Key result
Burn injury increases right ventricular β1-AR expression ~168% versus controls, indicating differential biventricular signaling.
Why the study?
Does severe burn injury differentially alter β-adrenergic receptor signaling in the right versus left ventricles in a rodent model?
Does severe burn injury differentially alter β-adrenergic receptor signaling in the right versus left ventricles in a rodent model?
Severe burn injury induces differential β-adrenergic receptor signaling alterations in the right versus left ventricles, suggesting non-canonical signaling pathways may be activated in the right ventricle.
Answers are grounded in this paper and cite their sources.
Rodent burn model shows RV β1-AR upregulation; hypothesis-generating for differential biventricular signaling, pending clinical validation.
Burn injury detrimentally affects 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. A rodent model with a scald burn of 60% of the total body surface area was used to test this hypothesis. Ventricles were isolated 7 days post-burn. We examined the expression of β-ARs via Western blotting and the mRNA expression of downstream signaling proteins via qRT-PCR. Cyclic adenosine monophosphate (cAMP) production and protein kinase A (PKA) activity were measured in membrane and cytosolic fractions, respectively, using enzyme immunoassay kits. β1-AR protein expression was significantly increased in the RV following burn injury compared to non-burned RV but not in the LV (p = 0.0022). In contrast, β2-AR expression was unaltered among the groups while Gαi expression was significantly higher in the LV post-burn (p = 0.023). B-arrestin-1 and G-protein coupled receptor kinase-2 mRNA expression were significantly increased in the left ventricle post-burn (p = 0.001, p<0.0001, respectively). cAMP production and PKA activity were significantly lower in the LV post-burn (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 activated in the RV as cAMP production and PKA activity were unchanged despite changes in β1-AR protein expression.
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Guillory et al. (2017) studied Burn injury. Scald burn injury vs. Non-burned control was evaluated on β1-AR protein expression in the right ventricle (p=0.0022). Burn injury significantly increased β1-AR protein expression in the right ventricle by 168% compared to non-burned controls, indicating differential biventricular β-adrenergic receptor signaling.
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