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Why is the partial oxygen pressure of human tissues a crucial parameter? Small molecules and hypoxia.

Carreau A, El Hafny-Rahbi B, Matejuk A, Grillon C, Kieda C - J. Cell. Mol. Med. (2011)

Bottom Line: The oxygen partial pressure (pO(2)), which is a key component of the physiological state of an organ, results from the balance between oxygen delivery and its consumption.More importantly we emphasize the discrepancy between in vivo and in vitro tissue and cells oxygen status which can have detrimental effects on experimental outcome.It is important to realize that most of the experiments performed in so-called normoxia might be dangerously misleading.

View Article: PubMed Central - PubMed

Affiliation: Centre de Biophysique Moléculaire, CNRS UPR, Orléans, France.

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Relative HIF-1 and HIF-2 contributions to the hypoxic response over time at 1% (A) and 5% (B) oxygen as demonstrated in human neuroblastoma cells. Model based on a summary of data obtained from protein level variations (Western blot), chromatin immunoprocipitations (ChIP) and activation of target genes ± siRNA treatment. Reproduced with permission from Lofstedt et al., Cell Cycle, 2007[80].
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fig06: Relative HIF-1 and HIF-2 contributions to the hypoxic response over time at 1% (A) and 5% (B) oxygen as demonstrated in human neuroblastoma cells. Model based on a summary of data obtained from protein level variations (Western blot), chromatin immunoprocipitations (ChIP) and activation of target genes ± siRNA treatment. Reproduced with permission from Lofstedt et al., Cell Cycle, 2007[80].

Mentions: HIF-1α stabilization in strong hypoxic conditions is primarily an acute response to hypoxia and the HIF-1α protein levels are reduced or disappear for prolonged hypoxia. HIF-2α levels, on the other hand, continue to increase with time in hypoxia and become more important during the later phases of hypoxia [80]. Moreover, prolonged moderate hypoxia (5% O2 or 38 mmHg) seems to be sufficient to stabilize HIF-2α, but not to induce HIF-1α as showed in Figure 6.


Why is the partial oxygen pressure of human tissues a crucial parameter? Small molecules and hypoxia.

Carreau A, El Hafny-Rahbi B, Matejuk A, Grillon C, Kieda C - J. Cell. Mol. Med. (2011)

Relative HIF-1 and HIF-2 contributions to the hypoxic response over time at 1% (A) and 5% (B) oxygen as demonstrated in human neuroblastoma cells. Model based on a summary of data obtained from protein level variations (Western blot), chromatin immunoprocipitations (ChIP) and activation of target genes ± siRNA treatment. Reproduced with permission from Lofstedt et al., Cell Cycle, 2007[80].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373326&req=5

fig06: Relative HIF-1 and HIF-2 contributions to the hypoxic response over time at 1% (A) and 5% (B) oxygen as demonstrated in human neuroblastoma cells. Model based on a summary of data obtained from protein level variations (Western blot), chromatin immunoprocipitations (ChIP) and activation of target genes ± siRNA treatment. Reproduced with permission from Lofstedt et al., Cell Cycle, 2007[80].
Mentions: HIF-1α stabilization in strong hypoxic conditions is primarily an acute response to hypoxia and the HIF-1α protein levels are reduced or disappear for prolonged hypoxia. HIF-2α levels, on the other hand, continue to increase with time in hypoxia and become more important during the later phases of hypoxia [80]. Moreover, prolonged moderate hypoxia (5% O2 or 38 mmHg) seems to be sufficient to stabilize HIF-2α, but not to induce HIF-1α as showed in Figure 6.

Bottom Line: The oxygen partial pressure (pO(2)), which is a key component of the physiological state of an organ, results from the balance between oxygen delivery and its consumption.More importantly we emphasize the discrepancy between in vivo and in vitro tissue and cells oxygen status which can have detrimental effects on experimental outcome.It is important to realize that most of the experiments performed in so-called normoxia might be dangerously misleading.

View Article: PubMed Central - PubMed

Affiliation: Centre de Biophysique Moléculaire, CNRS UPR, Orléans, France.

Show MeSH
Related in: MedlinePlus