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Biventricular Differences in β‐adrenergic Receptor Signaling Following Burn Injury
Author(s) -
Guillory Ashley,
El Ayadi Amina,
Mifflin Randy,
Herndon David,
Finnerty Celeste
Publication year - 2015
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.29.1_supplement.1025.8
Subject(s) - burn injury , ventricle , total body surface area , medicine , receptor , endocrinology , signal transduction , adrenergic , severe burn , protein expression , cardiology , chemistry , surgery , gene , biochemistry
Burn injury has been shown to have detrimental effects on the myocardium primarily due to over‐activation of β‐adrenergic receptors (β‐AR). Autopsy reports from our institution reveal that patients often suffer from right ventricle (RV) failure. Since burn injury affects β‐AR signaling in the left ventricle (LV), we proposed that β‐AR signaling may also be altered in the RV. We used a rat model of 60% total body surface area burn. Ventricles were isolated at 7 days post‐burn. We examined the expression of β‐ARs and downstream proteins via Western blotting. cAMP production and PKA activity were measured in membrane and cytosolic fractions, respectively, using enzyme immunoassay kits. β 1 ‐AR expression was significantly increased in the RV following burn injury compared to non‐burned RV but remained normal in the LV (p=0.0002). Similarly, G αs expression was increased in the RV post‐burn but not in the LV (p=0.04). There were no differences in β 2 ‐AR expression among the groups. G αi expression was significantly higher in the LV post‐burn compared to non‐burned LV, burned RV and non‐burned RV (p<0.0001). Similarly, cAMP production and PKA activity were significantly lower in the LV post‐burn compared to non‐burned LV, burned RV and non‐burned RV (p=0.0063, 0.0042, respectively). These data indicate that burn injury affects the β‐AR signaling pathway in the RV independently of the LV. Additionally, non‐canonical β‐AR signaling may be involved as cAMP production and PKA activity were unchanged. This study was supported by grants from the National Institutes of Health (P50‐GM60338, KL2RR029875, UL1RR029876) and Shriners Hospital for Children (80100, 84291, 80500, 84202, 71001).