PMID- 27220315
OWN - NLM
STAT- MEDLINE
DCOM- 20170406
LR  - 20170406
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 14
IP  - 1
DP  - 2016 Jul
TI  - Exogenous H2O2 induces growth inhibition and cell death of human pulmonary artery 
      smooth muscle cells via glutathione depletion.
PG  - 936-42
LID - 10.3892/mmr.2016.5307 [doi]
AB  - Reactive oxygen species (ROS) are associated with various pathophysiological 
      processes of vascular smooth muscle cells (VSMCs). Pyrogallol (PG) induces the 
      superoxide anion (O2*‑)‑mediated cell death of numerous cell types. The present 
      study aimed to investigate the effects of exogenous hydrogen peroxide (H2O2) and 
      PG treatment on the cell growth and death of human pulmonary artery smooth muscle 
      cells (HPASMCs), with regards to intracellular ROS and glutathione (GSH) levels, 
      as determined by MTT and cell number assays. H2O2 led to reduced growth of 
      HPASMCs, with a half maximal inhibitory concentration of 250‑500 microM at 24 h, and 
      induced apoptosis, as determined by Annexin V‑staining and 
      benzyloxycarbonyl‑Val‑Ala‑Asp‑fluoromethylketone treatment. However, PG did not 
      strongly induce growth inhibition and death of HPASMCs. In addition, H2O2 led to 
      increased ROS levels, including mitochondrial O2*‑, and induced GSH depletion in 
      HPASMCs. Treatment with N‑acetyl cysteine (NAC) attenuated apoptotic cell death 
      and ROS levels in H2O2‑treated HPASMCs, and also prevented GSH depletion. 
      Notably, PG treatment did not increase ROS levels, including mitochondrial O2*‑. 
      Furthermore, NAC induced a significant increase in mitochondrial O2*‑ levels in 
      PG‑treated HPASMCs, and cell death and GSH depletion were significantly 
      increased. L‑buthionine sulfoximine intensified cell death and GSH depletion in 
      PG‑treated HPASMCs. In conclusion, exogenous H2O2 induced growth inhibition and 
      cell death of HPASMCs via GSH depletion.
FAU - Park, Woo Hyun
AU  - Park WH
AD  - Department of Physiology, Medical School, Research Institute for Endocrine 
      Sciences, Chonbuk National University, Jeonju, North Jeolla 561‑180, Republic of 
      Korea.
LA  - eng
PT  - Journal Article
DEP - 20160519
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Apoptosis/drug effects
MH  - Cell Death/drug effects
MH  - Cell Proliferation/drug effects
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Glutathione/*metabolism
MH  - Humans
MH  - Hydrogen Peroxide/*pharmacology
MH  - Intracellular Space
MH  - Myocytes, Smooth Muscle/*drug effects/*metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Pulmonary Artery/*metabolism
MH  - Reactive Oxygen Species/metabolism
EDAT- 2016/05/26 06:00
MHDA- 2017/04/07 06:00
CRDT- 2016/05/26 06:00
PHST- 2015/07/08 00:00 [received]
PHST- 2016/05/10 00:00 [accepted]
PHST- 2016/05/26 06:00 [entrez]
PHST- 2016/05/26 06:00 [pubmed]
PHST- 2017/04/07 06:00 [medline]
AID - 10.3892/mmr.2016.5307 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Jul;14(1):936-42. doi: 10.3892/mmr.2016.5307. Epub 2016 May 19.