PMID- 18692603
OWN - NLM
STAT- MEDLINE
DCOM- 20090415
LR  - 20220311
IS  - 1569-9048 (Print)
IS  - 1878-1519 (Electronic)
IS  - 1569-9048 (Linking)
VI  - 164
IP  - 1-2
DP  - 2008 Dec 10
TI  - Transcriptional responses to intermittent hypoxia.
PG  - 277-81
LID - 10.1016/j.resp.2008.07.006 [doi]
AB  - Recurrent apneas are characterized by transient repetitive cessations of 
      breathing (two breaths duration or longer) resulting in periodic decreases in 
      arterial blood PO2 or chronic intermittent hypoxia (IH). Patients with recurrent 
      apneas and experimental animals exposed to chronic IH exhibit cardio-respiratory 
      morbidities. The purpose of this article is to highlight the current information 
      on the transcriptional mechanisms associated with chronic IH. Studies on rodents 
      and cell cultures have shown that IH activates a variety of transcription factors 
      including the hypoxia-inducible factor-1 (HIF-1), c-fos (immediate early gene), 
      nuclear factor of activated T-cells (NFAT), and nuclear factor kB (NF-kB). The 
      signaling pathways associated with transcriptional activation associated with IH 
      differ from continuous hypoxia (CH). Compared to same duration and intensity of 
      CH, IH is more potent in activating HIF-1 and c-fos and also results in 
      long-lasting accumulation of HIF-1alpha and c-fos mRNA, a phenomenon that was not 
      seen with CH. IH-evoked transcriptional activation by HIF-1, c-fos as well as the 
      resulting activator protein-1 (AP-1) requires reactive oxygen species 
      (ROS)-mediated signaling and involves complex feed forward interactions between 
      HIF-1 and ROS. Chronic IH-evoked cardio-respiratory responses are absent in 
      Hif-1alpha+/- mice, and hypertension elicited by chronic IH is absent in mice 
      lacking NFAT3c. These studies indicate that cardiorespiratory responses to 
      chronic IH depend on complex interactions between various transcription factors 
      resulting in alterations in several down stream genes and their protein products.
FAU - Nanduri, Jayasri
AU  - Nanduri J
AD  - The Center for Systems Biology, Department of Medicine, University of Chicago, MC 
      5068, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
FAU - Yuan, Guoxiang
AU  - Yuan G
FAU - Kumar, Ganesh K
AU  - Kumar GK
FAU - Semenza, Gregg L
AU  - Semenza GL
FAU - Prabhakar, Nanduri R
AU  - Prabhakar NR
LA  - eng
GR  - R01 HL076537/HL/NHLBI NIH HHS/United States
GR  - R01 HL086493/HL/NHLBI NIH HHS/United States
GR  - P01HL-90554/HL/NHLBI NIH HHS/United States
GR  - P01 HL090554/HL/NHLBI NIH HHS/United States
GR  - R01HL-76537/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - Netherlands
TA  - Respir Physiol Neurobiol
JT  - Respiratory physiology & neurobiology
JID - 101140022
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Hypoxia/genetics/*physiopathology
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/physiology
MH  - Transcription Factors/genetics/*metabolism
MH  - Transcription, Genetic/*physiology
PMC - PMC3390913
MID - NIHMS78666
EDAT- 2008/08/12 09:00
MHDA- 2009/04/16 09:00
PMCR- 2012/07/06
CRDT- 2008/08/12 09:00
PHST- 2008/04/02 00:00 [received]
PHST- 2008/07/07 00:00 [revised]
PHST- 2008/07/15 00:00 [accepted]
PHST- 2008/08/12 09:00 [pubmed]
PHST- 2009/04/16 09:00 [medline]
PHST- 2008/08/12 09:00 [entrez]
PHST- 2012/07/06 00:00 [pmc-release]
AID - S1569-9048(08)00194-8 [pii]
AID - 10.1016/j.resp.2008.07.006 [doi]
PST - ppublish
SO  - Respir Physiol Neurobiol. 2008 Dec 10;164(1-2):277-81. doi: 
      10.1016/j.resp.2008.07.006.