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14 results on '"Kong, Shiqi"'

11. Effects of IGFBP‐3 and GalNAc‐T14 on proliferation and cell cycle of glioblastoma cells and its mechanism.

Author

Yang, Jiao, Hu, Yuhua, Wu, Jianliang, and Kong, Shiqi

Subjects
CELL cycle, CELL proliferation, CELL cycle proteins, PROTEIN expression, WESTERN immunoblotting
Abstract

Objective: The purpose of this study was to determine the effects of IGFBP‐3 and GalNAc‐T14 on the proliferation and cell cycle of glioblastoma cells and to explore the mechanisms of action. Methods: U87MG and U251MG glioblastoma cells were treated with recombinant human IGFBP‐3 (rhIGFBP‐3). Furthermore, IGFBP‐3‐overexpressed cells and cells co‐overexpressing IGFBP‐3 and GalNAc‐T14 were constructed by transfection. Cell viability, cell colony formation ability, cell cycle and protein expression were determined by MTT assay, colony formation assay, flow cytometry and Western blotting, respectively. Key findings: Both rhIGFBP‐3 treatment and overexpression of IGFBP‐3 induced the proliferation, colony formation, and G1/S phase transformation of U87MG and U251MG cells. In addition, the expression of cyclinE, CDK2 and p‐ERK1/2 proteins was up‐regulated in the cells. In cells co‐overexpressing, IGFBP‐3 and GalNAc‐T14, cell proliferation, colony formation and G1/S phase transformation were inhibited, and the expression of CyclinE, CDK2 and p‐ERK1/2 was significantly down‐regulated, when compared with IGFBP‐3‐overexpressed cells. Conclusions: IGFBP‐3 can promote the proliferation, colony formation and G1/S phase transformation of U87MG and U251MG cells, which may be related to the activation of ERK signalling pathway and the up‐regulation of cyclinE and CDK2 proteins. Furthermore, our study demonstrated that GalNAc‐T14 can inhibit the functions of IGFBP‐3. [ABSTRACT FROM AUTHOR]

Published
2020
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12. The phosphatidylinositol-3 kinase/Akt pathway mediates geranylgeranylacetone-induced neuroprotection against cerebral infarction in rats

Author

Tatsuya Abe, Yasuyuki Nagai, Kong Shiqi, Minoru Fujiki, Keisuke Ishii, Takeshi Kubo, Hidenori Kobayashi, and Eiji Abe

Subjects
Brain Infarction, Male, Time Factors, ATP-sensitive potassium channel, Pharmacology, Neuroprotection, Wortmannin, Brain ischemia, Phosphatidylinositol 3-Kinases, chemistry.chemical_compound, KATP Channels, Diazoxide, Animals, Medicine, Enzyme Inhibitors, Rats, Wistar, Molecular Biology, Protein kinase B, PI3K/AKT/mTOR pathway, Phosphoinositide-3 Kinase Inhibitors, business.industry, Kinase, General Neuroscience, Brain, Infarction, Middle Cerebral Artery, medicine.disease, Rats, Androstadienes, Neuroprotective Agents, chemistry, Anesthesia, Neurology (clinical), Diterpenes, Hydroxy Acids, business, Decanoic Acids, Proto-Oncogene Proteins c-akt, Central Nervous System Agents, Signal Transduction, Developmental Biology, medicine.drug
Abstract

Previous studies demonstrated the cytoprotective effect of geranylgeranylacetone (GGA), a heat shock protein inducer, against ischemic insult. Phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is thought to be an important factor that mediates neuroprotection. However, the signaling pathways in the brain in vivo after oral GGA administration remain unclear. We measured and compared infarction volumes to investigate the effect of GGA on cerebral infarction induced by permanent middle cerebral artery occlusion in rats. We evaluated the effects of pretreatment with 5-hydroxydecanoate (5HD), a specific mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel inhibitor; diazoxide (DZX), a selective mitoK(ATP) channel opener and wortmannin (Wort), a specific PI3K inhibitor of GGA-induced neuroprotection against infarction volumes. To clarify the relationship between PI3K/Akt activation and neuroprotection, we used immunoblot analysis to determine the amount of p-Akt proteins present after GGA administration with or without Wort treatment. Neuroprotective effects of GGA (pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia) were prevented by 5HD, DZX and Wort pretreatment, which indicates that the selective mitoK(ATP) channel and the PI3K/Akt pathway may mediate GGA-dependent protection. Oral GGA-induced p-Akt and GGA pretreatment enhanced ischemia-induced p-Akt, both of which were prevented by Wort pretreatment. These results suggest that a single oral dose of GGA induces p-Akt and that GGA plays an important role in neuroprotection against cerebral ischemia through the mitoK(ATP) channel opening.

Published
2010
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13. Electroconvulsive seizure-induced VEGF is correlated with neuroprotective effects against cerebral infarction: Involvement of the phosphatidylinositol-3 kinase/Akt pathway

Author

Takeshi Kubo, Keisuke Ishii, Eiji Abe, Tatsuya Abe, Hidenori Kobayashi, Minoru Fujiki, Kong Shiqi, and Yasuyuki Nagai

Subjects
Male, Vascular Endothelial Growth Factor A, Time Factors, Blotting, Western, Ischemia, Pharmacology, Neuroprotection, Brain ischemia, Wortmannin, chemistry.chemical_compound, Phosphatidylinositol 3-Kinases, Developmental Neuroscience, Seizures, medicine, Animals, Phosphorylation, Rats, Wistar, Protein kinase B, PI3K/AKT/mTOR pathway, Analysis of Variance, Electroshock, business.industry, Cerebral infarction, Brain, Cerebral Infarction, medicine.disease, Rats, Vascular endothelial growth factor, Neurology, chemistry, Anesthesia, Cerebrovascular Circulation, business, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

The present study demonstrates the cytoprotective effect of electrical convulsive stimulation (ECS) as a potential neuroprotective vascular endothelial growth factor (VEGF) inducer against ischemic insult. Phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is thought to be an important factor that mediates neuroprotection. However, the signaling pathways in the brain in vivo after ECS remain unclear. We measured and compared infarction volumes to investigate the effect of ECS on cerebral infarction induced by permanent middle cerebral artery occlusion in rats. We evaluated the effects of pretreatment with Wortmannin (Wort), a specific PI3K inhibitor of ECS-induced neuroprotection against infarction volumes. To clarify the relationship between PI3K/Akt activation and neuroprotection, we used immunoblot analysis to determine the amounts of p-Akt and VEGF proteins present after ECS with or without Wort treatment. Neuroprotective effects of ECS (pretreatment with a single ECS 6 h before ischemia) were prevented by Wort pretreatment, which indicates that the PI3K/Akt pathway may mediate ECS-dependent protection. ECS induced p-Akt and VEGF and ECS pretreatment enhanced ischemia-induced VEGF, both of which were prevented by Wort pretreatment. These results suggest that a single ECS induces p-Akt and that ECS plays an important role in neuroprotection against the cerebral ischemia through VEGF induction.

Published
2010

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