炎症・再生
Online ISSN : 1880-5795
Print ISSN : 1346-8022
ISSN-L : 1346-8022
Mini Review
視細胞の分化調節機構—活性化STAT3による負の制御—
小澤 洋子中尾 啓子島崎 琢也岡野 栄之
著者情報
ジャーナル フリー

2005 年 25 巻 2 号 p. 118-122

詳細
抄録
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 Rhodopsin expression, although they 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.
著者関連情報
© 2005 日本炎症・再生医学会
前の記事 次の記事
feedback
Top