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NeuroD induces photoreceptor cell overproduction in vivo and de novo generation in vitro.

ABSTRACT: The molecular mechanisms underlying the generation of the various types of cells in the vertebrate retina are largely unknown. We investigated the possibility that genes belonging to the basic helix-loop-helix (bHLH) family of transcriptional factors participate in cell-type specification during retinal neurogenesis. Chick neuroD was isolated from an embryonic cDNA library and its deduced amino acid sequence showed 75% identity with mouse neuroD. In situ hybridization showed that neuroD was expressed in cells located at the outer portion of the developing retinal neuroepithelium, the location where prospective photoreceptors reside. Misexpression of neuroD in retinal neuroepithelium through replication-competent, transformation-deficient retroviruses produced a retina with three, instead of two, layers of photoreceptor cells; the number of cells that express visinin, a marker for cone photoreceptors, increased over 50% compared to control embryos misexpressing the green fluorescent protein. No significant changes were observed in the number of other retinal neurons, including those that express RA4 (ganglion cells), pax6 (ganglion cells and amacrine cells), and chx10 (bipolar cells). Retroviral-driven misexpression of neuroD in monolayer cultures of retinal pigment epithelium yielded de novo production of photoreceptor cells with no other types of retinal neurons detected. We propose that neuroD is important for photoreceptor cell production in the vertebrate retina.

SUBMITTER: Yan RT

PROVIDER: S-EPMC1764458 | biostudies-literature | 1998 Sep

REPOSITORIES: biostudies-literature

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neuroD induces photoreceptor cell overproduction in vivo and de novo generation in vitro.

Yan R T RT Wang S Z SZ

Journal of neurobiology 19980901 4

The molecular mechanisms underlying the generation of the various types of cells in the vertebrate retina are largely unknown. We investigated the possibility that genes belonging to the basic helix-loop-helix (bHLH) family of transcriptional factors participate in cell-type specification during retinal neurogenesis. Chick neuroD was isolated from an embryonic cDNA library and its deduced amino acid sequence showed 75% identity with mouse neuroD. In situ hybridization showed that neuroD was expr ...[more]

PMID: 9740021

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Project description:Background/objectivesFasting dyslipidemia is commonly observed in insulin resistant states and mechanistically linked to hepatic overproduction of very low density lipoprotein (VLDL). Recently, the incretin hormone glucagon-like peptide-1 (GLP-1) has been implicated in ameliorating dyslipidemia associated with insulin resistance and reducing hepatic lipid stores. Given that hepatic VLDL production is a key determinant of circulating lipid levels, we investigated the role of both peripheral and central GLP-1 receptor (GLP-1R) agonism in regulation of VLDL production.MethodsThe fructose-fed Syrian golden hamster was employed as a model of diet-induced insulin resistance and VLDL overproduction. Hamsters were treated with the GLP-1R agonist exendin-4 by intraperitoneal (ip) injection for peripheral studies or by intracerebroventricular (ICV) administration into the 3rd ventricle for central studies. Peripheral studies were repeated in vagotomised hamsters.ResultsShort term (7-10 day) peripheral exendin-4 enhanced satiety and also prevented fructose-induced fasting dyslipidemia and hyperinsulinemia. These changes were accompanied by decreased fasting plasma glucose levels, reduced hepatic lipid content and decreased levels of VLDL-TG and -apoB100 in plasma. The observed changes in fasting dyslipidemia could be partially explained by reduced respiratory exchange ratio (RER) thereby indicating a switch in energy utilization from carbohydrate to lipid. Additionally, exendin-4 reduced mRNA markers associated with hepatic de novo lipogenesis and inflammation. Despite these observations, GLP-1R activity could not be detected in primary hamster hepatocytes, thus leading to the investigation of a potential brain-liver axis functioning to regulate lipid metabolism. Short term (4 day) central administration of exendin-4 decreased body weight and food consumption and further prevented fructose-induced hypertriglyceridemia. Additionally, the peripheral lipid-lowering effects of exendin-4 were negated in vagotomised hamsters implicating the involvement of parasympathetic signaling.ConclusionExendin-4 prevents fructose-induced dyslipidemia and hepatic VLDL overproduction in insulin resistance through an indirect mechanism involving altered energy utilization, decreased hepatic lipid synthesis and also requires an intact parasympathetic signaling pathway.

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NeuroD induces photoreceptor cell overproduction in vivo and de novo generation in vitro.

Publications

neuroD induces photoreceptor cell overproduction in vivo and de novo generation in vitro.

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