Purpose:Oncostatin M(OSM) is a cytokine released by macrophages and lymphocytesthat can function as a growth regulator. A current study shows that leukemia inhibitoryfactor (LIF), a homologue of OSM, can prevent photo...Purpose:Oncostatin M(OSM) is a cytokine released by macrophages and lymphocytesthat can function as a growth regulator. A current study shows that leukemia inhibitoryfactor (LIF), a homologue of OSM, can prevent photoreceptor cell death when expressedin the lens of transgenic mice. We determined the efforts of lens-specific overexpressionof OSM on the development of eye.Methods: A truncated mouse OSM cDNA ( ～ 660 bp) was linked to the αA-crytallinpromoter, and injected into single-cell embryos with microinjection. Then, transgenic micewere established. The mRNA expression of transgene OSM was detected by in situhybridization. Immunohistochemistry was used to detect the expression of syntaxin, glialfibrillary acidic protein (GFAP), synaptophysin in the retinas of transgenic mice.Results: At embryonic day (E 17.5), the expression of the syntaxin at the inner and midportion of the retinas of transgenic mice was much higher than that of the retinas ofnon-transgenic mice. The expression of GFAP was detected in the retinas of transgenicmice, while no expression in non-transgenic normal FVB(FVB/N) mice was detected inthis stage. At postnatal day one (P1), the expression of synaptophysin was detected inthe retinas of transgenic mice, but there was no such expression in FVB/N mice.Conclusions: Lens-specific overexpression of OSM induces premature differentiation ofamacrine cells, gial cells, and photoreceptors in vivo.展开更多
文摘Purpose:Oncostatin M(OSM) is a cytokine released by macrophages and lymphocytesthat can function as a growth regulator. A current study shows that leukemia inhibitoryfactor (LIF), a homologue of OSM, can prevent photoreceptor cell death when expressedin the lens of transgenic mice. We determined the efforts of lens-specific overexpressionof OSM on the development of eye.Methods: A truncated mouse OSM cDNA ( ～ 660 bp) was linked to the αA-crytallinpromoter, and injected into single-cell embryos with microinjection. Then, transgenic micewere established. The mRNA expression of transgene OSM was detected by in situhybridization. Immunohistochemistry was used to detect the expression of syntaxin, glialfibrillary acidic protein (GFAP), synaptophysin in the retinas of transgenic mice.Results: At embryonic day (E 17.5), the expression of the syntaxin at the inner and midportion of the retinas of transgenic mice was much higher than that of the retinas ofnon-transgenic mice. The expression of GFAP was detected in the retinas of transgenicmice, while no expression in non-transgenic normal FVB(FVB/N) mice was detected inthis stage. At postnatal day one (P1), the expression of synaptophysin was detected inthe retinas of transgenic mice, but there was no such expression in FVB/N mice.Conclusions: Lens-specific overexpression of OSM induces premature differentiation ofamacrine cells, gial cells, and photoreceptors in vivo.
