PMID- 29387292
OWN - NLM
STAT- MEDLINE
DCOM- 20180813
LR  - 20181113
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2017
DP  - 2017
TI  - Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a 
      Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway.
PG  - 5262958
LID - 10.1155/2017/5262958 [doi]
LID - 5262958
AB  - Oxidative stress has both detrimental and beneficial effects. Kallistatin, a key 
      component of circulation, protects against vascular and organ injury. Serum 
      kallistatin levels are reduced in patients and animal models with hypertension, 
      diabetes, obesity, and cancer. Reduction of kallistatin levels is inversely 
      associated with elevated thiobarbituric acid-reactive substance. Kallistatin 
      therapy attenuates oxidative stress and increases endothelial nitric oxide 
      synthase (eNOS) and NO levels in animal models. However, kallistatin 
      administration increases reactive oxygen species formation in immune cells and 
      bacterial killing activity in septic mice. High oxygen inhibits kallistatin 
      expression via activating the JNK-FOXO1 pathway in endothelial cells. Conversely, 
      mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible 
      factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal 
      mice. Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense 
      RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of 
      kallistatin in mediating mild oxygen's stimulation on antioxidant genes. Protein 
      kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to 
      hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates 
      kallistatin-mediated HIF-1 and eNOS synthesis. In summary, oxidative stress 
      induces down- or upregulation of kallistatin expression, depending on oxygen 
      concentration, and kallistatin plays a novel role in mediating 
      oxygen/exercise-induced HIF-1-eNOS-NO pathway.
FAU - Chao, Julie
AU  - Chao J
AUID- ORCID: 0000-0001-7294-2636
AD  - Department of Biochemistry and Molecular Biology, Medical University of South 
      Carolina, Charleston, SC, USA.
FAU - Guo, Youming
AU  - Guo Y
AD  - Department of Biochemistry and Molecular Biology, Medical University of South 
      Carolina, Charleston, SC, USA.
FAU - Li, Pengfei
AU  - Li P
AD  - Department of Biochemistry and Molecular Biology, Medical University of South 
      Carolina, Charleston, SC, USA.
FAU - Chao, Lee
AU  - Chao L
AD  - Department of Biochemistry and Molecular Biology, Medical University of South 
      Carolina, Charleston, SC, USA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20171213
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Serpins)
RN  - 0 (kallistatin)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Hypoxia-Inducible Factor 1/*metabolism
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase Type III/*metabolism
MH  - Oxidative Stress
MH  - Oxygen/*metabolism
MH  - Serpins/*biosynthesis
MH  - *Signal Transduction
PMC - PMC5745740
EDAT- 2018/02/02 06:00
MHDA- 2018/08/14 06:00
PMCR- 2017/12/13
CRDT- 2018/02/02 06:00
PHST- 2017/08/17 00:00 [received]
PHST- 2017/10/25 00:00 [accepted]
PHST- 2018/02/02 06:00 [entrez]
PHST- 2018/02/02 06:00 [pubmed]
PHST- 2018/08/14 06:00 [medline]
PHST- 2017/12/13 00:00 [pmc-release]
AID - 10.1155/2017/5262958 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2017;2017:5262958. doi: 10.1155/2017/5262958. Epub 2017 Dec 
      13.