SCIRR39 Promotes Neurite Extension via RhoA in NGF-Induced PC12 Cells

Zhao, Chuanqi; Liu, Y; Ni, Yanli; Yang, Junning; Hui, Hua; Sun, Zhonglei; Liu, S J

doi:10.1159/000350715

Cited by 8 publications

(6 citation statements)

References 43 publications

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“…Y-27632, a ROCK inhibitor can enhance the efficacy of bone marrow-derived MSCs transdifferentiation into neurons and neuroglial cells [ 14 , 15 ]. SCIRR39, a gene usually upregulated in primary neuron injury and/or regeneration process, can increase the neurite extension in NGF-treated PC12 cells via RhoA [ 28 ]. Cyclic tensile loading, a mechanic methods used to promote neuronal transdifferentiation of MSCs is also partly through the regulation of Rho GTPases activity [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-124 Promote Neurogenic Transdifferentiation of Adipose Derived Mesenchymal Stromal Cells Partly through RhoA/ROCK1, but Not ROCK2 Signaling Pathway

Wang

Guo

2016

PLoS ONE

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ObjectiveSome recent studies suggest that multiple miRNAs might regulate neurogenic transdifferentiation of mesenchymal stromal cells (MSCs). In the present study, we hypothesized that the miR-124 can repress the expression of RhoA upon the neurogenesis of adipose derived MSCs (ADMSCs).MethodsMiRNA expression dynamics during neurogenic transdifferentiation of ADMSCs were measured. The expression of neuron-specific enolase (NSE), Tuj-1 (Neuron-specific class III beta-tubulin) and glial fibrillary acidic protein (GFAP), as well as electrophysiological properties, were detected after neurogenic transdifferentiation. The targeting of miR-124 over RhoA was verified by dual luciferase assay, qRT-PCR and western blot. The functions of miR-124 and the RhoA/ROCK signaling pathway were studied using gain and loss of function experiments in vitro.ResultsMiR-124 is significantly upregulated during neurogenic transdifferentiation of ADMSCs. Knockdown of endogenous miR-124 hampered neurogenic transdifferentiation and the acquired electrophysiological properties. MiR-124 could directly target RHOA mRNA and repress its expression, through which it increased the proportion of transdifferentiated (transdiff.) cells with positive NSE, Tuj-1 and GFAP. RhoA/ROCK1, but not ROCK2 is a downstream signaling pathway of miR-124 in the process of transdifferentiation.ConclusionMiR-124 is an important miRNA modulating neurogenic transdifferentiation of ADMSCs at least partly via the miR-124/RhoA/ROCK1 signaling pathway. These findings provided some fundamental information for future use of ADMSCs as an agent for regenerative medicine and cell therapy for neurological diseases.

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Section: Discussionmentioning

confidence: 99%

MiR-124 Promote Neurogenic Transdifferentiation of Adipose Derived Mesenchymal Stromal Cells Partly through RhoA/ROCK1, but Not ROCK2 Signaling Pathway

Wang

Guo

2016

PLoS ONE

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“…Interestingly, injured spinal cord neurons upregulate the rat Ribonuclease Inhibitor (RNH1, also known as SCIRR39) in vitro and in vivo (Zhao et al, ) and, in PC12 cells, overexpression of RNH1 enhances neurite outgrowth whilst knockdown of RNH1 reduces neurite outgrowth (Zhao et al, ). It is plausible therefore that RNH1 promotes neurite outgrowth by inhibiting ribonucleases although other mechanisms could be responsible [such as binding of PTEN (Kim et al, )].…”

Section: Might Attenuation Of Chromatolysis Be Therapeutically Benefimentioning

confidence: 99%

Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA?

Moon

2018

Developmental Neurobiology

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After axonal injury, chromatolysis (fragmentation of Nissl substance) can occur in the soma. Electron microscopy shows that chromatolysis involves fission of the rough endoplasmic reticulum. In CNS neurons (which do not regenerate axons back to their original targets) or in motor neurons or dorsal root ganglion neurons denied axon regeneration (e.g., by transection and ligation), chromatolysis is often accompanied by degranulation (loss of ribosomes from rough endoplasmic reticulum), disaggregation of polyribosomes and degradation of monoribosomes into dust-like particles. Ribosomes and rough endoplasmic reticulum may also be degraded in autophagic vacuoles by ribophagy and reticulophagy, respectively. In other words, chromatolysis is disruption of parts of the protein synthesis infrastructure. Whereas some neurons may show transient or no chromatolysis, severely injured neurons can remain chromatolytic and never again synthesize normal levels of protein; some may atrophy or die. Ribonuclease(s) might cause the following features of chromatolysis: fragmentation and degranulation of rough endoplasmic reticulum, disaggregation of polyribosomes and degradation of monoribosomes. For example, ribonucleases in the EndoU/PP11 family can modify rough endoplasmic reticulum; many ribonucleases can degrade mRNA causing polyribosomes to unchain and disperse, and they can disassemble monoribosomes; Ribonuclease 5 can control rRNA synthesis and degrade tRNA; Ribonuclease T2 can degrade ribosomes, endoplasmic reticulum and RNA within autophagic vacuoles; and Ribonuclease IRE1α acts as a stress sensor within the endoplasmic reticulum. Regeneration might be improved after axonal injury by protecting the protein synthesis machinery from catabolism; targeting ribonucleases using inhibitors can enhance neurite outgrowth and could be a profitable strategy in vivo. © 2018 Wiley Periodicals, Inc. Develop Neurobiol, 2018.

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“…These cells have been extensively used as a neural cell model of neurite outgrowth (12)(13)(14). Undifferentiated PC12 cells do not produce neurites (<1%), as reported in a previous study (15).…”

Section: Discussionmentioning

confidence: 68%

Tenuifoliside A promotes neurite outgrowth in PC12 cells via the PI3K/AKT and MEK/ERK/CREB signaling pathways

Liu

Wang

Lü

2015

Molecular Medicine Reports

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Abstract. Previous studies have demonstrated the neuroprotective effect of tenuifoliside A (TFSA) on corticosterone-induced neuron damage in SH-SY5Y cells, however, the effect of TFSA on the promotion of neurite outgrowth remains to be elucidated. PC12 cells were treated with TFSA or nerve growth factor, and the levels of proteins were evaluated by western blotting. In addition, for pharmacological experiments, inhibitors of the PD98059 mitogen-activated protein kinase kinase (MEK) and phosphatidylinositol 3-kinase (PI3K; LY294002) were added into the culture medium. The present study demonstrated that TFSA significantly increased the percentage of neurite-bearing cells and promoted neurite extension in PC12 cells. In addition, TFSA-treated PC12 cells also expressed increased levels of the 43 kD growth-associated protein (GAP-43) neural marker, comparable to those in nerve growth factor-treated cells. The present study also demonstrated that TFSA enhanced the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, which are important signaling molecules involved in neural differentiation in PC12 cells. Co-treatment of the PC12 cells with the PD98059 MEK inhibitor and LY294002 PI3K inhibitor inhibited the neurite outgrowth induced by TFSA. In addition, treatment with TFSA also promoted the phosphorylation of cyclic AMP response element-binding protein (CREB), which was inhibited completely by treatment with PD98059. In conclusion, the results of the present study demonstrated that TFSA induces neurite extension of PC12 cells and suggested that activation of the MEK/ERK/CREB and PI3K/Akt signaling pathways is involved in this process.

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SCIRR39 Promotes Neurite Extension via RhoA in NGF-Induced PC12 Cells

Cited by 8 publications

References 43 publications

MiR-124 Promote Neurogenic Transdifferentiation of Adipose Derived Mesenchymal Stromal Cells Partly through RhoA/ROCK1, but Not ROCK2 Signaling Pathway

MiR-124 Promote Neurogenic Transdifferentiation of Adipose Derived Mesenchymal Stromal Cells Partly through RhoA/ROCK1, but Not ROCK2 Signaling Pathway

Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA?

Tenuifoliside A promotes neurite outgrowth in PC12 cells via the PI3K/AKT and MEK/ERK/CREB signaling pathways

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