Retinal regeneration in adult zebrafish requires regulation of TGF signaling

被引：88

作者：

Lenkowski, Jenny R. ^{[1
]}

Qin, Zhao ^{[2
]}

Sifuentes, Christopher J. ^{[1
]}

Thummel, Ryan ^{[3
,4
]}

Soto, Celina M. ^{[1
]}

Moens, Cecilia B. ^{[5
]}

Raymond, Pamela A. ^{[1
]}

机构：

[1] Univ Michigan, Ann Arbor, MI 48109 USA

[2] NYU, Sch Med, Dev Genet Program, Skirball Inst Biomol Med, New York, NY USA

[3] Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA

[4] Wayne State Univ, Sch Med, Dept Ophthalmol, Detroit, MI USA

[5] Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98104 USA

来源：

GLIA | 2013年 / 61卷 / 10期

关键词：

Muller glia; photoreceptor; tgif1; six3b; stem cell; MULLER GLIA DEDIFFERENTIATION; CELL-PROLIFERATION; STEM-CELLS; TGIF; BETA; GENES; SIX3; PROGENITORS; SUFFICIENT; EXPRESSION;

D O I：

10.1002/glia.22549

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Muller glia are the resident radial glia in the vertebrate retina. The response of mammalian Muller glia to retinal damage often results in a glial scar and no functional replacement of lost neurons. Adult zebrafish Muller glia, in contrast, are considered tissue-specific stem cells that can self-renew and generate neurogenic progenitors to regenerate all retinal neurons after damage. Here, we demonstrate that regulation of TGF signaling by the corepressors Tgif1 and Six3b is critical for the proliferative response to photoreceptor destruction in the adult zebrafish retina. When function of these corepressors is disrupted, Muller glia and their progeny proliferate less, leading to a significant reduction in photoreceptor regeneration. Tgif1 expression and regulation of TGF signaling are implicated in the function of several types of stem cells, but this is the first demonstration that this regulatory network is necessary for regeneration of neurons. GLIA 2013;61:1687-1697

引用

页码：1687 / 1697

页数：11

共 58 条

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