March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
PTX3 Controls Activation of Matrix Metalloproteinase 1 and Apoptosis in Conjunctivochalasis Fibroblasts
Author Affiliations & Notes
  • Su-Zhen Zhang
    Ocular Surface Rsch Education Fndn, Miami, Florida
  • Ping Guo
    Ocular Surface Rsch Education Fndn, Miami, Florida
  • Hua He
    TissueTech, Inc., Miami, Florida
  • Ying-Ting Zhu
    TissueTech, Inc., Miami, Florida
  • Scheffer C. G. Tseng
    Ocular Surface Rsch Education Fndn, Miami, Florida
    TissueTech, Inc., Miami, Florida
  • Footnotes
    Commercial Relationships  Su-Zhen Zhang, None; Ping Guo, None; Hua He, Tissue Tech, Inc (E); Ying-Ting Zhu, Tissue Tech, Inc (E); Scheffer C. G. Tseng, Tissue Tech, Inc (I, P)
  • Footnotes
    Support  NIH, NEI, EY017497 and EY021045
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 4004. doi:
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      Su-Zhen Zhang, Ping Guo, Hua He, Ying-Ting Zhu, Scheffer C. G. Tseng; PTX3 Controls Activation of Matrix Metalloproteinase 1 and Apoptosis in Conjunctivochalasis Fibroblasts. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4004.

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

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Purpose: : Higher levels of MMP-1 and MMP-3 have been found in fibroblasts of conjunctivochalasis (CCh), which is an age-related inflammatory ocular surface disease manifesting redundant, loose conjunctiva folds. We would like to investigate whether the acute-phase protein PTX3, crucial for innate immunity and tissue inflammation, might play a pathogenic role in controlling upregulation of MMP-1 and MMP-3 in CCh.

Methods: : Immunostaining of PTX3 was carried out and compared between normal and CCh specimens containing the conjunctiva and the Tenon. Second to third passages of normal and CCh fibroblasts were treated with or without Aprotinin, Batimastat, or NNGH, followed by transfection with or without PTX3 siRNA, and stimulation with TNF-α or IL-1β. Cell lysates and culture media were collected to assess apoptosis measured by the Cell Death Detection ELISA and expression of PTX3, MMP-1 and MMP-3 transcripts and proteins by qRT-PCR and Western blot, respectively.

Results: : PTX3 immmunostaining was negative in normal specimens, but strongly positive in the subconjunctival stroma of CCh specimens. Expression of PTX3 transcript and protein was not constitutive in resting normal fibroblasts, but was upregulated in resting CCh fibroblasts and more by TNF-α or IL-1β in cell lysates and culture media of both fibroblasts. PTX3 siRNA further upregulated MMP-1 transcript more than MMP-3 transcript in resting normal and CCh fibroblasts, but synergistically with IL-1β upregulated the expression of actMMP-1 only in cell lysates and culture media of CCh fibroblasts. PTX3 siRNA knockdown also induced more cell death characterized by apoptosis and necrosis, and such cell death could be rescued by inhibitors against serinne proteinase, MMP1, or MMP3.

Conclusions: : Perturbation of PTX3 expression might partake in pathogenesis of CCh by upregulating transcription and translation of MMP-1 and MMP-3, and activation of MMP-1.

Keywords: conjunctiva • apoptosis/cell death • inflammation 

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