June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
GPR158 Modulates Expression of Genes Associated with Extracellular Matrix (ECM) Deposition in Trabecular Meshwork Cells
Author Affiliations & Notes
  • Maria Fernanda Suarez
    Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts, United States
    New England Eye Center, Tufts Medical Center, Boston, Massachusetts, United States
  • Satyabrata Pany
    Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts, United States
    New England Eye Center, Tufts Medical Center, Boston, Massachusetts, United States
  • Tatsuo Itakura
    USC Institute for Genetic Medicine, Los Angeles, California, United States
  • Shinwu Jeong
    USC Institute for Genetic Medicine, Los Angeles, California, United States
  • M Elizabeth Fini
    Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts, United States
    New England Eye Center, Tufts Medical Center, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Maria Fernanda Suarez, None; Satyabrata Pany, None; Tatsuo Itakura, None; Shinwu Jeong, None; M Elizabeth Fini, None
  • Footnotes
    Support  NIH/NEI Grant R01EY027315 - Massachusetts Lions Eye Research Fund -Research to Prevent Blindness
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 1243. doi:
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      Maria Fernanda Suarez, Satyabrata Pany, Tatsuo Itakura, Shinwu Jeong, M Elizabeth Fini; GPR158 Modulates Expression of Genes Associated with Extracellular Matrix (ECM) Deposition in Trabecular Meshwork Cells. Invest. Ophthalmol. Vis. Sci. 2020;61(7):1243.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : GPR158, a distant member of the G protein coupled receptor family C, was identified by our lab in a genomic screen for genes associated with susceptibility to glucocorticoid (GC)-induced ocular hypertension (OH). GPR158 is expressed in the trabecular meshwork (TM) and in TM cell cultures, and expression is stimulated by GC treatment (PMID: 23451275). In this study, we investigated the effects of GPR158 expression levels in trabecular meshwork cells.

Methods : An immortalized TM cell line (TM1) stably-transduced with GPR158 under doxycycline (Dox) regulation was created. For GPR158 over-expression, cells were treated with low Dox (100 ng/mL) or high Dox (500 ng/mL) for up to 96hs. For GPR158 knockdown, TM1 cells were transfected with a pool of three custom designed siRNA oligonucleotides. Gene expression microarray profiling was performed in over-expressing cells, and evaluated by Ingenuity Pathway Analysis (IPA). A group of regulated genes was further evaluated by qPCR and western blot blotting in both over-expressing and knockdown cells. Statistical significance was calculated using Student’s t-test (N=3; P≤0.05 considered significant).

Results : IPA revealed that GPR158 over-expression downregulates genes related to ECM deposition. Validation by qPCR showed that with low Dox, expression of ECM-associated genes TGFB2, COL1A1 and FN is downregulated (p>0.05), while SMAD3 is upregulated (p>0.05). At high Dox, TGFB2 and COL1A1 are still downregulated (p= 0.0109 and 0.002 respectively), but expression of FN and SMAD3 is increased (p>0.05 and p=0.01 respectively). Somewhat different behaviors were observed at the protein level. At low Dox, TGFB2 protein is decreased, but with high Dox it is increased (p>0.05). FN protein is upregulated at all conditions (p=0.028). SMAD3 protein is only increased with high Dox, but activated phosphorylated p-SMAD3 is decreased (p>0.05, both). When GPR158 expression was knocked down, TGFB2 was downregulated (~55%, p=0.037), but COL1A1, FN and SMAD3 did not show any changes

Conclusions : GPR158 modulates expression of genes associated with extracellular matrix deposition. This suggests a possible mechanism by which changes in GPR158 expression levels could contribute to SIOH susceptibility.

This is a 2020 ARVO Annual Meeting abstract.

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