In the present study, we therefore used microarray technology to investigate the concurrent expression of 1,178 genes in the rat retina both
following hypoxia and following a post-hypoxic 24 h reoxygenation period.
The expression of VEGF, Flk - 1, and EPO were significantly upregulated
following hypoxia.
These analyses revealed that expression of the metabotropic glutamate receptor family was also significantly enriched
following hypoxia and recovery
Thus, interactome hubs such as NR1 may exhibit low levels of change in individual gene expression
following hypoxia, but, based on analysis of interaction networks, are likely to play an important role in regulating the biologic response.
Of the 24 genes downregulated
following hypoxia, the expression of approximately half remained lower than control levels after recovery.
However, 24 genes were significantly downregulated
following hypoxia, with 12 still significantly downregulated after recovery.
Our results confirmed and extended previous observations that genes associated with hypoxia (specifically VEGF, Flk - 1, and EPO) are indeed elevated
following hypoxia in the retina.
Similarly, Bernaudin et al. [43] found increased expression of 18 genes in the neonatal rat brain
following hypoxia (8 % O2 for 3 h) including several known hypoxia inducible genes such as MAP kinase phosphatase - 1 (MKP - 1), several HIF - 1 target genes including VEGF and GLUT - 1, genes implicated in apoptosis, signal transduction molecules, and transcription factors.
Of the 119 genes upregulated
following hypoxia, 72 % remained upregulated after a 24 h period of recovery under normoxic conditions.
Of the total of 1,178 genes examined by microarray, 119 were significantly upregulated
following hypoxia.
Not exact matches
Homebirth is expected to cause a delay in diagnosis, delivery and / or transfer
following an acute intrapartum event with rapidly developing
hypoxia, acidosis and asphyxia.
The results demonstrated that the impairments
following microgravity were not aggravated by
hypoxia.
The research, published in PLOS ONE, found that several markers of insulin resistance were increased
following sustained exposure (6 - 8 weeks) to
hypoxia at high altitude and that this change was related to increased blood levels of markers of inflammation and oxidative stress.
The expression of a few retinal mRNAs known to be induced by
hypoxia, including HIF - 1α, was assessed by qRT — PCR analysis of total RNA isolated from retinal tissue
following exposure to 3 h of 6 % — 7 % O2.
Therefore, the primary novelty of the discoveries reported here is that programming by prenatal chronic
hypoxia of cardiac and vascular dysfunction in adulthood
follows the induction of oxidative stress in the fetal heart and vasculature, and that cardiac and endothelial dysfunction in adulthood can both be prevented by maternal treatment with antioxidants during pregnancy.
GSEA demonstrated significant enrichment in NMDAR subunit expression both during
hypoxia and
following recovery.
Additionally, expression of these mRNAs was also assessed
following 24 h of recovery from
hypoxia in room air compared to that in retinas isolated from control animals exposed only to air (Figure 2).
For microarray and qRT — PCR measurements (i.e., all molecular measurements except those for HIF - 1α message and protein), animals were sacrificed by decapitation without anesthesia either immediately
following 3 h of
hypoxia or
following a 24 h post-
hypoxia recovery period in normal air.
Here, we show that a non-adherent, stem - like, and metastatic CSC - enriched subpopulation could be isolated by exposing human metastatic breast cancer cell lines to cycles of chronic
hypoxia followed by reoxygenation.
Furthermore, susceptibility of genomic instability can vary after acute or chronic exposure to
hypoxia followed by reoxygenation [23].
Following in vitro culture in
hypoxia, cells were reexposed to atmospheric oxygen for up to 10 days before mammosphere culture.
$ 6.3 Million Jury Verdict —
Hypoxia brain injury
following minimally invasive surgery from drug interaction.