Biology of hypoxia

Juliann G. Kiang, Kong-Thon Tsen

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

Hypoxia is an often seen problem resulting from conditions such as ischemia, hemorrhage, stroke, premature birth, and other cardiovascular difficulties. To find useful remedies that are capable of ameliorating its casualty is an essential effort. Although the underlying mechanisms of the hypoxia-induce injury and cell death are still not fully understood, it has been shown that hypoxia induces nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression that play important roles in producing injury including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B 4 (LTB 4) generation. Moreover, it has been evident that transcription factors responsible for iNOS expression are also altered by hypoxia. Hypoxia also increases intracellular Ca 2+ concentration, tumor necrosis factor-α, lipid peroxidation, prostaglandin E 2 production, activity of caspase-3 and -9, and release of cytochrome c from mitochondria, apoptosis inducible factor, and endonuclease G. However, it has been shown that downregulation of iNOS can limit cell injury caused by hypoxia. In our laboratory, we have found that treatment with either iNOS inhibitors or iNOS siRNA inhibits iNOS expression, reduces lipid peroxidation, apoptosome formation, and cellular caspase-3 activity, preserves cellular ATP levels, and increases cell survival. Therefore, iNOS inhibition may be a novel mechanism for protection from hypoxia-induced injury and cell death.

Original languageEnglish (US)
Pages (from-to)223-233
Number of pages11
JournalChinese Journal of Physiology
Volume49
Issue number5
StatePublished - 2006

Fingerprint

Nitric Oxide Synthase Type II
Wounds and Injuries
Caspase 3
Lipid Peroxidation
Cell Death
Apoptosomes
Leukotriene B4
Neutrophil Infiltration
Caspase 9
Premature Birth
Prostaglandins E
Cytochromes c
Hypoxia
Small Interfering RNA
Cell Survival
Mitochondria
Nitric Oxide
Transcription Factors
Down-Regulation
Ischemia

Keywords

  • ATP
  • Calcium
  • Caspase
  • Free radical
  • Hypoxia
  • iNOS
  • NO

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Kiang, J. G., & Tsen, K-T. (2006). Biology of hypoxia. Chinese Journal of Physiology, 49(5), 223-233.

Biology of hypoxia. / Kiang, Juliann G.; Tsen, Kong-Thon.

In: Chinese Journal of Physiology, Vol. 49, No. 5, 2006, p. 223-233.

Research output: Contribution to journalArticle

Kiang, JG & Tsen, K-T 2006, 'Biology of hypoxia', Chinese Journal of Physiology, vol. 49, no. 5, pp. 223-233.
Kiang, Juliann G. ; Tsen, Kong-Thon. / Biology of hypoxia. In: Chinese Journal of Physiology. 2006 ; Vol. 49, No. 5. pp. 223-233.
@article{3f9f3db9f74b4ac093fd0608bd88f713,
title = "Biology of hypoxia",
abstract = "Hypoxia is an often seen problem resulting from conditions such as ischemia, hemorrhage, stroke, premature birth, and other cardiovascular difficulties. To find useful remedies that are capable of ameliorating its casualty is an essential effort. Although the underlying mechanisms of the hypoxia-induce injury and cell death are still not fully understood, it has been shown that hypoxia induces nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression that play important roles in producing injury including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B 4 (LTB 4) generation. Moreover, it has been evident that transcription factors responsible for iNOS expression are also altered by hypoxia. Hypoxia also increases intracellular Ca 2+ concentration, tumor necrosis factor-α, lipid peroxidation, prostaglandin E 2 production, activity of caspase-3 and -9, and release of cytochrome c from mitochondria, apoptosis inducible factor, and endonuclease G. However, it has been shown that downregulation of iNOS can limit cell injury caused by hypoxia. In our laboratory, we have found that treatment with either iNOS inhibitors or iNOS siRNA inhibits iNOS expression, reduces lipid peroxidation, apoptosome formation, and cellular caspase-3 activity, preserves cellular ATP levels, and increases cell survival. Therefore, iNOS inhibition may be a novel mechanism for protection from hypoxia-induced injury and cell death.",
keywords = "ATP, Calcium, Caspase, Free radical, Hypoxia, iNOS, NO",
author = "Kiang, {Juliann G.} and Kong-Thon Tsen",
year = "2006",
language = "English (US)",
volume = "49",
pages = "223--233",
journal = "Chinese Journal of Physiology",
issn = "0304-4920",
publisher = "Chinese Physiological Society",
number = "5",

}

TY - JOUR

T1 - Biology of hypoxia

AU - Kiang, Juliann G.

AU - Tsen, Kong-Thon

PY - 2006

Y1 - 2006

N2 - Hypoxia is an often seen problem resulting from conditions such as ischemia, hemorrhage, stroke, premature birth, and other cardiovascular difficulties. To find useful remedies that are capable of ameliorating its casualty is an essential effort. Although the underlying mechanisms of the hypoxia-induce injury and cell death are still not fully understood, it has been shown that hypoxia induces nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression that play important roles in producing injury including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B 4 (LTB 4) generation. Moreover, it has been evident that transcription factors responsible for iNOS expression are also altered by hypoxia. Hypoxia also increases intracellular Ca 2+ concentration, tumor necrosis factor-α, lipid peroxidation, prostaglandin E 2 production, activity of caspase-3 and -9, and release of cytochrome c from mitochondria, apoptosis inducible factor, and endonuclease G. However, it has been shown that downregulation of iNOS can limit cell injury caused by hypoxia. In our laboratory, we have found that treatment with either iNOS inhibitors or iNOS siRNA inhibits iNOS expression, reduces lipid peroxidation, apoptosome formation, and cellular caspase-3 activity, preserves cellular ATP levels, and increases cell survival. Therefore, iNOS inhibition may be a novel mechanism for protection from hypoxia-induced injury and cell death.

AB - Hypoxia is an often seen problem resulting from conditions such as ischemia, hemorrhage, stroke, premature birth, and other cardiovascular difficulties. To find useful remedies that are capable of ameliorating its casualty is an essential effort. Although the underlying mechanisms of the hypoxia-induce injury and cell death are still not fully understood, it has been shown that hypoxia induces nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression that play important roles in producing injury including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B 4 (LTB 4) generation. Moreover, it has been evident that transcription factors responsible for iNOS expression are also altered by hypoxia. Hypoxia also increases intracellular Ca 2+ concentration, tumor necrosis factor-α, lipid peroxidation, prostaglandin E 2 production, activity of caspase-3 and -9, and release of cytochrome c from mitochondria, apoptosis inducible factor, and endonuclease G. However, it has been shown that downregulation of iNOS can limit cell injury caused by hypoxia. In our laboratory, we have found that treatment with either iNOS inhibitors or iNOS siRNA inhibits iNOS expression, reduces lipid peroxidation, apoptosome formation, and cellular caspase-3 activity, preserves cellular ATP levels, and increases cell survival. Therefore, iNOS inhibition may be a novel mechanism for protection from hypoxia-induced injury and cell death.

KW - ATP

KW - Calcium

KW - Caspase

KW - Free radical

KW - Hypoxia

KW - iNOS

KW - NO

UR - http://www.scopus.com/inward/record.url?scp=33847758449&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847758449&partnerID=8YFLogxK

M3 - Article

C2 - 17294830

AN - SCOPUS:33847758449

VL - 49

SP - 223

EP - 233

JO - Chinese Journal of Physiology

JF - Chinese Journal of Physiology

SN - 0304-4920

IS - 5

ER -