MicroRNAs: recently discovered key regulators of proliferation and apoptosis in animal cells

Gammell, Patrick

doi:10.1007/s10616-007-9049-4

Cited by 67 publications

(51 citation statements)

References 113 publications

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“…Recent works demonstrate that HIF-1α may also serve as a transcription factor for the expression of noncoding genes, including microRNAs (miRs) (15). miRs are now known to play a key role in cell proliferation (16). We observed that ischemic wounds have a higher abundance of the HIF-1α-dependent miR-210 (Fig.…”

Section: Resultsmentioning

confidence: 73%

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

Biswas¹,

Roy²,

Banerjee³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

253

199

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Ischemia complicates wound closure. Here, we are unique in presenting a murine ischemic wound model that is based on bipedicle flap approach. Using this model of ischemic wounds we have sought to elucidate how microRNAs may be implicated in limiting wound reepithelialization under hypoxia, a major component of ischemia. Ischemia, evaluated by laser Doppler as well as hyperspectral imaging, limited blood flow and lowered tissue oxygen saturation. EPR oximetry demonstrated that the ischemic wound tissue had pO 2 <10 mm Hg. Ischemic wounds suffered from compromised macrophage recruitment and delayed wound epithelialization. Specifically, epithelial proliferation, as determined by Ki67 staining, was compromised. In vivo imaging showed massive hypoxia inducible factor-1α (HIF-1α) stabilization in ischemic wounds, where HIF-1α induced miR-210 expression that, in turn, silenced its target E2F3, which was markedly down-regulated in the wound-edge tissue of ischemic wounds. E2F3 was recognized as a key facilitator of cell proliferation. In keratinocytes, knock-down of E2F3 limited cell proliferation. Forced stabilization of HIF-1α using Ad-VP16-HIF-1α under normoxic conditions upregulated miR-210 expression, down-regulated E2F3, and limited cell proliferation. Studies using cellular delivery of miR-210 antagomir and mimic demonstrated a key role of miR-210 in limiting keratinocyte proliferation. In summary, these results are unique in presenting evidence demonstrating that the hypoxia component of ischemia may limit wound re-epithelialization by stabilizing HIF-1α, which induces miR-210 expression, resulting in the down-regulation of the cell-cycle regulatory protein E2F3.skin | tissue repair | wound healing

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Section: Resultsmentioning

confidence: 73%

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

Biswas¹,

Roy²,

Banerjee³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

253

199

View full text Add to dashboard Cite

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“…For example, the miR-34a, b, c, and miR-214 were observed to promote apoptosis by increasing the expression of Caspases, P21, P53, and Bax (Corney et al 2007, Gammell 2007, Zenz et al 2009). miR-210 and miR-155 repressed apoptosis by decreasing the expression of pro-apoptotic Caspases (Wang & Lee 2009).…”

Section: Discussionmentioning

confidence: 99%

microRNA 376a regulates follicle assembly by targeting Pcna in fetal and neonatal mouse ovaries

Zhang¹,

Jiang²,

Zhang³

et al. 2014

Reproduction

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In mammals, the primordial follicle pool, providing all oocytes available to a female throughout her reproductive life, is established perinatally. Dysregulation of primordial follicle assembly results in female reproductive diseases, such as premature ovarian insufficiency and infertility. Female mice lacking Dicer1 (Dicer), a gene required for biogenesis of microRNAs, show abnormal morphology of follicles and infertility. However, the contribution of individual microRNAs to primordial follicle assembly remains largely unknown. Here, we report that microRNA 376a (miR-376a) regulates primordial follicle assembly by modulating the expression of proliferating cell nuclear antigen (Pcna), a gene we previously reported to regulate primordial follicle assembly by regulating oocyte apoptosis in mouse ovaries. miR-376a was shown to be negatively correlated with Pcna mRNA expression in fetal and neonatal mouse ovaries and to directly bind to Pcna mRNA 3 0 untranslated region. Cultured 18.5 days postcoitum mouse ovaries transfected with miR-376a exhibited decreased Pcna expression both in protein and mRNA levels. Moreover, miR-376a overexpression significantly increased primordial follicles and reduced apoptosis of oocytes, which was very similar to those in ovaries co-transfected with miR-376a and siRNAs targeting Pcna. Taken together, our results demonstrate that miR-376a regulates primordial follicle assembly by modulating the expression of Pcna. To our knowledge, this is the first microRNA-target mRNA pair that has been reported to regulate mammalian primordial follicle assembly and further our understanding of the regulation of primordial follicle assembly.

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“…One of the hottest new topics in metabolic regulation is the control of mRNA expression by microRNA (miRNA). miRNAs are small non-coding transcripts (19-25 nucleotides long) that bind to target mRNAs; a perfect sequence match between a miRNA species and its target typically directs the mRNA into degradation pathways, whereas an imperfect match leads to translational inhibition via storage in cytoplasmic P-bodies [30] . Regulation by miRNA control over mRNA translation is now known to be particularly important in the regulation of development, and aberrant miRNA expression patterns have been linked with multiple diseases [31] .…”

Section: Global Metabolic Arrestmentioning

confidence: 99%

Out Cold: Biochemical Regulation of Mammalian Hibernation – A Mini-Review

Storey¹

2009

Gerontology

176

203

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Hibernating mammals offer an intriguing example of natural torpor and illustrate the regulatory mechanisms that control metabolic rate depression and the cell preservation strategies that support long-term viability in a hypometabolic state. These suggest applied strategies for improving the hypothermic preservation of human organs for transplant, and guidelines that could aid the development of torpor as an intervention strategy in human medicine. Recent advances in hibernation research have illustrated mechanisms that contribute to metabolic depression by orchestrating the global suppression of ATP-expensive transcription and translation including multiple forms of post-translational modification of proteins/enzymes (phosphorylation, acetylation, SUMOylation), mRNA storage mechanisms, and differential expression of microRNA species. DNA-screening technologies have also contributed new advances in understanding the range of cell functions that are impacted during torpor and point out some critical preservation strategies that aid long-term viability in a torpid state. These include antioxidant defenses, chaperones and the implementation of the unfolded protein response, and the enhancement of serpins (serine protease inhibitors) to control the actions of extracellular proteases in clotting and inflammation responses.

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MicroRNAs: recently discovered key regulators of proliferation and apoptosis in animal cells

Cited by 67 publications

References 113 publications

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

microRNA 376a regulates follicle assembly by targeting Pcna in fetal and neonatal mouse ovaries

Out Cold: Biochemical Regulation of Mammalian Hibernation – A Mini-Review

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