z-logo
Premium
Receptor for advanced glycation end products is involved in remodeling of diabetic coronary arterioles
Author(s) -
Trask Aaron J,
Katz Paige S,
Stewart James A,
Lucchesi Pamela A
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.1025.11
Subject(s) - glycation , medicine , endocrinology , receptor , lumen (anatomy) , chemistry , myograph , rage (emotion) , biology , endothelium , neuroscience
The aim of this study was to determine whether the receptor for advanced glycation end products (RAGE) contributes to remodeling of type 2 diabetic coronary arterioles (<150 μm diameter) of leptin‐receptor deficient db/db mice. Coronary arterioles isolated from control Db/db, type 2 diabetic db/db, and RAGE −/− × db/db mice at 16 weeks of age were mounted on a pressure myograph to measure and record wall thickness and diameters over a range of pressures (0–125 mmHg). Coronary arterioles isolated from db/db mice exhibited decreased luminal diameter (Db/db: 118 ± 5 μm vs. db/db: 103 ± 4 μm p < 0.05) with thicker microvascular walls (Db/db: 6.9 ± 0.6 μm vs. db/db: 9.7 ± 0.5 μm p < 0.01), which significantly increased the wall:lumen ratio (Db/db: 6.0 ± 0.8 vs. db/db: 9.5 ± 0.4, p < 0.01). Compared to db/db mice, coronary arterioles isolated from RAGE −/− x db/db mice had similar internal diameter (104 ± 9 μm, p > 0.05), while wall thickness (6.1 ± 0.5 μm, p < 0.001), wall:lumen ratio (6.2 ± 0.8 μm, p < 0.01), and growth index (db/db: 28.1 vs. RAGE −/− x db/db: 22.3, % of control) were reduced. External diameters were not different among groups, although there was a tendency for reduced external diameter in RAGE −/− x db/db. These data suggest that the RAGE receptor is at least partially responsible for inward hypertrophic remodeling observed in coronary arterioles of type 2 diabetic mice. Support: NIH T32HL098039 to AJT; NIH HL056046 to PAL .

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here