Adipokinetic hormone exerts its anti-oxidative effects using a conserved signal-transduction mechanism involving both PKC and cAMP by mobilizing extra- and intracellular Ca2+ stores
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.
PubMed
23845878
DOI
10.1016/j.cbpc.2013.07.002
PII: S1532-0456(13)00082-3
Knihovny.cz E-resources
- Keywords
- 4-HNE, 4-hydroxy-2-nonenal, AKH, Adipokinetic hormone, Calcium channel, Cell signaling, Hydrogen peroxide, Membrane fluidity, Oxidative stress, PKC, Protein kinase, adipokinetic hormone, cAMP, cyclic adenosine monophosphate, protein kinase C,
- MeSH
- Aldehydes metabolism MeSH
- Cyclic AMP metabolism MeSH
- Calcium Channel Blockers pharmacology MeSH
- Membrane Fluidity drug effects MeSH
- Heteroptera MeSH
- Insect Hormones physiology MeSH
- Pyrrolidonecarboxylic Acid analogs & derivatives MeSH
- Oligopeptides physiology MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- Protein Kinase C metabolism MeSH
- Signal Transduction drug effects physiology MeSH
- Tetradecanoylphorbol Acetate pharmacology MeSH
- Calcium metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Names of Substances
- 4-hydroxy-2-nonenal MeSH Browser
- adipokinetic hormone MeSH Browser
- Aldehydes MeSH
- Cyclic AMP MeSH
- Calcium Channel Blockers MeSH
- Insect Hormones MeSH
- Pyrrolidonecarboxylic Acid MeSH
- Oligopeptides MeSH
- Protein Kinase C MeSH
- Tetradecanoylphorbol Acetate MeSH
- Calcium MeSH
The involvement of members of the adipokinetic hormone (AKH) family in regulation of response to oxidative stress (OS) has been reported recently. However, despite these neuropeptides being the best studied family of insect hormones, their precise signaling pathways in their OS responsive role remain to be elucidated. In this study, we have used an in vitro assay to determine the importance of extra and intra-cellular Ca(2+) stores as well as the involvement of protein kinase C (PKC) and cyclic adenosine 3',5'-monophosphate (cAMP) pathways by which AKH exerts its anti-oxidative effects. Lipid peroxidation product (4-HNE) was significantly enhanced and membrane fluidity reduced in microsomal fractions of isolated brains (CNS) of Pyrrhocoris apterus when treated with hydrogen peroxide (H2O2), whereas these biomarkers of OS were reduced to control levels when H2O2 was co-treated with Pyrap-AKH. The effects of mitigation of OS in isolated CNS by AKH were negated when these treatments were conducted in the presence of Ca(2+) channel inhibitors (CdCl2 and thapsigargin). Presence of either bisindolylmaliemide or chelyrythrine chloride (inhibitors of PKC) in the incubating medium also compromised the anti-oxidative function of AKH. However, supplementing the medium with either phorbol myristate acetate (PMA, an activator of PKC) or forskolin (an activator of cAMP) restored the protective effects of exogenous AKH treatment by reducing 4-HNE levels and increasing membrane fluidity to control levels. Taken together, our results strongly implicate the importance of both PKC and cAMP pathways in AKHs' anti-oxidative action by mobilizing both extra and intra-cellular stores of Ca(2+).
References provided by Crossref.org
Unusual functions of insect vitellogenins: minireview
Hormonal Regulation of Response to Oxidative Stress in Insects-An Update
