PMID- 29623927
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1673-5374 (Print)
IS  - 1876-7958 (Electronic)
IS  - 1673-5374 (Linking)
VI  - 13
IP  - 3
DP  - 2018 Mar
TI  - Progesterone modulates mTOR in the hippocampus of mice after traumatic brain 
      injury.
PG  - 434-439
LID - 10.4103/1673-5374.228725 [doi]
AB  - The mechanistic target of rapamycin (mTOR) is an intracellular protein kinase 
      that functions as an energy and nutrient sensor in the cellular microenvironment 
      of neurons. Modulation of mTOR is vital when nutrient and energy sources become 
      limited. Hypoxia, traumatic brain injury, cellular energy states, and growth 
      factors all regulate the phosphorylation and total levels of mTOR in cells. 
      Alterations in the microenvironment induce transduction of signals to downstream 
      proteins by mTOR allowing for cells to make the necessary adjustments to 
      counteract stressors and survive. Progesterone, a hydrophobic steroid hormone, 
      has been shown in studies of non-neural tissue to be a suppressor of mTOR and 
      modulator of mTOR phosphorylation. Our study tested the effects of progesterone 
      on mTOR expression following traumatic brain injury. C57BL/6 mice were treated 
      with progesterone (8 mg/kg) at 1 (intraperitoneal), 6 (subcutaneous), 24 
      (subcutaneous), and 48 (subcutaneous) hours post closed skull traumatic brain 
      injury. The hippocampus was then harvested 72 hours post injury and prepared for 
      western blot analysis. We found that progesterone significantly decreased total 
      mTOR levels in all groups compared to sham treated with vehicle. This was further 
      confirmed by immunostaining showing decreased cytoplasmic mTOR levels compared to 
      sham. Our study shows progesterone is a significant modulator of mTOR levels in 
      the hippocampus of mice following traumatic brain injury.
FAU - Garling, Richard Justin
AU  - Garling RJ
AD  - Department of Neurosurgery, Wayne State University, Detroit, MI; School of 
      Medicine, The University of Texas Health Science Center at San Antonio, San 
      Antonio, TX, USA.
FAU - Watts, Lora Talley
AU  - Watts LT
AD  - School of Medicine, The University of Texas Health Science Center at San Antonio, 
      San Antonio, TX, USA.
FAU - Sprague, Shane
AU  - Sprague S
AD  - Department of Neurosurgery, The University of Texas Health Science Center at San 
      Antonio, San Antonio, TX, USA.
FAU - Digicaylioglu, Murat
AU  - Digicaylioglu M
AD  - Department of Neurosurgery, The University of Texas Health Science Center at San 
      Antonio, San Antonio, TX, USA.
LA  - eng
PT  - Journal Article
PL  - India
TA  - Neural Regen Res
JT  - Neural regeneration research
JID - 101316351
PMC - PMC5900505
OTO - NOTNLM
OT  - closed skull head injury
OT  - nerve regeneration
OT  - neural regeneration
OT  - neuroprotection
OT  - neurotrauma
OT  - pneumatic injury model
OT  - progesterone
OT  - traumatic brain injury
COIS- There are no conflicts of interest to declare
EDAT- 2018/04/07 06:00
MHDA- 2018/04/07 06:01
PMCR- 2018/03/01
CRDT- 2018/04/07 06:00
PHST- 2018/04/07 06:00 [entrez]
PHST- 2018/04/07 06:00 [pubmed]
PHST- 2018/04/07 06:01 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
AID - NeuralRegenRes_2018_13_3_434_228725 [pii]
AID - NRR-13-434 [pii]
AID - 10.4103/1673-5374.228725 [doi]
PST - ppublish
SO  - Neural Regen Res. 2018 Mar;13(3):434-439. doi: 10.4103/1673-5374.228725.