May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Prenatal Malnourishment Accelerates Vascular Apoptosis in Rat Retinas
Author Affiliations & Notes
  • S. Roy
    Medicine, Boston University School of Medicine, Boston, Massachusetts
  • J. Tonkiss
    Medicine, Boston University School of Medicine, Boston, Massachusetts
  • S. Roy
    Medicine, Boston University School of Medicine, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  S. Roy, None; J. Tonkiss, None; S. Roy, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 3988. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      S. Roy, J. Tonkiss, S. Roy; Prenatal Malnourishment Accelerates Vascular Apoptosis in Rat Retinas. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3988.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : To determine whether prenatal malnourishment accelerates the development of retinal vascular cell loss, a characteristic lesion of diabetic retinopathy, in aged rats. In particular, the study addresses whether the effect of prenatal malnourishment may eventually lead to retinal vascular cell apoptosis and development of acellular capillaries and pericyte loss later in adult life.

Methods: : Female Long Evans rats were maintained on a low protein diet (6% casein) from 5 weeks prior to, and during their entire pregnancy such that the pups born to these rats were prenatally, protein-malnourished. Immediately after birth, these pups were cross-fostered to well-nourished rats, fed a regular 25% casein diet. After weaning, these rats were maintained on a regular laboratory chow diet until they were killed at 22 months of age. In parallel, three well-nourished groups were used as control, each consisting of pups born to rats fed a regular 25% casein diet 5 weeks prior to, and during pregnancy. These rats were also maintained on regular chow diet following weaning. Control rats were sacrificed at 12 months, 18 months, or 22 months of age. After death, eyes were enucleated, and retinal trypsin digests (RTDs) were prepared. To determine the number of cells undergoing apoptosis, TUNEL assays were performed on RTDs from all four groups: 12 month, 18 month, 22 month, and 22 month-prenatally-malnourished. To determine the number of pericyte loss and acellular capillaries, RTDs were counter-stained with Hematoxylin and PAS, images were photographed, and acellular capillaries and pericyte losses were scored.

Results: : The number of cells undergoing apoptosis was significantly increased in the 22 month-prenatally-malnourished rat retinas compared to those of the 22 month-control rats (177% of 22-month control). Furthermore, the 22 month-control retinas showed significantly increased apoptosis compared to those of the 18 month-control and 12 month-control rats (62% of 22-month control, 28% of 22 month-control, respectively), suggesting that aging could contribute to increased apoptosis. The number of acellular capillaries and pericyte loss was significantly increased in the 22 month prenatally-malnourished retinas compared to those of 22 month-control rats (14%, 38%, p<0.05, respectively).

Conclusions: : Our findings indicate that the effect of prenatal malnourishment is manifested in the retina later in adult life. Results suggest that prenatal malnourishment may accelerate the development of vascular lesions characteristic of diabetic retinopathy.

Keywords: apoptosis/cell death • aging 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×