In Vitro Evidence Suggests That miR-133a-mediated Regulation of Uncoupling Protein 2 (UCP2) Is an Indispensable Step in Myogenic Differentiation

Chen, Xi; Wang, Kehui; Chen, Jiangning; Guo, Jigang; Yin, Yuan; Cai, Xing Fu; Guo, Xing; Wang, Guoqiang; Yang, Rong; Zhu, Lingyun; Zhang, Yan; Wang, Jin; Xiang, Yang; Weng, Chun-Yue; Zen, Ke; Zhang, Junfeng; Zhang, Chenyu

doi:10.1074/jbc.m807523200

Cited by 89 publications

(67 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Importantly in both cardiac and skeletal muscle, mitochondrial UPC2/UCP3 uncoupling proteins regulate energy homeostasis and the rate of development and differentiation, with UPC2 repressing differentiation and promoting cell proliferation. However, MyoD activates miR133a expression which in turn directly downregulates UCP2 mRNA to alleviate the develop mental repression, suggesting a feedback network involving MyoDmiR133aUCP2 [56] . Additionally, over expression of myogenin and MyoD in mouse C2C12 myoblasts [57] increase expression strongly from the UCP3…”

Section: Muscle Mitochondrial Functionmentioning

confidence: 99%

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

140

132

View full text Add to dashboard Cite

MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

show abstract

Section: Muscle Mitochondrial Functionmentioning

confidence: 99%

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

140

132

View full text Add to dashboard Cite

show abstract

“…4A) was fused into a luciferase reporter plasmid. The resultant plasmid and control plasmid (b-gal) were introduced into 293T cells (22). Because miR-21 was also widely reported to target the PTEN (36-40), miR-19a (37), we further compared the PTEN-binding seed sequence between miR-21 and miR-214 (Fig.…”

Section: Identification Of Monocytic Pten As a Target Gene Of Mir-214mentioning

confidence: 99%

“…THP-1 cells (∼10 6 ), seeded on six-well plates or 60-mm dishes, were transfected with pre-miR-214 or miR-214 ASOs using Lipofectamine 2000 (Invitrogen), according to the manufacturer's instructions (22). For miR-214 overexpression, 100 pmol pre-miR-214 or scrambled control oligonucleotide was used.…”

Section: Overexpression or Knockdown Of Mir-214mentioning

confidence: 99%

See 1 more Smart Citation

Role of MicroRNA-214–Targeting Phosphatase and Tensin Homolog in Advanced Glycation End Product-Induced Apoptosis Delay in Monocytes

Liu

Hou

Guo

et al. 2011

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Advanced glycation end products (AGEs) delay spontaneous apoptosis of monocytes and contribute to the development of inflammatory responses. However, the mechanism by which AGEs affect monocyte apoptosis is unclear. We studied the role of microRNA-214 (miR-214) and its target gene in AGE-induced monocytic apoptosis delay. Using microRNA (miRNA) microarray and stem-loop, quantitative RT-PCR assay, we studied genome-wide miRNA expression in THP-1 cells treated with or without AGEs. Significant upregulation of miR-214 was consistently observed in THP-1 and human monocytes treated with various AGEs, and AGE-induced monocytic miR-214 upregulation was likely through activation of receptor for AGEs. A striking increase in miR-214 was also detected in monocytes from patients with chronic renal failure. Luciferase reporter assay showed that miR-214 specifically binds to the phosphatase and tensin homolog (PTEN) mRNA 3′-untranslated region, implicating PTEN as a target gene of miR-214. PTEN expression is inversely correlated with miR-214 level in monocytes. Compared with normal monocytes, AGE-treated monocytes and monocytes from chronic renal failure patients exhibited lower PTEN levels and delayed apoptosis. Overexpression of pre–miR-214 led to impaired PTEN expression and delayed apoptosis of THP-1 cells, whereas knockdown of miR-214 level largely abolished AGE-induced cell survival. Our findings define a new role for miR-214–targeting PTEN in AGE-induced monocyte survival.

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

In Vitro Evidence Suggests That miR-133a-mediated Regulation of Uncoupling Protein 2 (UCP2) Is an Indispensable Step in Myogenic Differentiation

Cited by 89 publications

References 33 publications

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Role of MicroRNA-214–Targeting Phosphatase and Tensin Homolog in Advanced Glycation End Product-Induced Apoptosis Delay in Monocytes

Epigenetic Diabetic Vascular Complications

Contact Info

Product

Resources

About