June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
LOXL1-AS1 regulates extracellular matrix remodeling, mechanotransduction responses, and cellular morphology in human outflow cells.
Author Affiliations & Notes
  • Kristyn Hake
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Heather Schmitt
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • William Johnson
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Maria Gomez-Caraballo
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Kristin Perkumas
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Michael A Hauser
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Daniel W Stamer
    Ophthalmology, Duke University, Durham, North Carolina, United States
  • Footnotes
    Commercial Relationships   Kristyn Hake, None; Heather Schmitt, None; William Johnson, None; Maria Gomez-Caraballo, None; Kristin Perkumas, None; Michael Hauser, None; Daniel Stamer, None
  • Footnotes
    Support  R01EY030617, P30EYE005722, Research to Prevent Blindness Foundation, L.C. Industries, The Glaucoma Foundation, Fight for Sight
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 558. doi:
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      Kristyn Hake, Heather Schmitt, William Johnson, Maria Gomez-Caraballo, Kristin Perkumas, Michael A Hauser, Daniel W Stamer; LOXL1-AS1 regulates extracellular matrix remodeling, mechanotransduction responses, and cellular morphology in human outflow cells.. Invest. Ophthalmol. Vis. Sci. 2021;62(8):558.

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

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Abstract

Purpose : Pseudoexfoliation glaucoma (PEXG) is a form of open angle glaucoma that is characterized by outflow resistance dysregulation and elevated intraocular pressure (IOP). The LOXL1-AS1 gene codes for a long non-coding RNA, whereby polymorphisms decrease its expression and are associated with risk of PEXG. Since LOXL1-AS1 influences the transcription of many genes, we hypothesize that LOXL1-AS1 in outflow cells regulates the expression of gene-products known to participate in outflow resistance regulation, including extracellular matrix (ECM), cell adhesion and mechanotransduction signaling proteins.

Methods : Knockdown of LOXL1-AS1 expression was achieved in primary cultures of human trabecular meshwork (TM) and Schlemm’s canal (SC) cells using a targeted Ad-shRNA, or by introducing targeted siRNA into HLE-B3 cells. Knockdown efficiency of LOXL1-AS1 and ECM gene expression was assessed using qPCR. Western blots were used to monitor ECM and mechanotransduction protein expression after LOXL1-AS1 knockdown, comparing to scrambled controls. Lastly, morphological changes due to LOXL1-AS1 knockdown in HLE-B3, SC, and TM cells were evaluated by calculating semi-axis ratios using FIJI.

Results : Knockdown of LOXL1-AS1 in HLE-B3 cells significantly altered the expression of seven ECM proteins (p<0.05, n=3), but did not change phosphorylation status of candidate mechanotransduction proteins AKT, MAPK, FAK (p>0.05, n=3). Experiments in one TM cell strain show that knockdown of LOXL1-AS1 results in dysregulation of ECM target genes including, but not limited to, MMP2, MMP14, MMP28, and MYC. In SC cells, knockdown of LOXL1-AS1 led to significant expression changes in ECM target genes including neuronal adhesion protein, vascular adhesion protein, integrin alpha 2, and laminin gamma 1 (p<0.05, n=4). With LOXL1-AS1 knockdown, SC cells significantly increased the proportion of phosphorylated AKT (p=0.008, n=4), but no changes were observed with phosphorylation status of FAK or MAPK. Knockdown of LOXL1-AS1 resulted in a shortening of the major axis of SC cells (p=0.006, n=3).

Conclusions : LOXL1-AS1 regulates genes involved in ECM remodeling and mechanotransduction signaling in human ocular cells. These data indicate that LOXL1-AS1 has a regulatory role in outflow resistance homeostasis, and represents a potential target for PEXG therapies.

This is a 2021 ARVO Annual Meeting abstract.

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