MiR-133b Promotes Neurite Outgrowth by Targeting RhoA Expression

Lu, Xiao Cheng; Zheng, Jin Yu; Tang, Lin; Huang, Bao Sheng; Li, Kai; Tao, Yi Ting; Wan, Yu; Zhu, Rong Lan; Li, Shuai; Li, Lixin

doi:10.1159/000369692

Cited by 65 publications

(57 citation statements)

References 48 publications

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“…RhoA plays important pathophysiological roles in the cardiovascular system and in disease states such as hypertension, heart failure, stroke, diabetes and others [22,23]. We found that RhoA activation and geranylgeranylation of RhoA in the tissue of the heart increased at week 6 of SHR although there was no significant difference, but it significantly increased at week 12 of SHR (data not shown).…”

Section: Discussionmentioning

confidence: 76%

Alteration of RhoA Prenylation Ameliorates Cardiac and Vascular Remodeling in Spontaneously Hypertensive Rats

Yang

Chen²,

Xu³

et al. 2016

Cell Physiol Biochem

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Background: In our previous study, farnesyl pyrophosphate synthase (FPPS) was shown to be increased in spontaneously hypertensive rats (SHR) and in mice with angiotensin-II induced cardiac hypertrophy. Overexpression of FPPS induced cardiac hypertrophy and fibrosis in mice, accompanied by an increase in the synthesis of farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). In the present study, we investigated the mechanisms of reversing cardiovascular remodeling in SHR by inhibiting FPPS. Methods and Results: Six-week-old rats were given vehicle or an FPPS inhibitor (alendronate, 100 ug/kg/d) daily for twelve weeks by osmotic mini-pump. The results demonstrated that FPPS inhibition attenuated cardiac hypertrophy and fibrosis in SHR as shown by the heart weight to body weight ratio, echocardiographic parameters, and histological examination. In addition, FPPS inhibition attenuated aortic remodeling as shown by reduced media thickness, media cross-sectional area and collagen of the aorta as well as SBP, DBP, MBP. Furthermore, 12 weeks of alendronate treatment significantly decreased FPP and GGPP levels, RhoA activation and geranylgeranylation in the heart and aorta, all of which were significantly upregulated in SHR compared with normotensive Wistar-Kyoto rats. Conclusion: Taken together, these results indicate that chronic treatment with alendronate decreases the development of cardiac and aortic remodeling, by a pathway which involves inhibition of the geranylgeranylation and activation of RhoA.

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Section: Discussionmentioning

confidence: 76%

Alteration of RhoA Prenylation Ameliorates Cardiac and Vascular Remodeling in Spontaneously Hypertensive Rats

Yang

Chen²,

Xu³

et al. 2016

Cell Physiol Biochem

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“…The ROCK2 transcript is highly expressed in muscle and brain tissues, whereas the ROCK1 is localized in nonnerves tissues [37]. RhoA/ROCK pathway has been shown to play an important role in neurite growth inhibition from CSPG after CNS injury [38]. Several preclinical and clinical studies have utilized inhibitors of Rho/ROCK signaling pathway for anticancer therapeutics in prostate, lung, melanoma, and many other tumor types with remarkable success [39][40][41].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124 (MiR-124) Inhibits Cell Proliferation, Metastasis and Invasion in Colorectal Cancer by Downregulating Rho-Associated Protein Kinase 1(ROCK1)

Zhou

Xiaoqiang

et al. 2016

Cell Physiol Biochem

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Background/Aims: MiR-124 inhibits neoplastic transformation, cell proliferation, and metastasis and downregulates Rho-associated protein kinase (ROCK1) in Colorectal Cancer (CRC). The aim of this study was to further investigate the roles and interactions of ROCK1 and miR-124 and the effects of knockdown of ROCK1and MiR-124 in human Colorectal Cancer (CRC). Methods: Three Colorectal cancer cell lines (HCT116, HT29 and SW620) and one Human Colonic Mucosa Epithelial cell line (NCM460) were studied. The protein expression of ROCK1 was examined by Western-blot and qRT-PCR were performed to examine the expression levels of ROCK1 mRNA and miR-124. Furthermore, We performed transfection of cancer cell line (SW620) with pre-miR-124(mimics), anti-miR-124(inhibitor), ROCK1 siRNA and the control, then observed the affects of ROCK1 protein expression by westen-blot, cell proliferation by EDU (5-ethynyl-2'deoxyuridine assay) and expression levels of ROCK1mRNA by qRT-PCR . A soft agar formation assay, Migration and invasion assays were used to determine the effect of regulation of miR-124 and ROCK1, and survivin on the transformation and invasion capability of colorectal cancer cell. Results: MiR-124 expression was significantly downregulated in CRC cell lines compare to normal (P < 0.05). In contrast, ROCK1 protein expression was significantly increased in CRC cell lines compared to the normal (P < 0.05), whereas the gene (ROCK1mRNA) expression remained unaltered (P > 0.05). ROCK1 mRNA was unaltered in cells transfected with miR-124 mimic and miR-124 inhibitor, compared to normal controls. There was a significant reduction in ROCK1 protein in cells transfected with miR-124 mimic and a significant increase in cells transfected with miR-124 inhibitor (P < 0.05). Cell proliferation, transformation and invasion of cells transfected with miR-124 inhibitor were significantly increased compared to those in normal controls (P<0.05). However, cell proliferation, transformation and invasion of cells transfected with ROCK1 siRNA were significantly decreased compared to control (P < 0.05). Conclusions: In conclusion, our results demonstrated that miR-124 not only promoted cancer cell hyperplasia and significantly associated with CRC metastasis and progression, but also downregulated ROCK1 protein expression. More importantly, increased ROCK1 expression or inhibited miR-124 expression may constitute effective new therapeutic strategies for the treatment of renal cancer in the future.

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“…For example, miR-133b, which is specifically expressed in mammalian midbrain dopaminergic neurons (DNs) and is deficient in midbrain tissue from patients with Parkinson's disease [89], has been proved as an important determinant in spinal cord regeneration in adult zebra fish by directly reducing RhoA protein levels [90]. miR-133b has also been shown to be promoting neurite outgrowth in the primary cortical neurons and PC12 cells [91]. miR-133b increases axon growth and attenuates axon growth restrictions from CSPG in PCNs via ERK1/2 and PI3K/Akt signaling pathway by suppressing RhoA [91].…”

Section: Micrornas and Intrinsic Determinants Of Axon Regenerationmentioning

confidence: 99%

“…miR-133b has also been shown to be promoting neurite outgrowth in the primary cortical neurons and PC12 cells [91]. miR-133b increases axon growth and attenuates axon growth restrictions from CSPG in PCNs via ERK1/2 and PI3K/Akt signaling pathway by suppressing RhoA [91]. …”

Section: Micrornas and Intrinsic Determinants Of Axon Regenerationmentioning

confidence: 99%

Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury

Teng

Liu

2016

Neural Plasticity

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Spinal cord injury is a devastating disease which disrupts the connections between the brain and spinal cord, often resulting in the loss of sensory and motor function below the lesion site. Most injured neurons fail to regenerate in the central nervous system after injury. Multiple intrinsic and extrinsic factors contribute to the general failure of axonal regeneration after injury. MicroRNAs can modulate multiple genes' expression and are tightly controlled during nerve development or the injury process. Evidence has demonstrated that microRNAs and their signaling pathways play important roles in mediating axon regeneration and glial scar formation after spinal cord injury. This article reviews the role and mechanism of differentially expressed microRNAs in regulating axon regeneration and glial scar formation after spinal cord injury, as well as their therapeutic potential for promoting axonal regeneration and repair of the injured spinal cord.

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MiR-133b Promotes Neurite Outgrowth by Targeting RhoA Expression

Cited by 65 publications

References 48 publications

Alteration of RhoA Prenylation Ameliorates Cardiac and Vascular Remodeling in Spontaneously Hypertensive Rats

Alteration of RhoA Prenylation Ameliorates Cardiac and Vascular Remodeling in Spontaneously Hypertensive Rats

MicroRNA-124 (MiR-124) Inhibits Cell Proliferation, Metastasis and Invasion in Colorectal Cancer by Downregulating Rho-Associated Protein Kinase 1(ROCK1)

Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury

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