MicroRNA-210 overexpression induces angiogenesis and neurogenesis in the normal adult mouse brain

Zeng, Lili; He, Xingxing; Wang, Y; Tang, Yaohui; Zheng, Chao; Cai, Hao; Liu, Jing; Fu, Yue; Gy, Yang

doi:10.1038/gt.2013.55

Cited by 162 publications

(133 citation statements)

References 42 publications

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“…Altered miRNA expression in gastric cancer has been found in many different studies. Several deregulated miRNAs in gastric cancer such as miR-185, miR-107, miR-210, miR-99, miR-155 and miR-95 have been shown to regulate cell growth, apoptosis, migration and invasion (10)(11)(12)(13)(14). These findings suggest that deregulation of miRNA may be associated with tumorigenesis of gastric cancer.…”

Section: Introductionmentioning

confidence: 69%

MicroRNA-224 aggrevates tumor growth and progression by targeting mTOR in gastric cancer

Zhang

et al. 2016

International Journal of Oncology

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Abstract. Growing evidence suggests that microRNA plays an essential role in the development and metastasis of many tumors, including gastric cancer. Aberrant miR-224 expression has been indicated in tumor growth, the mechanism of miR-224 promoting the proliferation and metastatic ability for gastric cancer remains unclear. Accumulating evidence reports that mTOR signal pathway plays an important role in the cellular process, such as apoptosis, cell growth and proliferation. The goal of the present study was to identify whether miR-224 could inhibit the growth, migration, invasion, proliferation and metastasis of gastric cancer through targeting mTOR expression. Real-time PCR (RT-PCR) was used to quantify miR-224 expression in vitro and in vivo experiments. Luciferase reporter assays were performed to confirm the activity of mTOR pathway, and immunofluorescence staining assay was conducted to observe apoptosis and cell proliferation ability. Bioinformatics as well as cell luciferase function studies distinguished the direct modulation of miR-224 on the 3'-UTR of the mTOR, which leads to the inactivation of apoptosis signaling and the activation of cell proliferation. In addition, inhibition of miR-224 significantly reduced the expression of mTOR and improved caspase-9/3 expression while decreased cyclin D1/2 levels, attenuating gastric cancer cell proliferation. Therefore, the present study revealed the mechanistic links between miR-224 and mTOR in the pathogenesis of gastric cancer through modulation of caspase-9/3 and cyclin D1/2. In addition, targeting miR-224 could serve as a novel strategy for future gastric cancer therapy.

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Section: Introductionmentioning

confidence: 69%

MicroRNA-224 aggrevates tumor growth and progression by targeting mTOR in gastric cancer

Zhang

et al. 2016

International Journal of Oncology

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“…microRNAs) [6][7][8][9] regulate the neurogenic niche. MicroRNAs (miR) are able to regulate hundreds of genes [10] at the posttranscriptional level by inhibiting mRNA translation or inducing mRNA degradation [11].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

142

128

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Modulation of the subventricular zone (SVZ) neurogenic niche can enhance brain repair in several disorders including Parkinson's disease (PD). Herein, we used biocompatible and traceable polymeric nanoparticles (NPs) containing perfluoro-1,5-crown ether (PFCE) and coated with protamine sulfate to complex microRNA-124 (miR-124), a neuronal fate determinant. The ability of NPs to efficiently deliver miR-124 and prompt SVZ neurogenesis and brain repair in PD was evaluated. In vitro, miR-124 NPs were efficiently internalized by neural stem/progenitors cells and neuroblasts and promoted their neuronal commitment and maturation. The expression of Sox9 and Jagged1, two miR-124 targets and stemness-related genes, were also decreased upon miR-124 NP treatment. In vivo, the intracerebral administration of miR-124 NPs increased the number of migrating neuroblasts that reached the granule cell layer of the olfactory bulb, both in healthy and in a 6-hydroxydopamine (6-OHDA) mouse model for PD.MiR-124 NPs were also able to induce migration of neurons into the lesioned striatum of 6-OHDA-treated mice. Most importantly, miR-124 NPs proved to ameliorate motor symptoms of 6-OHDA mice, monitored by the apomorphine-induced rotation test.Altogether, we provide clear evidences to support the use of miR-124 NPs as a new therapeutic approach to boost endogenous brain repair mechanisms in a setting of neurodegeneration.

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“…microRNA-210 has been indicated to exert neuroprotective effects against oxygen-glucose deprivation through apoptosis inhibition in PC12 cells, 28) and to induce angiogenesis and neurogenesis in the normal adult mouse brain. 29) The protective role of micro-RNA-210 has also been recognized in hypoxic cardiomyocytes through Akt-and p53-dependent pathways. 26) And what is more in a rat model indicates that injection of ds microRNA-210 is effective in promoting the healing of partially torn anterior cruciate ligaments through enhancement of angiogenesis.…”

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confidence: 99%

HIF-1α-induced microRNA-210 reduces hypoxia-induced osteoblast MG-63 cell apoptosis

Sun

Peng

2015

Bioscience, Biotechnology, and Biochemistry

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To better understand the ischemic-hypoxia-induced fracture healing impairment, we determined in this study the microRNA-210 expression in broken bone specimens and in osteoblasts under hypoxia and then determined the influence of microRNA-210 overexpression on the osteoblast cell proliferation and apoptosis. Results demonstrated that microRNA-210 expression was upregulated with an association with HIF-1α overexpression in clinical human catagmatic tissues and was upregulated HIF-1α-dependently in response to hypoxia in osteoblast MG-63 cells. CCK-8 assay indicated that microRNA-210 upregulation by microRNA-210 mimics reduced the chemotherapeutic 5-FU-induced osteoblast cell death, and colony formation assay demonstrated that microRNA-210 mimics promoted osteoblast cells growth. Moreover, the microRNA-210 mimics transfection inhibited the hypoxia-induced MG-63 cell apoptosis via inhibiting the activation of caspase 3 and caspase 9. Therefore, our research indicated a protective role of microRNA-210 in response to hypoxia. And microRNA-210 might serve as a protective role in bone fracture healing.

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MicroRNA-210 overexpression induces angiogenesis and neurogenesis in the normal adult mouse brain

Cited by 162 publications

References 42 publications

MicroRNA-224 aggrevates tumor growth and progression by targeting mTOR in gastric cancer

MicroRNA-224 aggrevates tumor growth and progression by targeting mTOR in gastric cancer

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

HIF-1α-induced microRNA-210 reduces hypoxia-induced osteoblast MG-63 cell apoptosis

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