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Decreased protein expression and activity of transglutaminases 1 and 2 in arteries from DOCA‐salt rats
Author(s) -
Petersen-Jones Humphrey,
Johnson Kyle B.,
Thompson Janice M.,
Watts Staphanie W.
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.870.23
Subject(s) - aorta , western blot , medicine , immunohistochemistry , endocrinology , blot , protein expression , chemistry , thoracic aorta , biology , biochemistry , gene
Transglutaminases (TGs) catalyze a variety of protein modification reactions in the vasculature, and TG‐mediated protein remodeling has been implicated in hypertension. We hypothesized that there would be a higher expression of TGs in hypertensive vs normotensive vasculature due to protein cross‐linking catalyzed by the TGs. We used aorta (RA) from deoxycorticosterone acetate (DOCA)‐salt (hypertensive) and sham (normotensive) control rats. Methods included immunohistochemistry (IHC), Western blot analysis, and in situ fluorescent detection of active TGs using the K5 (TG1) and T26 (TG2) peptides. IHC showed a decreased expression of TG1 and TG2 in DOCA‐salt rat aorta (TG1: DOCA 1.22, sham 1.44; TG2: DOCA 0.61, sham 1.61 arbitrary rank units) and in situ detection showed decreased activity of TG1 and TG2 in DOCA‐salt rat aorta (TG1: DOCA 2.0, sham 2.72; TG2: DOCA 1.79, sham 2.56 arbitrary rank units). Similarly, protein expressions of TG1 and TG2 in DOCA‐salt rat aorta were diminished compared to the control (TG1: DOCA 27.8 ± 2.52, sham 51.9 ± 13.0; TG2: DOCA 83.2 ± 3.85, sham 108 ± 5.83 arbitrary densitometry units/alpha actin; p<0.05). We conclude that there is less activity and decreased levels of TG1 and TG2 in hypertensive rat aorta compared to sham. This contradicts our hypothesis and supports the idea that lack of compensatory TGs may a role in the pathology of hypertension. POIHC70687