Downregulation of STAT3 activation is required for presumptive rod photoreceptor cells to differentiate in the postnatal retina

Yoko Ozawa, Keiko Nakao, Takuya Shimazaki, Junji Takeda, Shizuo Akira, Katsuhiko Ishihara, Toshio Hirano, Yoshihisa Oguchi, Hideyuki Okano

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Ciliary neurotrophic factor (CNTF) has been known to inhibit the differentiation of presumptive rod photoreceptor cells; however, the underlying mechanisms have remained to be elucidated. We demonstrated that STAT3 activation, but not SHP2 activation, is responsible for the CNTF/gp130 signaling that inhibits expression of Rhodopsin and its upstream activator, crx, in the retinal explants derived from P0 mice (P0 retinal explants), utilizing STAT3-deficient retina and electroporation of dominant-negative form of STAT3 (STAT3F). We also demonstrated that STAT3 activation in presumptive rod photoreceptor cells at E18.5 is rapidly downregulated at P0, when Rhodopsin expression starts during retinal development. Persistent STAT3 activation in the P0 retinal explants prevented Rhodopsin expression and rapid upregulation of crx expression. STAT3-deficient retinas did not exhibit precocious rod photoreceptor cell differentiation as a whole, although they occasionally exhibited precocious upregulation of crx mRNA. Thus, we conclude that downregulation of STAT3 activation is required, but insufficient, for rod photoreceptor cell differentiation in the postnatal retina.

Original languageEnglish
Pages (from-to)258-270
Number of pages13
JournalMolecular and Cellular Neuroscience
Volume26
Issue number2
DOIs
Publication statusPublished - 2004 Jun 1

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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