Harikumar

et al. 2013

Journal of Biological Chemistry

108

View full text Add to dashboard Cite

Background: miR1 is a muscle-specific microRNA, however, its role in muscle atrophy is unclear. Results: Excess dexamethasone and myostatin induced miR1 via glucocorticoid receptor, resulting in reduced HSP70 and development of muscle atrophy. Conclusion: miR1 mediates muscle atrophy by regulating the levels of HSP70. Significance: Given that miR1 has a role in muscle atrophy, its antagonism may be beneficial during atrophy.

show abstract

“…Over-expressed miR-133 can impel QT interval prolongation in patients with diabetes (89). However, down-regulation of both miR-1 and miR-133a occurred in insulin-deficiency and in cardiac hypertrophy and heart failure (90,91). Remarkably, a recent study found correlation between miR-126 levels and the onset of DVC was contradictory (92).…”

Section: Mirnamentioning

confidence: 99%

Epigenetic Diabetic Vascular Complications

Ahmadzadeh-Amiri

2016

J Pediatr Rev

View full text Add to dashboard Cite

Diabetic vascular complications (DVC) influence several vital organ systems including cardiovascular, renal, ocular and nervous systems making it a major public health problem. Although extensive researches were performed in this field, the exact mechanisms responsible for these organ damages in diabetes remain obscure. Several metabolic disturbances have been involved in its complication and change in genes associated with these pathways occurred. Gene expression to produce a biologically active protein can be controlled by transcriptional and translational alteration on the head of genes without change in nucleotide composition. These epigenetic adjustments are steady, but possibly reversible and can be transmitted to future generation. Gene expression can be regulated by three epigenetic mechanisms including DNA methylation, histone modifications and noncoding microRNAs (miRNAs) activity. Epigenetic studies must be directed to better realize the role of epigenetic changes to the etiology of DVC and knowledge of epigenetic would play a pivotal role in the application of individualized medicine. Application and development of high technology sequencing combined with more sensitive and advanced methodologies for epigenome studying help to determine specific epigenetic events that stimulate gene responses in patients with diabetes mellitus.

show abstract

miR‐1/miR‐206 regulate Hsp60 expression contributing to glucose‐mediated apoptosis in cardiomyocytes

Cited by 182 publications

References 39 publications

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Muscle-specific MicroRNA1 (miR1) Targets Heat Shock Protein 70 (HSP70) during Dexamethasone-mediated Atrophy*

Epigenetic Diabetic Vascular Complications

Contact Info

Product

Resources

About