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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.
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Image Search Results


Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.

Journal: Cells

Article Title: The Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

doi: 10.3390/cells12222626

Figure Lengend Snippet: Repetitive IOP spikes induce the activation of inflammatory biomarkers and RGC dysfunction and loss. ( A ) Experimental paradigm of the spiking OHT (spOHS) model and steady OHT (stOHT) control; ( B ) qRT-PCR data on relative changes in transcript abundances of inflammasome pathway genes in retinas. Mean fold change vs. naïve ± SE, * p < 0.05, n = 3–5. ( C ) Intravitreal IL1-β measured at 6, 12, and 24 h after spOHT (red) and stOHT eyes (OD, blue). Mean ± SE, * p < 0.05, n = 5. Negative control: Casp1 −/− eyes (Cs1KO). ( D ) Quantification for HIF1a fluorescent labeling in retina wholemounts from eyes exposed to sham, stOHT, spOHT, or IR. Mean percentile change vs. sham ± SE, ** p < 0.05, n = 5.

Article Snippet: ELISA kits for mouse IL-1β (R&D ID# MBL00C) or Ella SimplePlex for IL1β, TNFα, and MCP1/CCL2 (Protein Simple, Bio-Techne Inc., Minneapolis, MN, USA), as described in [ ], were used to measure the cytokines released into the vitreous.

Techniques: Activation Assay, Quantitative RT-PCR, Negative Control, Labeling

Pro-inflammatory cytokines in the spOHT-challenged retina. Immunolabeling for IL-1β (blue) co-localized with neurons in the GCL and INL; TNFα-specific labelling (green) confined to GFAP + astroglia (arrows), infiltrating monocytes (arrowheads) in the retina 48 h after the spOHT challenge. ASC-citrine specks (magenta) co-localized with the GFAP + TNFα + astrocytes and Muller glia (yellow arrows) in the inner retina, and with astrocytes in the optic nerve. In control stOHT-treated retinas (bottom panels), both TNFα- and IL1β-specific labeling were reduced; no infiltrating monocytes were detected. Size bars in µm.

Journal: Cells

Article Title: The Inflammasome-Dependent Dysfunction and Death of Retinal Ganglion Cells after Repetitive Intraocular Pressure Spikes

doi: 10.3390/cells12222626

Figure Lengend Snippet: Pro-inflammatory cytokines in the spOHT-challenged retina. Immunolabeling for IL-1β (blue) co-localized with neurons in the GCL and INL; TNFα-specific labelling (green) confined to GFAP + astroglia (arrows), infiltrating monocytes (arrowheads) in the retina 48 h after the spOHT challenge. ASC-citrine specks (magenta) co-localized with the GFAP + TNFα + astrocytes and Muller glia (yellow arrows) in the inner retina, and with astrocytes in the optic nerve. In control stOHT-treated retinas (bottom panels), both TNFα- and IL1β-specific labeling were reduced; no infiltrating monocytes were detected. Size bars in µm.

Article Snippet: ELISA kits for mouse IL-1β (R&D ID# MBL00C) or Ella SimplePlex for IL1β, TNFα, and MCP1/CCL2 (Protein Simple, Bio-Techne Inc., Minneapolis, MN, USA), as described in [ ], were used to measure the cytokines released into the vitreous.

Techniques: Immunolabeling, Labeling