Exploring the Roles of CREBRF and TRIM2 in the Regulation of Angiogenesis by High-Density Lipoproteins

被引:14
|
作者
Wong, Nathan K. P. [1 ,2 ,3 ]
Cheung, Helena [1 ,2 ]
Solly, Emma L. [3 ]
Vanags, Laura Z. [1 ,2 ]
Ritchie, William [2 ,4 ,5 ]
Nicholls, Stephen J. [3 ,6 ]
Ng, Martin K. C. [2 ,7 ]
Bursill, Christina A. [1 ,2 ,3 ,6 ]
Tan, Joanne T. M. [1 ,2 ,3 ,6 ]
机构
[1] Heart Res Inst, Immunobiol Res Grp, 7 Eliza St, Newtown, NSW 2042, Australia
[2] Univ Sydney, Sch Med, Discipline Med, Camperdown, NSW 2006, Australia
[3] South Australian Hlth & Med Res Inst, Heart Hlth Theme, North Terrace, Adelaide, SA 5000, Australia
[4] Royal Prince Alfred Hosp, Centenary Inst, Camperdown, NSW 2050, Australia
[5] Inst Human Genet, CNRS, 141 Rue Cardonille, F-34396 Montpellier 5, France
[6] Univ Adelaide, Adelaide Med Sch, Fac Hlth & Med Sci, Adelaide, SA 5000, Australia
[7] Royal Prince Alfred Hosp, Dept Cardiol, Camperdown, NSW 2050, Australia
基金
英国医学研究理事会;
关键词
angiogenesis; high-density lipoproteins; hypoxia; inflammation; TRIM2; CREBRF; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; UBIQUITIN LIGASE TRIM2; GLOBAL BURDEN; INFLAMMATION; INHIBIT; CANCER; DEFICIENCY; ISCHEMIA; HYPOXIA;
D O I
10.3390/ijms19071903
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Angiogenesis, the process of forming new blood vessels, is crucial in the physiological response to ischemia, though it can be detrimental as part of inflammation and tumorigenesis. We have previously shown that high-density lipoproteins (HDL) modulate angiogenesis in a context-specific manner via distinct classical signalling pathways, enhancing hypoxia-induced angiogenesis while suppressing inflammatory-driven angiogenesis. Whether additional novel targets exist to account for these effects are unknown. A microarray approach identified two novel genes, cyclic-adenosine-monophosphate-response-element-binding protein 3 regulatory factor (CREBRF) and tripartite motif-containing protein 2 (TRIM2) that were upregulated by reconstituted HDL (rHDL). We measured CREBRF and TRIM2 expression in human coronary artery endothelial cells following incubation with rHDL and exposure to either hypoxia or an inflammatory stimulus. We found that CREBRF and TRIM2 mRNA were significantly upregulated by rHDL, particularly in response to its phospholipid component 1-palmitoyl-2-linoleoyl-phosphatidylcholine, however, protein expression was not significantly altered. Knockdown of TRIM2 impaired endothelial cell tubulogenesis in vitro in both hypoxia and inflammation, implying a necessary role in angiogenesis. Furthermore, TRIM2 knockdown attenuated rHDL-induced tubule formation in hypoxia, suggesting that it is important in mediating the pro-angiogenic action of rHDL. Our study has implications for understanding the regulation of angiogenesis in both of these pathophysiological contexts by HDL.
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页数:17
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