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1.
Chinese Journal of Pathophysiology ; (12): 572-576, 2018.
Article in Chinese | WPRIM | ID: wpr-701163

ABSTRACT

Stroke is one of the major causes of death and disability in China and even worldwide.At present, treatment of stroke has been traditionally focused on reducing death of ischemic cells.However,clinical trials have shown that none of neuroprotective drugs tested achieve clinical benefit after acute stroke.Exosomes are 30~100 nm extracellular vesicles derived from cells with cell membrane structure.Many studies suggest exosomes play essential roles in intercellular communication by transferring their cargo between source and target cells in brain.Emerging data show that exsomes also make a contribution to brain recovery via regulating highly interactive process pathway after stroke.Here,we review these advances and highlight the potential therapeutic functions of exosomes in brain remodeling after stroke.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 558-563, 2016.
Article in English | WPRIM | ID: wpr-285229

ABSTRACT

Pituitary adenomas (PAs) are well known as a common intracranial benign tumor, and a portion of PAs are refractory to current therapeutic methods. ErbB receptors family signaling pathway regulates the expression of PAs activation associated gene. Inhibition of epidermal growth factor receptor (EGFR) can inhibit proliferation of PAs. Leucine-rich repeats and immunoglobulin-like domains protein 1 ( LRIG1), a negative mediated gene of ErbB receptors family, plays a role in many tumors. However, there are seldom researches about the functional role of LRIG1 in PAs. The aim of this study is to explore the potential effect of LRIG1 and its regulating mechanism in PAs. First, we investigated the role of LRIG1 in cell migration, invasion of PAs with transfected LRIG1 or control. Then, we explored its impact on cell proliferation and apoptosis of PAs in vivo. To study the regulating mechanism of LRIG1, we examined the expression of molecular factor of PI3K/AKT and Ras/Raf/ERK pathway using Western blotting in vitro and RT-PCR in vitro and in vivo. It was found that LRIG1 over-expression inhibited cell migration, invasion and proliferation, and promoted apoptosis of PAs in vivo and in vitro. Furthermore, LRIG1 suppressed the expression of signaling of PI3K/AKT and Ras/Raf/ERK pathways in PAs. LRIG1, as a negative mediated gene of tumor, can inhibit biological function of PAs via inhibiting PI3K/AKT and Ras/Raf/ERK pathways, and it might be a new target for gene therapy of PAs.


Subject(s)
Animals , Female , Humans , Mice , Apoptosis , Genetics , Brain Neoplasms , Genetics , Pathology , Cell Line, Tumor , Cell Movement , Genetics , Cell Proliferation , Genetics , Gene Expression Regulation, Neoplastic , MAP Kinase Signaling System , Genetics , Membrane Glycoproteins , Genetics , Oncogene Protein v-akt , Phosphatidylinositol 3-Kinases , Genetics , Pituitary Neoplasms , Genetics , Pathology , Xenograft Model Antitumor Assays , raf Kinases , Genetics
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