Lipidized Prolactin-Releasing Peptide Agonist Attenuates Hypothermia-Induced Tau Hyperphosphorylation in Neurons
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30689580
DOI
10.3233/jad-180837
PII: JAD180837
Knihovny.cz E-resources
- Keywords
- Hypothermia, SH-SY5Y, lipidization, primary neuronal culture, prolactin-releasing peptide, tau phosphorylation,
- MeSH
- Cell Line MeSH
- Phosphorylation drug effects MeSH
- Glucagon-Like Peptide 1 agonists MeSH
- Prolactin-Releasing Hormone analogs & derivatives pharmacology MeSH
- Rats MeSH
- Humans MeSH
- Liraglutide pharmacology MeSH
- Neurodegenerative Diseases drug therapy metabolism MeSH
- Neurons * drug effects metabolism MeSH
- Neuroprotective Agents pharmacology MeSH
- tau Proteins metabolism MeSH
- Hypothermia, Induced MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glucagon-Like Peptide 1 MeSH
- Prolactin-Releasing Hormone MeSH
- Liraglutide MeSH
- Neuroprotective Agents MeSH
- palm11-PrRP31 MeSH Browser
- tau Proteins MeSH
Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by the accumulation of extracellular amyloid plaques and intraneuronal neurofibrillary tangles. These tangles mainly consist of hyperphosphorylated tau protein. As it induces tau hyperphosphorylation in vitro and in vivo, hypothermia is a useful tool for screening potential neuroprotective compounds that ameliorate tau pathology. In this study, we examined the effect of prolactin-releasing peptide (PrRP), its lipidized analog palm11-PrRP31 and glucagon-like-peptide-1 agonist liraglutide, substances with anorexigenic and antidiabetic properties, on tau phosphorylation and on the main kinases and phosphatases involved in AD development. Our study was conducted in a neuroblastoma cell line SH-SY5Y and rat primary neuronal cultures under normothermic and hypothermic conditions. Hypothermia induced a significant increase in tau phosphorylation at the pThr212 and pSer396/pSer404 epitopes. The palmitoylated analogs liraglutide and palm11-PrRP31 attenuated tau hyperphosphorylation, suggesting their potential use in the treatment of neurodegenerative diseases.
Institute of Organic Chemistry and Biochemistry AS CR Prague Czech Republic
References provided by Crossref.org
Prolactin-Releasing Peptide: Physiological and Pharmacological Properties
