April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Intravitreal Administration Of Adult Stem/progenitor Cells And Their Secreted Proteins Delays Retinal Degeneration By Decreasing Apoptosis In Two Rat Models
Author Affiliations & Notes
  • Gavin W. Roddy
    Texas A&M Health Science Center College of Medicine Institute for Regenerative Medicine at Scott & White, Temple, Texas
  • Robert H. Rosa, Jr.
    Texas A&M Health Science Center College of Medicine Institute for Regenerative Medicine at Scott & White, Temple, Texas
  • Matthew M. LaVail
    Beckman Vision Center, UCSF School of Medicine, San Francisco, California
  • Michael T. Matthes
    Beckman Vision Center, UCSF School of Medicine, San Francisco, California
  • Douglas Yasumura
    Beckman Vision Center, UCSF School of Medicine, San Francisco, California
  • Joo Youn Oh
    Texas A&M Health Science Center College of Medicine Institute for Regenerative Medicine at Scott & White, Temple, Texas
  • Darwin J. Prockop
    Texas A&M Health Science Center College of Medicine Institute for Regenerative Medicine at Scott & White, Temple, Texas
  • Footnotes
    Commercial Relationships  Gavin W. Roddy, None; Robert H. Rosa, Jr., None; Matthew M. LaVail, None; Michael T. Matthes, None; Douglas Yasumura, None; Joo Youn Oh, None; Darwin J. Prockop, None
  • Footnotes
    Support  Scott & White Research Grants Program (RHR, DJP), Foundation Fighting Blindness (ML), NIH grants EY001919 (ML), EY006842 (ML), EY016143 (RHR)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2218. doi:
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      Gavin W. Roddy, Robert H. Rosa, Jr., Matthew M. LaVail, Michael T. Matthes, Douglas Yasumura, Joo Youn Oh, Darwin J. Prockop; Intravitreal Administration Of Adult Stem/progenitor Cells And Their Secreted Proteins Delays Retinal Degeneration By Decreasing Apoptosis In Two Rat Models. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2218.

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

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Abstract

Purpose: : Therapeutic benefits have been observed with administration of adult stem/progenitor cells from bone marrow (mesenchymal stem cells, or MSCs). MSCs may engraft and differentiate to replace injured tissues; however, the cells more frequently produce improvements by expressing therapeutic factors, such as the anti-apoptotic protein stanniocalcin-1 (STC-1). Previous reports indicated that subretinal administration of MSCs delayed photoreceptor degeneration in vivo. We tested the hypothesis that intravitreal injection of MSCs or STC-1 may delay retinal degeneration by decreasing apoptosis.

Methods: : In preliminary experiments, cultures of retinal pigment epithelial cells (ARPE-19) were injured with hydrogen peroxide and treated with MSCs or STC-1. Viability was detected using MTT, and apoptosis was detected by measuring caspase activity and annexin V/PI uptake. Also, we administered STC-1 or MSCs via intravitreal injection in two models of retinal degeneration: the Royal College of Surgeons (RCS) rat and the S334ter-3 rhodopsin transgenic rat. Photoreceptor rescue was assessed by measurement of outer nuclear layer (ONL) thickness and quantitative gene expression assays for markers of photoreceptors and apoptosis.

Results: : The in vitro studies demonstrated that MSCs and STC-1 reduced apoptosis of ARPE-19. In the RCS rat model, injection of MSCs or STC-1 blunted the decrease in photoreceptor gene expression and reduced markers of apoptosis. In the S334ter-3 rats, injections of STC-1 reduced the decline in ONL thickness.

Conclusions: : STC-1 was effective in decreasing apoptosis induced by oxidative damage to ARPE-19. In addition, intravitreal administration of STC-1 rescued photoreceptors in two different rodent models of retinal degeneration, apparently by decreasing apoptosis. The results raise the possibility that intravitreal administration of either MSCs or STC-1 may be an effective and less invasive therapy for retinal degeneration than subretinal injection of MSCs or other stem/progenitor cells.

Keywords: retina • retinal degenerations: cell biology • neuroprotection 
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