Erratum to “Cytokines and the regulation of hypoxia-inducible factor (HIF)-1α" [International Immunopharmacology 5 (2005) 461-483]

Haddad, John J.; Harb, Hisham L.

doi:10.1016/j.intimp.2006.03.013

Cited by 1 publication

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“…It is fi rmly established that hypoxia can induce both proinfl ammatory (TNF-α, IL-1, IL-6) and antiinfl ammatory (IL-10) cytokines [8]. The cytokines are the low-molecular regulator polypeptides or glycoproteins produced by leukocytes, macrophages, platelets, and endothelial or some other cells, which play the key roles in orchestrated immune response of the organism to acute and chronic stress (hypoxia included), their level being increased manifold during such defense or adaptive reactions [8].…”

Section: Resultsmentioning

confidence: 99%

“…The cytokines are the low-molecular regulator polypeptides or glycoproteins produced by leukocytes, macrophages, platelets, and endothelial or some other cells, which play the key roles in orchestrated immune response of the organism to acute and chronic stress (hypoxia included), their level being increased manifold during such defense or adaptive reactions [8]. Thus, hypoxia can promote the chronic infl ammation.…”

Section: Resultsmentioning

confidence: 99%

“…In the same periods, the degree of adaptation to hypoxia was assessed by the changes in their total resistance (by strengthening the ability to cope with acute hypobaric hypoxia incompatible with life assessed by the hypoxic lifetime, LT) [4]. The changes of HIF-1α in neocortex were assessed with the Western blotting [8]. The contents of HIF-1α -dependent vascular endothelial growth factor (VEGF), proinfl ammatory cytokines (IL-6, IL-1, TNF-α), and anti-infl ammatory cytokine IL-10 were assayed in blood serum with VEGF ELISA kit, Quantikine human VEGF, R&D Systems, ELISA (BioSource International) test systems.…”

Section: Methodsmentioning

confidence: 99%

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Role of Proinfl ammatory Factors, Nitric Oxide, and Some Parameters of Lipid Metabolism in the Development of Immediate Adaptation to Hypoxia and HIF-1α Accumulation

2013

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The development of immediate and delayed long-term resistance to hypoxia during a course of intermittent normobaric hypoxia (15 daily sessions of alternating exposure to 10% O2 and atmospheric air for 1 h) correlated with biphasic expression of HIF-1α in neocortex of hypoxia-intolerant rats, which suggests involvement of this protein factor not only in the formation of long-term adaptation, but also in triggering immediate adaptation to hypoxia. Both processes develop under conditions promoting down-regulation of oxidative modification of LDL and increasing tolerance of biological membranes to hypoxia in the absence of activation of the free radical processes, which therefore do not trigger HIF-1α expression under these conditions. Neither cytokines nor NO are the inducers of immediate adaptation, and they are not related to HIF-1α expression during the early post-hypoxic period. In contrast, long-term adaptation in response to the course of intermittent normobaric hypoxia develops against the background of enhanced NO production, activation of pro- and anti-inflammatory factors, and expression of VEGF, the marker of angiogenesis. Therefore, all these factors can promote activation of transcription processes required to form the long-term adaptation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%