Effects of targeted modulation of miR-762 on expression of the IFITM5 gene in Saos-2 cells

Mo, Xinkai; Li, Yanqin; Han, Jinxiang

doi:10.5582/irdr.3.12

Cited by 6 publications

(5 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-762 is reportedly upregulated in human corneal epithelial cells induced by tear fluid and Pseudomonas aeruginosa antigens, which act by targeting a number of important genes, such as RNase7 and ST2 23 . Moreover, miR-762 is involved in bone mineralization by repressing the expression of IFITM5 in Saos-2 cells 24 . In addition, miR-762 was shown to increase breast cancer cell proliferation and invasion by targeting IRF7 expression 25 .…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial miR-762 regulates apoptosis and myocardial infarction by impairing ND2

Zhai

et al. 2019

Cell Death Dis

View full text Add to dashboard Cite

Mitochondrial dysfunction plays a major role in the pathogenesis of cardiovascular diseases. MicroRNAs (miRNAs) are small RNAs that act as negative regulators of gene expression, but how miRNAs affect mitochondrial function in the heart is unclear. Using a miRNA microarray assay, we found that miR-762 predominantly translocated in the mitochondria and was significantly upregulated upon anoxia/reoxygenation (A/R) treatment. Knockdown of endogenous miR-762 significantly attenuated the decrease in intracellular ATP levels, the increase in ROS levels, the decrease in mitochondrial complex I enzyme activity and the increase in apoptotic cell death in cardiomyocytes, which was induced by A/R treatment. In addition, knockdown of miR-762 ameliorated myocardial ischemia/reperfusion (I/R) injury in mice. Mechanistically, we showed that enforced expression of miR-762 dramatically decreased the protein levels of endogenous NADH dehydrogenase subunit 2 (ND2) but had no effect on the transcript levels of ND2. The luciferase reporter assay showed that miR-762 bound to the coding sequence of ND2. In addition, knockdown of endogenous ND2 significantly decreased intracellular ATP levels, increased ROS levels, reduced mitochondrial complex I enzyme activity and increased apoptotic cell death in cardiomyocytes, which was induced by A/R treatment. Furthermore, we found that the inhibitory effect of miR-762 downregulation was attenuated by ND2 knockdown. Thus, our findings suggest that miR-762 participates in the regulation of mitochondrial function and cardiomyocyte apoptosis by ND2, a core assembly subunit of mitochondrial complex I. Our results revealed that mitochondrial miR-762, as a new player in mitochondrial dysfunction, may provide a new therapeutic target for myocardial infarction.

show abstract

Section: Discussionmentioning

confidence: 99%

Mitochondrial miR-762 regulates apoptosis and myocardial infarction by impairing ND2

Zhai

et al. 2019

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…Previous study has shown that miR‐762 is up‐regulated in human corneal epithelial cells in response to tear fluid and Pseudomonas aeruginosa antigens, and genes coding for RNase7 and ST2 have been identified as target genes of miR‐762 . Moreover, miR‐762 suppresses expression of IFITM5 at the translational level in Saos‐2 cells, and probably contributes to progression of bone mineralization . However, the role of miR‐762 in breast cancer has remained unclear.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐762 promotes breast cancer cell proliferation and invasion by targeting IRF7 expression

Huang

Wang

et al. 2015

Cell Proliferation

View full text Add to dashboard Cite

show abstract

“…It has been reported that miR-762 could promote the development of ovarian cancer by suppressing Menin 20 . miR-762 has also been reported to regulate Interferon-induced transmembrane protein 5 (IFITM5), an osteoblast-specific membrane protein 21 . This is the first study to reveal miR-762’s role in myogenesis.…”

Section: Discussionmentioning

confidence: 77%

Long Noncoding RNA lncMUMA Reverses Established Skeletal Muscle Atrophy following Mechanical Unloading

Guan

Liang

et al. 2018

Molecular Therapy

View full text Add to dashboard Cite

Reversing established muscle atrophy following mechanical unloading is of great clinical challenge. Long noncoding RNAs (lncRNAs) have been demonstrated to play important roles in myogenesis. Here we identified a lncRNA (mechanical unloading-induced muscle atrophy-related lncRNA [lncMUMA]) enriched in muscle, which was the most downregulated lncRNA during muscle atrophy development in hindlimb suspension (HLS) mice. The in vitro and in vivo data demonstrated that the decreased expression levels of lncMUMA closely associated with a reduction of myogenesis during mechanical unloading. Mechanistically, lncMUMA promoted myogenic differentiation by functioning as a miR-762 sponge to regulate the core myogenic regulator MyoD in vitro. The enforced expression of lncMUMA relieved the decreases in MyoD protein and muscle mass in miR-762 knockin mice. Therapeutically, the enforced expression of lncMUMA improved the in vitro myogenic differentiation of myoblasts under microgravity simulation, prevented the muscle atrophy development, and reversed the established muscle atrophy in HLS mice. These findings identify lncMUMA as an anabolic regulator to reverse established muscle atrophy following mechanical unloading.

show abstract

Effects of targeted modulation of miR-762 on expression of the IFITM5 gene in Saos-2 cells

Cited by 6 publications

References 30 publications

Mitochondrial miR-762 regulates apoptosis and myocardial infarction by impairing ND2

Mitochondrial miR-762 regulates apoptosis and myocardial infarction by impairing ND2

microRNA‐762 promotes breast cancer cell proliferation and invasion by targeting IRF7 expression

Long Noncoding RNA lncMUMA Reverses Established Skeletal Muscle Atrophy following Mechanical Unloading

Contact Info

Product

Resources

About