Expression of Long Non-Coding RNAs by Human Retinal Müller Glial Cells Infected with Clonal and Exotic Virulent <i>Toxoplasma gondii</i>

• Main Authors: Elise Rochet, Binoy Appukuttan, Yuefang Ma, Liam M. Ashander, Justine R. Smith
• Format: Article
• Language: English
• Published: MDPI AG 2019-09-01
• Series: Non-Coding RNA
• Subjects: Toxoplasma gondii; toxoplasmosis; human; eye; retina; Müller cells; long non-coding RNA
• Online Access: https://www.mdpi.com/2311-553X/5/4/48

Retinal infection with <i>Toxoplasma gondii</i>&#8212;ocular toxoplasmosis&#8212;is a common cause of vision impairment worldwide. Pathology combines parasite-induced retinal cell death and reactive intraocular inflammation. M&#252;ller glial cells, which represent the supporting cell population of the retina, are relatively susceptible to infection with <i>T. gondii</i>. We investigated expression of long non-coding RNAs (lncRNAs) with immunologic regulatory activity in M&#252;ller cells infected with virulent <i>T. gondii </i>strains&#8212;GT1 (haplogroup 1, type I) and GPHT (haplogroup 6). We first confirmed expression of 33 lncRNA in primary cell isolates. MIO-M1 human retinal M&#252;ller cell monolayers were infected with <i>T. gondii</i> tachyzoites (multiplicity of infection = 5) and harvested at 4, 12, 24, and 36 h post-infection, with infection being tracked by the expression of parasite surface antigen 1 (SAG1). Significant fold-changes were observed for 31 lncRNAs at one or more time intervals. Similar changes between strains were measured for BANCR, CYTOR, FOXD3-AS1, GAS5, GSTT1-AS1, LINC-ROR, LUCAT1, MALAT1, MIR22HG, MIR143HG, PVT1, RMRP, SNHG15, and SOCS2-AS1. Changes differing between strains were measured for APTR, FIRRE, HOTAIR, HOXD-AS1, KCNQ1OT1, LINC00968, LINC01105, lnc-SGK1, MEG3, MHRT, MIAT, MIR17HG, MIR155HG, NEAT1, NeST, NRON, and PACER. Our findings suggest roles for lncRNAs in regulating retinal M&#252;ller cell immune responses to <i>T. gondii</i>, and encourage future studies on lncRNA as biomarkers and/or drug targets in ocular toxoplasmosis.