Insulin growth factor-1 (IGF-1) enhances hippocampal excitatory and seizure activity through IGF-1 receptor-mediated mechanisms in the epileptic brain

Jiang, Guohui; Wang, Wei; Cao, Qingqing; Gu, Juan; Mi, Xiujuan; Wang, Kewei; Chen, Guojun; Wang, Xuefeng

doi:10.1042/cs20150312

Cited by 35 publications

(30 citation statements)

References 43 publications

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“…In the present study, the activation of ERK1/2 was found to be attenuated as well when the activity of IGF-1R was inhibited by Linsitinib or shRNA targeted to IGF-1R, suggesting that IGF-1R activation of ERK1/2 contributes to the mechanism by which chondrocytes sense and respond to periodic mechanical stress. Our present observation seems consistent with the reports of IGF-1R modulations and interactions with ERK1/2 in other cell types [30,31]. However, this relationship has not been investigated in chondrocytes under mechanical stimulation.…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andsupporting

confidence: 83%

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

Tang

Jiang

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: The biological effects of periodic mechanical stress on the mitogenesis of chondrocytes have been studied extensively over the past few years. However, the mechanisms underlying the ability of chondrocytes to sense and respond to mechanical stimuli remain to be determined. In the current study, we analyzed the mechanisms by which periodic mechanical stress is translated into biochemical signals and verified the key role of non-integrin mechanosensors including Caveolin-1 (Cav-1), and insulin-like growth factor-1 receptor (IGF-1R) in chondrocyte proliferation. Methods: Two steps were undertaken in the experiment. In the first step, the cells were maintained under static conditions or periodic mechanical stress for 0 h and 1 h prior to Western blot analysis. In the second step, the cells were pretreated with short hairpin RNA (shRNA) targeted to Cav-1 or IGF-1R or control scrambled shRNA. Moreover, they were pretreated with their selective inhibitors methyl β-cyclodextrin (MCD) or Linsitinib (OSI-906). They were maintained under static conditions or periodic mechanical stress for 1 h prior to Western blot analysis, and for 3 days, 8 h per day, prior to direct cell counting and CCK-8 assay, respectively. Results: Periodic mechanical stress significantly induced sustained phosphorylation of Cav-1 at Tyr 14 and IGF-1R at Tyr 1135/1136 . Proliferation was inhibited by pretreatment with Cav-1 inhibitor MCD and by shRNA targeted to Cav-1 in chondrocytes in response to periodic mechanical stress. Meantime, MCD and shRNA targeted to Cav-1 also attenuated IGF-1R, and extracellular signal-regulated kinase (ERK)1/2 activation. In addition, inhibiting IGF-1R activity by Linsitinib and shRNA targeted to

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Section: Cellular Physiology and Biochemistry Cellular Physiology Andsupporting

confidence: 83%

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

Tang

Jiang

Sun

et al. 2018

Cell Physiol Biochem

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“…On the contrary, the hsa-let-7c over-expression downregulated the level of IGF-1R and decreased the odonto/osteogenic differentiation in IGF-1-treated SCAPs. It is commonly believed that IGF-1 takes actions mostly via IGF-1R2324. These findings indicate that IGF-1, IGF-1R and hsa-let-7c act as a whole especially in the process of cell differentiation.…”

Section: Discussionmentioning

confidence: 88%

IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla

Ma¹,

Liu

Lin

et al. 2016

Sci Rep

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Insulin-like growth factor-1 (IGF-1) and its receptor IGF-1R play a paramount role in tooth/bone formation while hsa-let-7c actively participates in the osteogenic differentiation of mesenchymal stem cells. However, the interaction between IGF-1/IGF-1R and hsa-let-7c on the committed differentiation of stem cells from apical papilla (SCAPs) remains unclear. In this study, human SCAPs were isolated and treated with IGF-1 and hsa-let-7c over/low-expression viruses. The odonto/osteogenic differentiation of these stem cells and the involvement of mitogen-activated protein kinase (MAPK) pathway were subsequently investigated. Alizarin red staining showed that hsa-let-7c low-expression can significantly promote the mineralization of IGF-1 treated SCAPs, while hsa-let-7c over-expression can decrease the calcium deposition of IGF-1 treated SCAPs. Western blot assay and real-time reverse transcription polymerase chain reaction further demonstrated that the expression of odonto/osteogenic markers (ALP, RUNX2/RUNX2, OSX/OSX, OCN/OCN, COL-I/COL-I, DSPP/DSP, and DMP-1/DMP-1) in IGF-1 treated SCAPs were significantly upregulated in Let-7c-low group. On the contrary, hsa-let-7c over-expression could downregulate the expression of these odonto/osteogenic markers. Moreover, western blot assay showed that the JNK and p38 MAPK signaling pathways were activated in Let-7c-low SCAPs but inhibited in Let-7c-over SCAPs. Together, the IGF-1/IGF-1R/hsa-let-7c axis can control the odonto/osteogenic differentiation of IGF-1-treated SCAPs via the regulation of JNK and p38 MAPK signaling pathways.

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“…IGF is a polypeptide mitogen that is similar to proinsulin; therefore, it has an important role in regulating cell proliferation, differentiation and apoptosis and mediates cell growth, synthetic metabolism, glucose reduction and immune regulation ( 18 ). Pinzani and Marra ( 4 ) previously demonstrated that PDGF enhanced the secretion and release of IGF and its binding proteins in rat HSCs and also promoted HSC division and proliferation by stimulating DNA synthesis in cells.…”

Section: Discussionmentioning

confidence: 99%

Influence of amygdalin on PDG, IGF and PDGFR expression in HSC-T6 cells

et al. 2018

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The aim of the present study was to elucidate the mechanism of amygdalin treatment on reducing liver fibrosis by investigating its role in regulating the expression level of platelet-derived growth factor (PDGF), insulin-like growth factor (IGF) and PDGF receptor (PDGFR) in the hepatic stellate cell (HSC)-T6 line. HSC-T6 cells were used as an in vitro model and randomly assigned into four groups: control, high-dose amygdalin, mid-dose amygdalin and low-dose amygdalin. Following amygdalin treatment, compared with the control, a high dose of amygdalin significantly suppressed the mRNA expression of PDGF and IGF (each P<0.05), whereas moderate and low doses showed no significant effect, relatively low doses of amygdalin are not sufficient to transfer signals to its receptor. The high-dose amygdalin and low-dose amygdalin displayed suppressed protein expression of PDGF at 24, 48 and 72 h, with the high-dose group exhibiting the most marked suppression at all three time points. By reducing the transcription of PDGF and IGF mRNA and the expression of PDGF protein, amygdalin decreased the synthesis and release of PDGF and IGF, thereby reducing the influence of PDGF and IGF on HSCs, thus protecting the liver from fibrosis.

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Insulin growth factor-1 (IGF-1) enhances hippocampal excitatory and seizure activity through IGF-1 receptor-mediated mechanisms in the epileptic brain

Cited by 35 publications

References 43 publications

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

IGF-1/IGF-1R/hsa-let-7c axis regulates the committed differentiation of stem cells from apical papilla

Influence of amygdalin on PDG, IGF and PDGFR expression in HSC-T6 cells

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