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. 2019 May 24;27(1):176–191. doi: 10.1038/s41418-019-0351-4

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© ADMC Associazione Differenziamento e Morte Cellulare 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Predominant role of H19 in microglial pyroptosis and neuronal apoptosis. a Heat map listed the top 16 dysregulated lncRNAs in response to I/R injury. LncRNA H19 (red box) was the most upregulated lncRNA in the I/R retina. b Retinas exposed to I/R injury displayed a significant decrease in IPL thickness. This I/R-induced IPL attenuation was significantly ameliorated in dH19 mice and aggravated by H19 overexpression in retinas. c Iba-1+ microglia (red) had increased GSDMD-N (green) localized in the plasma membrane of I/R-treated mice compared with that of control retinas. Of note, less co-expression of Iba-1 and GSDMD-N was observed in the retina of dH19 mice. H19 overexpression promoted GSDMD-N augmentation in activated microglia (Iba-1+). d As measured by FG retro-labeling, viable RGC was presented as gold dots in flat-mounted retina. The RGC survival rate was noticeably decreased in response to I/R injury. H19 overexpression accentuated RGC apoptosis with less viable RGCs in retinas, which was prevented by H19 knockout. e Compared with the wild type counterparts, the dH19 retina had less TUNEL-positive cells (black arrows) in response to I/R injury, indicating that apoptosis was inhibited by H19 knockout. However, H19 overexpression markedly increased TUNEL-positive cells in GCL. f In retinal homogenates, H19 excision effectively inhibited the I/R-mediated overproduction of IL-1β and IL-18. This anti-inflammatory effect was abolished by H19 overexpression as measured by ELISA. g H19 knockout effectively prevented I/R-induced caspase-3 cleavage, indicating the pro-apoptotic effect of H19. Also, the retinas of H19-null mice exhibited lower protein levels of Iba-1, cleaved-GSDMD, IL-1β, and IL-18. The relative level of each target protein was normalized to β-actin from the same sample (Fig. S2F). Scale bar = 100 μm. Data were represented as means ± SD (n = 6). Compared with the normal control (CON): **P < 0.01. Compared with the I/R retina: ^##P < 0.01. I/R, ischemia and reperfusion; dH19, H19 knockout; oH19, H19 overexpression; GCL, ganglion cell layer; IPL, inner plexiform layer; FG, flurogold