Loading...
|
Please use this identifier to cite or link to this item:
https://ir.csmu.edu.tw:8080/ir/handle/310902500/11598
|
| Title: | Enhancement of AG1024-Induced H9c2 Cardiomyoblast Cell Apoptosis via the Interaction of IGF2R with Gα Proteins and Its Downstream PKA and PLC-β Modulators by IGF-II |
| Authors: | Chu, Chun-Hsien
Huang, Chih-Yang
Lu, Ming-Chin
James, A.Lin
Tsai, Fuu-Jen
Tsai, Chang-Hai
Chu, Chia-Yih
Kuo, Wu-Hsien
Chen, Li-Mien
Chen, Ling-Yun |
| Contributors: | 中山醫學大學 |
| Keywords: | IGF-II, apoptosis, Gα, IGF2R |
| Date: | 2009 |
| Issue Date: | 2015-07-23T09:45:59Z (UTC)
|
| ISSN: | 0304-4920 |
| Abstract: | Our previous studies found that insulin-like growth factor-I receptor (IGF1R) signaling blockade
caused cardiac hypertrophy, and that apoptosis is required for upregulating the IGF-II and the IGF-II/
mannose 6-phosphate receptor (IGF2R) gene. However, the role of IGF-II in the regulation of cell
apoptosis through IGF2R is little known. In this study, we hypothesized that IGF-II may induce cell
apoptosis through IGF2R but is dependent on IGF1R activity. Western blots and TUNEL assay revealed
that in the presence of IGF1R, exogenous IGF-II acts, like IGF-I, would increase phospho-Akt through
IGF1R, but does not affect the caspase 3 activation and apoptotic induction in H9c2 cardiomyoblast
cells. Conversely, AG1024, an inhibitor of IGF1R activity, causes cell apoptosis, and the
treatment with IGF-II further enhances this process, implying that it occurs through IGF2R. Moreover,
immunoprecipitation assay revealed that treatment with IGF-II could enhance the interaction of IGF2R
with Gαi and Gαq but reduce its binding with Gαs, resulting in the reduction of phospho-PKA and the
activation of PLC-β. Taken together, these data provide new insight into the dual role of IGF-II in the
control of IGF1R dependent cell apoptosis and involved activation of IGF2R signaling. Improving
IGF1R activity and suppressing IGF2R may be a good strategy to prevent the progression of heart
disease with cardiomyocyte apoptosis. |
| URI: | https://ir.csmu.edu.tw:8080/ir/handle/310902500/11598
http://dx.doi.org/10.4077/CJP.2009.AMH004 |
| Relation: | Chinese Journal of Physiology 52(1): 31-37, 2009 |
| Appears in Collections: | [醫學系] 期刊論文
|
Files in This Item:
| File |
Description |
Size | Format | |
|---|
| index.html | 期刊論文 | 0Kb | HTML | 293 | View/Open | | index.html | | 0Kb | HTML | 297 | View/Open |
|
All items in CSMUIR are protected by copyright, with all rights reserved.
|
