The function of Connective Tissue Growth Factor (CCN2) in ischemia-reperfusion injury and chronic pressure overload is the main theme of Tuyet Anh Pham‘s PhD thesis.
MAIN RESULTS:
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Connective Tissue Growth Factor activates cytoprotective signaling in cardiomyocytes and endothelial cells.
- Connective Tissue Growth Factor protects cardiomyocytes and endothelial cells agains ischemia-reperfusion injury and oxidative stress.
- Connective Tissue Growth Factor reduces angiotensin II- and stretch-induced cardiomyocyte hypertrophy.
THESIS DEFENCE:
Thesis: A study on the cytoprotective actions of CCN2 and the role of CCN2 in angiotensin 2-induced myocardial hypertrophy
Candidate: Tuyet Anh Pham
Time: February 14, 2020 at 13:15
Place: University of Oslo, Domus Medica: Nye auditorium 13
Link to university website
SUMMARY:
(1) Connective Tissue Growth Factor (CCN2) protects against oxidative stress and cell death by activating the cytoprotective signaling pathway PI3-kinase/Akt/GSK-3β in adult cardiomyocytes and endothelial cells. Cardioprotective genes are upregulated in cardiomyocytes stimulated with CCN2. This cardioprotection is attenuated when a PI3-kinase inhibitor or Akt-inhibitor is present.
(2) Mice with overexpression of CCN2 in the heart showed attenuated hypertrophy compared to wild type mice when subjected to angiotensin II-infusion. Pro-hypertrophic NFAT-activity was reduced when CCN2 was present in neonatal cardiomyocytes exposed to mechanical stretch, indicating that CCN2 protects against hypertrophy through modulation of NFAT-activity.
REFERENCES:
(1) Moe, I. T., Pham, T. A., Hagelin, E. M. V., Ahmed, M. S., & Attramadal, H. (2013). CCN2 exerts direct cytoprotective actions in adult cardiac myocytes by activation of the PI3-kinase/Akt/GSK-3β signaling pathway. Journal of cell communication and signaling, 7(1), 31-47.
