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Toll‐like receptor 2 is elevated in rat corpus cavernosum in response to nitric oxide deficiency
Author(s) -
Davis Jason,
Nunes Kenia,
Webb R. Clinton
Publication year - 2012
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.26.1_supplement.1131.1
Subject(s) - nitric oxide , endothelial dysfunction , innate immune system , endocrinology , tlr2 , medicine , nitric oxide synthase , erectile dysfunction , receptor , vasodilation , diabetes mellitus , chemistry
The prevalence of erectile dysfunction (ED) is significantly higher among men with comorbid diseases, such as cardiovascular disease and or diabetes mellitus. One common underlying vascular condition that has been shown in both diseases when associated with ED is endothelial dysfunction, a process in which nitric oxide (NO) bioavailability, is reduced. Thus, our objective was to reveal that in the early stages of ED, an innate immune reaction is generated in response to endothelial dysfunction. Therefore, our hypothesis is that toll‐like receptor 2 (TLR2), a key player in innate immunity, is increased in the corpus cavernosum following treatment with N (G)‐nitro‐L‐arginine methyl ester (L‐NAME), an endothelium nitric oxide synthase inhibitor, that mimics endothelial dysfunction. Corpus cavernosum tissues from male Sprague‐Dawley (SD) rats were incubated with L‐NAME (100 uM) for 6, 12 or 24 hours, respectively. Western blot analysis demonstrated that, TLR2 expression is augmented in a time dependent manner, (6hrs:0.007±0.002, 12hrs:0.015±0.008, 24hrs:0.066±0.022), in response to L‐NAME. These results suggest a novel role of TLR2 activation in the causal path leading to ED.