NDP-α-MSH attenuates heart and liver responses to myocardial reperfusion via the vagus nerve and JAK/ERK/STAT signaling

Eur J Pharmacol. 2015 Dec 15:769:22-32. doi: 10.1016/j.ejphar.2015.10.022. Epub 2015 Oct 22.

Abstract

Melanocortin peptides afford cardioprotection during myocardial ischemia/reperfusion via janus kinases (JAK), extracellular signal-regulated kinases (ERK) and signal transducers/activators of transcription (STAT) pathways. Here we investigated whether melanocortin-induced modulation of the JAK/ERK/STAT signaling occurs via the cholinergic anti-inflammatory pathway, focusing our study on cardiac and hepatic responses to prolonged myocardial ischemia/reperfusion. Ischemia was produced in rats by ligature of the left anterior descending coronary artery for 30min; effects of ischemia/reperfusion were evaluated using Western blot of heart and liver proteins. Intravenous treatment, during coronary artery occlusion, with the melanocortin analog (Nle(4), D-Phe(7))α-melanocyte-stimulating hormone (NDP-α-MSH) induced a left ventricle up-regulation of the cardioprotective transcription factors pJAK2, pERK1/2 and pTyr-STAT3 (JAK-dependent), and a reduction in the levels of the inflammatory mediators tumor necrosis factor-α (TNF-α) and pJNK (a transcription factor also involved in apoptosis), as assessed at the end of the 2-h reperfusion period. Further, these beneficial effects of NDP-α-MSH were associated with heart over-expression of the pro-survival proteins heme oxygenase-1 (HO-1) and Bcl-XL, and decrease of ventricular arrhythmias and infarct size. In the liver NDP-α-MSH induced a decrease in the pJAK2 and pTyr-STAT3 levels, and strongly reduced pERK1/2 expression. In the liver of ischemic rats NDP-α-MSH also blunted pJNK activity and TNF-α expression, and up-regulated Bcl-XL. Bilateral cervical vagotomy prevented all effects of NDP-α-MSH, both in the heart and liver. These results indicate that melanocortins inhibit heart and liver damage triggered by prolonged myocardial ischemia/reperfusion likely, as main mechanism, via the vagus nerve-mediated modulation of the JAK/STAT/ERK signaling pathways.

Keywords: Inhibition of local and systemic responses; JAK/ERK/STAT signaling; Liver; Melanocortins; Myocardial ischemia/reperfusion; NDP-alpha-MSH (PubChem CID: 44277697); Vagus nerve.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / metabolism
  • Animals
  • Apoptosis / drug effects
  • Blood Pressure / drug effects
  • Cardiotonic Agents / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Heart / drug effects
  • Heart / physiopathology
  • Janus Kinases / metabolism*
  • Liver / drug effects
  • Liver / pathology
  • Liver / physiopathology
  • Male
  • Myocardial Reperfusion Injury / pathology
  • Myocardial Reperfusion Injury / physiopathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Myocardium / pathology
  • Rats
  • Rats, Wistar
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / drug effects*
  • Vagus Nerve / drug effects*
  • alpha-MSH / analogs & derivatives*
  • alpha-MSH / pharmacology

Substances

  • Cardiotonic Agents
  • STAT3 Transcription Factor
  • alpha-MSH
  • MSH, 4-Nle-7-Phe-alpha-
  • Janus Kinases
  • Extracellular Signal-Regulated MAP Kinases
  • Acetylcholine