All-trans retinoic acid reduces mammalian target of rapamycin via a Sirtuin1-dependent mechanism in neurons.
Neuroreport
; 32(12): 975-982, 2021 08 11.
Article
in En
| MEDLINE
| ID: mdl-34050114
ABSTRACT
Neuroinflammation has emerged as a key contributor in the pathogenesis of Alzheimer's disease (AD). Mammalian target of rapamycin (mTOR) is a key regulator of metabolism, cell growth and protein synthesis. And an elevated mTOR activity has been detected in AD-affected brain areas. Previous studies have suggested that all-trans retinoic acid (atRA) and rapamycin (RAPA), an mTOR inhibitor, protect lipopolysaccharide (LPS)-induced neuronal inflammation through inhibiting nuclear import of NFκB. The aim of this study was to test the effects of atRA on mTOR expression. Here we discovered that mTOR and p-mTOR expression are elevated in LPS-treated mice or primary rat neurons, while atRA blocks the mTOR gene upregulation via a SIRT1-dependent mechanism. The results of this study demonstrated that atRA may protect LPS-induced neuronal inflammation through suppressing mTOR signaling.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Tretinoin
/
Sirtuin 1
/
TOR Serine-Threonine Kinases
/
Neurons
Limits:
Animals
Language:
En
Journal:
Neuroreport
Journal subject:
NEUROLOGIA
Year:
2021
Document type:
Article