June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Characterization of Primary Open Angle Glaucomatous Sclera
Author Affiliations & Notes
  • Alex Huang
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • Karen Xuandao Duong-Polk
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • Christopher Heichel
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • Felipe Medeiros
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • James Lindsey
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • Robert Weinreb
    Ophthalmology, Shiley Eye Center, La Jolla, CA
  • Footnotes
    Commercial Relationships Alex Huang, None; Karen Xuandao Duong-Polk, None; Christopher Heichel, None; Felipe Medeiros, Carl-Zeiss (F), Heidelberg Engineering (F), Topcon (F), Alcon (F), Allergan (F), Sensimed (F), Reichert (F); James Lindsey, None; Robert Weinreb, Aerie (F), Alcon (C), Allergan (C), Altheos (C), Amakem (C), Bausch&Lomb (C), Carl Zeiss-Meditec (C), Genentech (F), Haag-Streit (F), Heidelberg Engineering (F), Konan (F), Lumenis (F), National Eye Institute (F), Nidek (F), Optovue (C), Quark (C), Solx (C), Topcon (C)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 785. doi:
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      Alex Huang, Karen Xuandao Duong-Polk, Christopher Heichel, Felipe Medeiros, James Lindsey, Robert Weinreb; Characterization of Primary Open Angle Glaucomatous Sclera. Invest. Ophthalmol. Vis. Sci. 2013;54(15):785.

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

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To study biochemical and cellular changes in primary open angle glaucomatous (POAG) sclera. TGF-β is a soluble protein known to be elevated in POAG and implicated in trabecular meshwork (TM) pathologic changes leading to increased aqueous humor outflow resistance and elevated intraocular pressure. As the TM is not entirely occluded in POAG, this soluble factor can still travel beyond the TM into the distal outflow pathway, including the intrascleral venous plexus, where it can mediate pathologic alterations such as myofibroblastic differentiation and elevated α-smooth muscle actin expression.


Scleral samples have been collected from an age-matched pair of 60 year-old glaucomatous and non-glaucomatous patients. Glaucomatous sclera was collected during canaloplasty surgery from a female with a five-year history of glaucoma with visual field defects and elevated intraocular pressures (20-40 mm Hg) despite multiple aqueous suppressants and a prostaglandin. Control sclera was collected from remnant corneo-scleral rim after corneal transplantation. Scleral samples were homogenized and myofibroblastic activation was evaluated by assessing α-smooth muscle actin expression. GAPDH levels served as protein loading controls.


Expression of α-smooth muscle actin expression was greater in glaucomatous sclera than in age-matched non-glaucomatous sclera.


Elevated α-smooth muscle actin levels in glaucomatous sclera are consistent with TGF-β mediated alterations and scleral myofibroblastic induction. These results support further evaluation of TGF-β mediated scleral changes and the relevance of myofibroblastic activation in glaucoma. Additional scleral samples from glaucomatous and control patients will be collected and evaluated. Primary culture fibroblasts will also be generated from normal and glaucomatous sclera and compared.

Keywords: 708 sclera • 519 extracellular matrix • 568 intraocular pressure  

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