Functional Studies of microRNAs in Neural Stem Cells: Problems and Perspectives

Åkerblom, Malin; Sachdeva, Rohit; Jakobsson, Johan

doi:10.3389/fnins.2012.00014

Cited by 26 publications

(23 citation statements)

References 106 publications

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“…miRNAs also regulate neural stem cell function in the adult brain (39-46). The biological function of miRNAs in neurogenesis has recently been reviewed (39,47-51). Emerging data indicate that adult neural stem cells express miRNAs and that cerebral infarction substantially alters miRNA profiles in neural stem cells.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs in Cerebral Ischemia-Induced Neurogenesis

Liu

Chopp

Zhang

et al. 2013

J Neuropathol Exp Neurol

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Cerebral ischemia induces neurogenesis including proliferation and differentiation of neural progenitor cells and migration of newly generated neuroblasts. microRNAs (miRNAs) are small non-coding RNAs that decrease gene expression through mRNA destabilization and/or translational repression. Emerging data indicate that miRNAs have a role in mediating processes of proliferation and differentiation of adult neural progenitor cells. This article reviews recent findings on miRNA profile changes in neural progenitor cells after cerebral infarction and the contributions of miRNAs to their ischemia-induced proliferation and differentiation. We highlight interactions between the miR-124 and the miR17-92 cluster and the Notch and Sonic hedgehog signaling pathways in mediating stroke-induced neurogenesis.

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Section: Introductionmentioning

confidence: 99%

MicroRNAs in Cerebral Ischemia-Induced Neurogenesis

Liu

Chopp

Zhang

et al. 2013

J Neuropathol Exp Neurol

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“…34,35 Studies in cancer and neuronal cells have began to establish the downstream targets of miR-124, which may associate with proliferation or other aspects of activated cell phenotype, such as Sox9, Jag1, polypyrimidine tract–binding protein 1 (PTBP1), small C-terminal domain phosphatase 1, ephrin-B1, NfatC3, and monocyte chemotactic protein-1 (MCP-1). 27,36,37 PTBP1 is especially interesting because of its effects on Notch signaling and other aspects of proliferation in cancer cell types. 38 …”

mentioning

confidence: 99%

MicroRNA-124 Controls the Proliferative, Migratory, and Inflammatory Phenotype of Pulmonary Vascular Fibroblasts

Wang

Zhang

et al. 2014

Circulation Research

178

179

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Rationale Pulmonary hypertensive remodeling is characterized by excessive proliferation, migration, and proinflammatory activation of adventitial fibroblasts. In culture, fibroblasts maintain a similar activated phenotype. The mechanisms responsible for generation/maintenance of this phenotype remain unknown. Objective We hypothesized that aberrant expression of microRNA-124 (miR-124) regulates this activated fibroblast phenotype and sought to determine the signaling pathways through which miR-124 exerts effects. Methods and Results We detected significant decreases in miR-124 expression in fibroblasts isolated from calves and humans with severe pulmonary hypertension. Overexpression of miR-124 by mimic transfection significantly attenuated proliferation, migration, and monocyte chemotactic protein-1 expression of hypertensive fibroblasts, whereas anti–miR-124 treatment of control fibroblasts resulted in their increased proliferation, migration, and monocyte chemotactic protein-1 expression. Furthermore, the alternative splicing factor, polypyrimidine tract–binding protein 1, was shown to be a direct target of miR-124 and to be upregulated both in vivo and in vitro in bovine and human pulmonary hypertensive fibroblasts. The effects of miR-124 on fibroblast proliferation were mediated via direct binding to the 3′ untranslated region of polypyrimidine tract–binding protein 1 and subsequent regulation of Notch1/phosphatase and tensin homolog/FOXO3/p21Cip1 and p27Kip1 signaling. We showed that miR-124 directly regulates monocyte chemotactic protein-1 expression in pulmonary hypertension/idiopathic pulmonary arterial hypertension fibroblasts. Furthermore, we demonstrated that miR-124 expression is suppressed by histone deacetylases and that treatment of hypertensive fibroblasts with histone deacetylase inhibitors increased miR-124 expression and decreased proliferation and monocyte chemotactic protein-1 production. Conclusions Stable decreases in miR-124 expression contribute to an epigenetically reprogrammed, highly proliferative, migratory, and inflammatory phenotype of hypertensive pulmonary adventitial fibroblasts. Thus, therapies directed at restoring miR-124 function, including histone deacetylase inhibitors, should be investigated.

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“…MyoD Prevent difference of postnatal myogenic progenitors [125] miR-128 Phf6, Bmi-1, P70S6K1 Control of neurogenesis and synaptogenesis suppress tumor proliferation and self-renewal [102,126] miR-294…”

Section: Coup-tfii Lefty1 Lefty2mentioning

confidence: 99%

“…As for astrocyte reprogramming caused by numerous TFs and microRNAs, there are numerous participants same as the abovementioned. To date, four microRNAs (miRNA9, miRNA124, miRNA125, and miRNA128) were chosen as candidates on the basis of their known roles in stem cell maintenance or neurogenesis [102]. Due to the multitude of miRNA complimentary targets in the genome and the complexity of miRNA gene regulation, the complete network of miRNAs and their targets in astrocyte reprogramming implicate a huge challenge to unravel the regulation of networks.…”

Section: C-mycmentioning

confidence: 99%

Therapeutical Strategies for Spinal Cord Injury and a Promising Autologous Astrocyte-Based Therapy Using Efficient Reprogramming Techniques

et al. 2015

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Spinal cord injury (SCI) is a traumatic event resulting in disturbances to normal sensory, motor, or autonomic functions, which ultimately impacts a patient's physical, psychological, and social well-being. Until now, no available therapy for SCI can effectively slow down or halt the disease progression. Compared to traditional treatments, e.g., medication, surgery, and functional electrical stimulation, stem cell replacement therapy shows high potential for repair and functional plasticity. Thus, stem cell therapy may provide a promising strategy in curative treatment of SCI, specifically when considering the requirement of neuron replenishment in the spinal cord after distinct acute injuries. However, the therapeutic application of neural stem cells (NSCs) still faces enormous challenges, such as ethical issues, possible inflammatory reactions, graft rejection, and tumor formation. Therefore, it is of vital interest to identify more suitable sources of cells with stem cell potential, which might potentially be harnessed for local neural repair. Due to abovementioned possible drawbacks, these cells should be autologous. Reprogramming of astrocytes to generate the desired neuronal cell types would open the door to autologous cell transplantation and treatment of SCI without possible severe side effects. In this paper, we review the relevant therapeutic strategies for SCI, and conversion of astrocyte into NSCs, suggesting this procedure as a possible treatment option.

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Functional Studies of microRNAs in Neural Stem Cells: Problems and Perspectives

Cited by 26 publications

References 106 publications

MicroRNAs in Cerebral Ischemia-Induced Neurogenesis

MicroRNAs in Cerebral Ischemia-Induced Neurogenesis

MicroRNA-124 Controls the Proliferative, Migratory, and Inflammatory Phenotype of Pulmonary Vascular Fibroblasts

Therapeutical Strategies for Spinal Cord Injury and a Promising Autologous Astrocyte-Based Therapy Using Efficient Reprogramming Techniques

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