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Post‐burn alterations in cardiac Erk1/2 signaling (850.4)
Author(s) -
Guillory Ashley,
El Ayadi Amina,
Herndon David,
Finnerty Celeste
Publication year - 2014
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.28.1_supplement.850.4
Subject(s) - phosphorylation , protein kinase b , western blot , signal transduction , burn injury , kinase , medicine , endocrinology , catecholamine , total body surface area , apoptosis , extracellular , chemistry , biology , microbiology and biotechnology , surgery , biochemistry , gene
. Severe burn trauma causes a catecholamine surge that has been demonstrated, in pediatric patients, to last up to 3 years post injury. The detrimental cardiac effects of the catecholamine surge include a reduction of functional β‐adrenergic receptors (β‐AR) and alterations in various signaling pathways such as that of extracellular signal regulated kinase (Erk1/2). Methods. We used a rat model of 60% total body surface area burn to investigate burn‐induced changes in cardiac signaling pathways. Animals were sacrificed and hearts were isolated 24 hrs and 7 days post injury. The expression and phosphorylation of proteins involved in Erk1/2 signaling were examined via Western Blot. Results. β 1 ‐AR expression levels were significantly increased 24 hrs post‐burn (p=0.009) but returned to control levels by 7 days post‐burn. No changes were observed in β 2 ‐AR expression levels. G i expression was initially depressed post‐burn but was increased at 7 days post‐burn (p=0.0009). Similarly, Erk1/2 phosphorylation was increased by 7 days post‐burn (p=0.036). However, Akt phosphorylation was decreased at 7 days post‐burn (p=0.01). Conclusion. These data indicate that burn injury alters Erk1/2 activation and activity, which may promote pro‐hypertrophic and pro‐apoptotic signaling. Furthermore, in the long‐term, these changes may underlie burn induced cardiac dysfunction and subsequent mortality. Grant Funding Source : Supported by grants from the NIH (P50‐GM60338, KL2RR029875,UL1RR029876) and SHC (80100, 71001).