Lipidized Prolactin-Releasing Peptide Agonist Attenuates Hypothermia-Induced Tau Hyperphosphorylation in Neurons
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
30689580
DOI
10.3233/jad-180837
PII: JAD180837
Knihovny.cz E-zdroje
- Klíčová slova
- Hypothermia, SH-SY5Y, lipidization, primary neuronal culture, prolactin-releasing peptide, tau phosphorylation,
- MeSH
- buněčné linie MeSH
- fosforylace účinky léků MeSH
- glukagonu podobný peptid 1 agonisté MeSH
- hormon uvolňující prolaktin analogy a deriváty farmakologie MeSH
- krysa rodu Rattus MeSH
- lidé MeSH
- liraglutid farmakologie MeSH
- neurodegenerativní nemoci farmakoterapie metabolismus MeSH
- neurony * účinky léků metabolismus MeSH
- neuroprotektivní látky farmakologie MeSH
- proteiny tau metabolismus MeSH
- terapeutická hypotermie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- glukagonu podobný peptid 1 MeSH
- hormon uvolňující prolaktin MeSH
- liraglutid MeSH
- neuroprotektivní látky MeSH
- palm11-PrRP31 MeSH Prohlížeč
- proteiny tau 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
Citace poskytuje Crossref.org
Prolactin-Releasing Peptide: Physiological and Pharmacological Properties
