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Transient Receptor Potential Type C Channels Play a Critical Role in Angiogenesis
Author(s) -
Zouein Fouad A.,
Sebastian Thomas,
Farley Jerry M.,
Booz George W.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1091.12
Subject(s) - trpc , trpc3 , trpc1 , transient receptor potential channel , trpc6 , angiogenesis , trpc5 , matrigel , microbiology and biotechnology , chemistry , biology , receptor , cancer research , biochemistry
Recent genetic studies indicate that transient receptor potential type C (TRPC) channels play a critical but undefined role in angiogenesis. Here we sought to establish their importance in new blood vessel formation using an in vitro assay. RNA was isolated from human microvascular endothelial cells (HMEC1) obtained from the CDC and human coronary microvascular endothelial cells (HCEC) from a deceased individual and analyzed by RT‐PCR. Results indicated that HMEC1 express mRNA for TRPC1, TRPC3, TRPC4, and TRPC6. HCEC express TRPC1 and TRPC4. Western blots showed that HMEC1 express TRPC1, TRPC3, and TRPC6 proteins. A matrigel assay was done to assess the effect of TRPC channel inhibitor BTP2 on angiogenesis. Treatment of HMEC1 with μM BTP2 reduced the number of branching intersections by 68% from 31.3 ± 2.3 for vehicle control cultures to 9.8 ± 1.8 (mean ± SD, n=3, P<0.001). The density of sprouts per surface area was reduced by 48% from 1.32 ± 0.10 to 0.69 ± 0.06 (P<0.001). Finally, intracellular calcium levels in HMEC1 exhibited oscillations which were reduced by BTP2. Our findings establish the utility of HMEC1 and HCEC as model systems to explore the molecular role of TRPC channels in angiogenesis. Strategies aimed at exploiting their activity may be of benefit in reparative angiogenesis of the heart after myocardial infarction or in heart failure.