Increase in bfgf and cntf proteins in rat retina induced by mechanical injury

M. Peng, C. Liu, R. Wen

Research output: Contribution to journalArticlepeer-review


Purpose. It has been shown that mechanical injury to the retina upregulates mRNA expression of two neurotrohpic factors, bFGF and CNTF, in the retina. Here we report that bFGF and CNTF proteins was also increased in the retina after focal mechanical injury. Methods. Adult male Sprague-Dawley rats were anesthetized with halothan. Focal mechanical injury was produced by an incision (1 mm) through the sciera down to the subretinal space in each eye. Relinas were collected 0.5, 1, 2, 3, or 6 days after injury. Control animals received no injury. Western blot analysis was conducted to assess the protein levels of bFGF and CNTF in the retina. Results. Significant increase in both bFGF and CNTF proteins was observed after injury. The increase in bFGF protein was progressive throughout the 6-day period of the experiment starting at day 1 after injury. In the case of CNTF, the increase was also observed I day after injury, which reached a maximum by 2 days after injury, and then slightly decline from its peak by day 3 and day 6. The time courses of protein expression of bFGF and CNTF are quite different from the time courses of their mRNA expression after injury (Wen, et al, 1995, J. Neurosci. 15:7377-85). Conclusions. These results show that mechanical injury upregulates bFGF and CNTF proteins in the retina, thus more neurotrophic factors are available for photoreceptors and other retinal neurons. Since exogenous bFGF or CNTF protects photoreceptors from degeneration, our results support the hypothesis that endogenous neurotrophic factors are responsible for injury-induced photoreceptor rescue.

Original languageEnglish (US)
Pages (from-to)S604
JournalInvestigative Ophthalmology and Visual Science
Issue number4
StatePublished - 1997
Externally publishedYes

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


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