Effects of Stress (Hypoxia) on Pro-Inflammatory Cytokine Production from Astrocytes
Abstract
Our research dealt with astrocytes in the human optic nerve head and studying their production of pro-inflammatory cytokines under hypoxic conditions. Retinal ganglion cells, neurons of the eye, die during the progression of glaucoma. Our lab believes that hypoxia in astrocytes from the optic nerve head contribute to retinal ganglion cell death via upregulation of pro-inflammatory cytokines. In the experiment, astrocytes from various human donors were incubated for 24 hours under normoxia and hypoxia. After 24 hours, immunocytochemistry was performed on the cells to view TNF-α, HIF-1α, and IL-1β production under a confocal microscope. Cells were stained with anti-rabbit primary and secondary antibodies at a dilution of 1:100 and 1:200, respectively. Our results showed that production of pro-inflammatory cytokines was enhanced, but the increase in production was not drastic. TNF-α and IL-1β were upregulated by a reasonable amount. It was hypothesized that, because cytokines are secretory in nature, the cytokines could have been released into the media the cells were in. Because of this, the next direction for the lab is to investigate the media for the presence of the cytokines. These results support our lab’s hypothesis that pro-inflammatory cytokines produced from astrocytes are upregulated in hypoxic conditions, similar to glaucoma. Understanding more about how glaucoma progresses would lead to better treatment in the near future.
Effects of Stress (Hypoxia) on Pro-Inflammatory Cytokine Production from Astrocytes
Founders Hall 142 A
Our research dealt with astrocytes in the human optic nerve head and studying their production of pro-inflammatory cytokines under hypoxic conditions. Retinal ganglion cells, neurons of the eye, die during the progression of glaucoma. Our lab believes that hypoxia in astrocytes from the optic nerve head contribute to retinal ganglion cell death via upregulation of pro-inflammatory cytokines. In the experiment, astrocytes from various human donors were incubated for 24 hours under normoxia and hypoxia. After 24 hours, immunocytochemistry was performed on the cells to view TNF-α, HIF-1α, and IL-1β production under a confocal microscope. Cells were stained with anti-rabbit primary and secondary antibodies at a dilution of 1:100 and 1:200, respectively. Our results showed that production of pro-inflammatory cytokines was enhanced, but the increase in production was not drastic. TNF-α and IL-1β were upregulated by a reasonable amount. It was hypothesized that, because cytokines are secretory in nature, the cytokines could have been released into the media the cells were in. Because of this, the next direction for the lab is to investigate the media for the presence of the cytokines. These results support our lab’s hypothesis that pro-inflammatory cytokines produced from astrocytes are upregulated in hypoxic conditions, similar to glaucoma. Understanding more about how glaucoma progresses would lead to better treatment in the near future.
