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Cardiomyoblast apoptosis induced by insulin-like growth factor (IGF)-I resistance is IGF-II dependent and synergistically enhanced by angiotensin II.
Apoptosis. 2006 Jul; 11(7):1075-89.A

Abstract

OBJECTIVE

This study explores the synergistic effect of cardiomyoblast apoptosis induced by angiotensin II (Ang II) and Insulin-like growth factor (IGF)-I resistance, and elucidates the role of IGF-II via IGF-II receptor (R) and calcineurin pathways in apoptosis induced by Ang II and IGF-I resistance.

METHODS

Apoptosis of cultured cardiomyoblast H9c2 cells was assessed by DNA fragmentation on agarose gel electrophoresis, nuclear condensation stained with DAPI, and Western blot analysis of pro-apoptotic Bad and cytochrome c in various combinations of control, Ang II, antisense IGF (I or II), IGF (I or II) antibody, IGF (I or II) receptor (R) antibody, or calcineurin inhibitor (Cyclosporine A, (CsA)).

RESULTS

We found the following: (1) The combination of Ang II and IGF-I deficiencies had a synergistic effect on apoptosis, confirmed by DNA fragmentation, nuclei condensation, and increases in such pro-apoptotic proteins as Bad, cytochrome c, caspase 9, and caspase 3 in H9c2 cells. (2) IGF-II and IGF-IIR protein products were increased by antisense IGF-I and IGF-I resistance, but these IGF-II protein products were not affected by sense IGF-I and non-specific antibody IgG in H9c2 cells. (3) The alteration of Bad protein level and the release of cytochrome c, both induced by treatments containing combinations of Ang II and antisense IGF-I, IGF-I antibody or IGF-IR antibody, were inhibited by IGF-II antibody. (4) DNA fragmentation, Bad, and cytochrome c which was induced by treatments combining IGF-IR antibody with Ang II or combining IGF-IR antibody with IGF-II were remarkably attenuated by CsA.

CONCLUSION

IGF-I deficiency and/or IGF-IR resistance induced apoptosis in cardiomyoblast cells. The apoptosis, which might have been caused by the upregulation of IGF-II and IGF-IIR genes possibly activated the downstream calcineurin pathway, was synergistically augmented by Ang II.

Authors+Show Affiliations

Department of Biological Science and Technology, China Medical University, No. 91 Hsueh-Shih Road, Taichung 404, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16699953

Citation

Kuo, Wei-Wen, et al. "Cardiomyoblast Apoptosis Induced By Insulin-like Growth Factor (IGF)-I Resistance Is IGF-II Dependent and Synergistically Enhanced By Angiotensin II." Apoptosis : an International Journal On Programmed Cell Death, vol. 11, no. 7, 2006, pp. 1075-89.
Kuo WW, Liu CJ, Chen LM, et al. Cardiomyoblast apoptosis induced by insulin-like growth factor (IGF)-I resistance is IGF-II dependent and synergistically enhanced by angiotensin II. Apoptosis. 2006;11(7):1075-89.
Kuo, W. W., Liu, C. J., Chen, L. M., Wu, C. H., Chu, C. H., Liu, J. Y., Lu, M. C., Lin, J. A., Lee, S. D., & Huang, C. Y. (2006). Cardiomyoblast apoptosis induced by insulin-like growth factor (IGF)-I resistance is IGF-II dependent and synergistically enhanced by angiotensin II. Apoptosis : an International Journal On Programmed Cell Death, 11(7), 1075-89.
Kuo WW, et al. Cardiomyoblast Apoptosis Induced By Insulin-like Growth Factor (IGF)-I Resistance Is IGF-II Dependent and Synergistically Enhanced By Angiotensin II. Apoptosis. 2006;11(7):1075-89. PubMed PMID: 16699953.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardiomyoblast apoptosis induced by insulin-like growth factor (IGF)-I resistance is IGF-II dependent and synergistically enhanced by angiotensin II. AU - Kuo,Wei-Wen, AU - Liu,Chung-Jung, AU - Chen,Li-Ming, AU - Wu,Chieh-Hsi, AU - Chu,Chun-Hsien, AU - Liu,Jer-Yuh, AU - Lu,Min-Chi, AU - Lin,James A, AU - Lee,Shin-Da, AU - Huang,Chih-Yang, PY - 2006/5/16/pubmed PY - 2006/9/12/medline PY - 2006/5/16/entrez SP - 1075 EP - 89 JF - Apoptosis : an international journal on programmed cell death JO - Apoptosis VL - 11 IS - 7 N2 - OBJECTIVE: This study explores the synergistic effect of cardiomyoblast apoptosis induced by angiotensin II (Ang II) and Insulin-like growth factor (IGF)-I resistance, and elucidates the role of IGF-II via IGF-II receptor (R) and calcineurin pathways in apoptosis induced by Ang II and IGF-I resistance. METHODS: Apoptosis of cultured cardiomyoblast H9c2 cells was assessed by DNA fragmentation on agarose gel electrophoresis, nuclear condensation stained with DAPI, and Western blot analysis of pro-apoptotic Bad and cytochrome c in various combinations of control, Ang II, antisense IGF (I or II), IGF (I or II) antibody, IGF (I or II) receptor (R) antibody, or calcineurin inhibitor (Cyclosporine A, (CsA)). RESULTS: We found the following: (1) The combination of Ang II and IGF-I deficiencies had a synergistic effect on apoptosis, confirmed by DNA fragmentation, nuclei condensation, and increases in such pro-apoptotic proteins as Bad, cytochrome c, caspase 9, and caspase 3 in H9c2 cells. (2) IGF-II and IGF-IIR protein products were increased by antisense IGF-I and IGF-I resistance, but these IGF-II protein products were not affected by sense IGF-I and non-specific antibody IgG in H9c2 cells. (3) The alteration of Bad protein level and the release of cytochrome c, both induced by treatments containing combinations of Ang II and antisense IGF-I, IGF-I antibody or IGF-IR antibody, were inhibited by IGF-II antibody. (4) DNA fragmentation, Bad, and cytochrome c which was induced by treatments combining IGF-IR antibody with Ang II or combining IGF-IR antibody with IGF-II were remarkably attenuated by CsA. CONCLUSION: IGF-I deficiency and/or IGF-IR resistance induced apoptosis in cardiomyoblast cells. The apoptosis, which might have been caused by the upregulation of IGF-II and IGF-IIR genes possibly activated the downstream calcineurin pathway, was synergistically augmented by Ang II. SN - 1360-8185 UR - https://www.unboundmedicine.com/medline/citation/16699953/Cardiomyoblast_apoptosis_induced_by_insulin_like_growth_factor__IGF__I_resistance_is_IGF_II_dependent_and_synergistically_enhanced_by_angiotensin_II_ L2 - https://doi.org/10.1007/s10495-006-7028-4 DB - PRIME DP - Unbound Medicine ER -