Abstract
Excess accumulation of vascular extracellular matrix (ECM) is an important pathological process in cardiovascular diseases including diabetes-associated atherosclerosis. We explored how a recently identified molecule, cell division autoantigen 1 (CDA1), influences the profibrotic TGF-beta pathway leading to vascular ECM accumulation.
Expression levels of genes encoding for CDA1, TGF-beta and connective tissue growth factor (CTGF) were examined in aorta from Apoe(-/-) mice with or without diabetes. We used retroviral and adenoviral constructs to knockdown or overexpress Tspyl2, the gene encoding CDA1, in mouse vascular smooth muscle cells (VSMCs) with or without TGF-beta treatment in order to demonstrate the role of CDA1 in TGF-beta signalling.
| Original language | English |
|---|---|
| Pages (from-to) | 170 - 179 |
| Number of pages | 10 |
| Journal | Diabetologia |
| Volume | 53 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2010 |
Cite this
Pham, Y., Tu, Y., Wu, T., Allen, T. J., Calkin, A., Watson, A. M., Li, J., Jandeleit-Dahm, K. A., Toh, B-H., Cao, Z. M., Cooper, M. E., & Chai, Z. (2010). Cell division autoantigen 1 plays a profibrotic role by modulating downstream signalling of TGF-? in a murine diabetic model of atherosclerosis. Diabetologia, 53(1), 170 - 179. https://doi.org/10.1007/s00125-009-1555-9