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MicroRNA-212 inhibits oligodendrocytes during maturation by down-regulation of differentiation-associated gene
Chih-Yen Wang1, Benjamin Deneen2, Shun-Fen Tzeng1
1Department of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Abstract:
MicroRNA-212 (mir-212) has been reported to regulate neuronal development and functioning. However, its expression and function in glia are not yet known. Here, we demonstrate that the level of microRNA-212 (mir-212) was reduced in spinal cord lesion site at 1 week and 1 month after a contusive spinal cord injury. In addition to its expression in neurons, mir-212 expression was detected in oligodendrocytes (OLGs) and glial progenitor cells (GPCs) in adult CNS. The addition of antagomir-212 to reduce mir-212 expression enabled to improve the cell process outgrowth of OLGs along with the up-regulation of the genes associated with OLG differentiation and maturation, including OLIG1, SOX10, myelin basic protein (MBP), and proteolipid protein 1 (PLP1). In contrast, these genes were significantly down-regulated by an increased expression of mir-212 in GPCs or in OLG progenitor cells (OPCs) through lentivirus-mediated gene delivery approach. Moreover, we found that PLP1 was the direct target molecule of mir-212. Furthermore, mir-212 over-expression diminished the protein production of OLGs markers including 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase), MBP, and PLP. Additionally, mir-212 over-expression decreased the number of mature OLGs expressing MBP, and the expression of galactocerebroside (GC). Complementary studies in a hippocampal neuron-OLG co-culture model and an ex vivo cerebellar slice system indicated that OLGs derived from GPCs with mir-212 over-expression exhibited decreased ability to interact with neuronal axons. Collectively, our findings demonstrate that mir-212 repressed the expression of OLG maturation-associated proteins and inhibited OLG cell process extension, indicating that mir-212 has negative regulatory effect on OLG lineage progression.
Insights
MicroRNA-212 (mir-212) levels decrease after spinal cord injury. Inhibiting mir-212 promotes oligodendrocyte maturation and process outgrowth, suggesting mir-212 negatively regulates glial lineage progression.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- MicroRNA-212 (mir-212) is known to regulate neuronal functions.
- The role of mir-212 in glial cells, particularly oligodendrocytes (OLGs) and glial progenitor cells (GPCs), remains largely unexplored.
- Spinal cord injury (SCI) impacts glial cell function and regeneration.
Purpose of the Study:
- To investigate the expression and function of mir-212 in glial cells following SCI.
- To determine the effect of mir-212 on oligodendrocyte differentiation, maturation, and function.
- To identify the molecular targets and regulatory mechanisms of mir-212 in OLG lineage progression.
Main Methods:
- Quantification of mir-212 levels in spinal cord lesion sites.
- Detection of mir-212 expression in neurons, oligodendrocytes, and glial progenitor cells.
- Manipulation of mir-212 levels using antagomir-212 and lentivirus-mediated gene delivery.
- Analysis of gene and protein expression related to OLG differentiation and maturation (e.g., OLIG1, SOX10, MBP, PLP1, CNPase, GC).
- Co-culture and ex vivo slice experiments to assess OLG-axon interactions.
Main Results:
- Mir-212 levels were reduced in the spinal cord lesion site post-injury.
- Mir-212 expression was detected in oligodendrocytes and glial progenitor cells.
- Reducing mir-212 enhanced OLG process outgrowth and upregulated OLG differentiation/maturation genes.
- Overexpressing mir-212 downregulated these genes and inhibited OLG maturation markers.
- Proteolipid protein 1 (PLP1) was identified as a direct target of mir-212.
- Mir-212 overexpression impaired OLG interaction with neuronal axons.
Conclusions:
- Mir-212 negatively regulates oligodendrocyte lineage progression by repressing maturation-associated proteins and inhibiting cell process extension.
- Mir-212 plays a critical role in glial response to spinal cord injury.
- Targeting mir-212 may offer a therapeutic strategy to promote glial repair after SCI.
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