April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
β3 Integrin Signaling Is Involved In Dexamethasone-induced Cross-linked Actin Network (CLAN) Formation In Human Trabecular Meshwork (HTM) Cells
Author Affiliations & Notes
  • M. Filla
    Ophthalmology & Visual Sciences,
    Pathology & Lab. Medicine,
    U. Wisconsin-Madison, Madison, Wisconsin
  • M. Schwinn
    Pathology & Lab. Medicine,
    U. Wisconsin-Madison, Madison, Wisconsin
  • A. Nosie
    Pathology & Lab. Medicine,
    U. Wisconsin-Madison, Madison, Wisconsin
  • R. Clark
    Pathology & Lab. Medicine,
    U. Wisconsin-Madison, Madison, Wisconsin
  • D. Peters
    Ophthalmology & Visual Sciences,
    Pathology & Lab. Medicine,
    U. Wisconsin-Madison, Madison, Wisconsin
  • Footnotes
    Commercial Relationships  M. Filla, Wisconsin Alumni Research Foundation (P); M. Schwinn, None; A. Nosie, None; R. Clark, None; D. Peters, Wisconsin Alumni Research Foundation (P)
  • Footnotes
    Support  NIHI grants EY017006, EY0020490 (D.M.P.); EY018274 (M.K.S.); P30 EY016665 (Core grant to the Dept. of Ophthalmology and Visual Sciences)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4656. doi:
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    • Get Citation

      M. Filla, M. Schwinn, A. Nosie, R. Clark, D. Peters; β3 Integrin Signaling Is Involved In Dexamethasone-induced Cross-linked Actin Network (CLAN) Formation In Human Trabecular Meshwork (HTM) Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4656.

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

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Abstract

Purpose: : To determine if cross-linked actin networks (CLANs) induced by dexamethasone (DEX) in human trabecular meshwork (HTM) cells are structurally similar to those formed following β3 integrin activation and involve αvβ3 integrin signaling.

Methods: : Two HTM cell strains and the immortalized TM-1 cell line overexpressing αvβ3 integrin were used. DEX- or ethanol-pre-treated HTM cells were treated with cycloheximide to block de novo protein synthesis prior to being re-plated on fibronectin with or without β3 integrin-activating mAb AP-5. Fluorescence microscopy was used to identify phalloidin-labeled CLANs and to ascertain the presence of α-actinin, PIP2 and syndecan-4 within them. β3 integrin signaling involvement was determined using a PI3-kinase (LY294002) or Rac1/Trio (NSC23766) inhibitor. αvβ3 integrin expression levels and the β3 integrin activation state were determined by FACS analysis and fluorescence microscopy.

Results: : CLANs induced by either DEX or activating β3 integrin contained syndecan-4, PIP2, and α-actinin. PI3-kinase inhibition did not affect DEX-induced CLAN formation while Rac1/Trio inhibition decreased the percentage of CLAN-positive cells by 80%. In contrast, inhibition of PI3-kinase or Rac1/Trio decreased β3 integrin-induced CLAN formation in the presence of DEX. DEX pre-treatment increased β3 integrin-induced CLAN formation ~ 6-fold and the level of αvβ3 integrin expression and activation 3-fold relative to control cells. Focal adhesions containing activated β3 integrin also increased ~ 5-fold in DEX-treated cells. Finally, the overexpression of αvβ3 integrin in TM-1 cells increased CLAN formation 2-fold.

Conclusions: : DEX-induced CLAN formation in HTM cells involved αvβ3 integrin activation and the Rac1/Trio signaling pathway previously shown to be associated with αvβ3-induced CLAN formation. Together these data suggest that steroid-induced CLAN formation may involve enhanced β3 integrin signaling in HTM cells possibly via an inside-out signaling mechanism. However, we can not exclude a role for β1 integrin signaling.

Keywords: trabecular meshwork • cytoskeleton • corticosteroids 
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