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Lgi4 promotes the proliferation and differentiation of glial lineage cells throughout the developing peripheral nervous system.
The mechanisms that regulate peripheral nervous system (PNS) gliogenesis are incompletely understood. For example, gut neural crest stem cells (NCSCs) do not respond to known gliogenic factors, suggesting that yet-unidentified factors regulate gut gliogenesis. To identify new mechanisms, we performed gene expression profiling to identify factors secreted by gut NCSCs during the gliogenic phase of development. These cells highly expressed leucine-rich glioma inactivated 4 (Lgi4) despite the fact that Lgi4 has never been implicated in stem cell function or enteric nervous system development. Lgi4 is known to regulate peripheral nerve myelination (having been identified as the mutated gene in spontaneously arising claw paw mutant mice), but Lgi4 is not known to play any role in PNS development outside of peripheral nerves. To systematically analyze Lgi4 function, we generated gene-targeted mice. Lgi4-deficient mice exhibited a more severe phenotype than claw paw mice and had gliogenic defects in sensory, sympathetic, and enteric ganglia. We found that Lgi4 is required for the proliferation and differentiation of glial-restricted progenitors throughout the PNS. Analysis of compound-mutant mice revealed that the mechanism by which Lgi4 promotes enteric gliogenesis involves binding the ADAM22 receptor. Our results identify a new mechanism regulating enteric gliogenesis as well as novel functions for Lgi4 regulating the proliferation and maturation of glial lineage cells throughout the PNS.
Document Type:

Reference

Product Catalog Number:

Multiple
Product Catalog Name:

Multiple
Angiotensin Receptor Mediated Oxidative Stress Is Associated with Impaired Cardiac Redox Signaling and Mitochondrial Function in Insulin Resistant Rats.
Activation of angiotensin receptor type 1 (AT1) contributes to NADPH oxidase (Nox)-derived oxidative stress during metabolic syndrome. However, AT1 activation in modulating redox signaling, mitochondrial function and oxidative stress in the heart during metabolic syndrome remains more elusive. To test the hypothesis that AT1 activation increases oxidative stress while impairing redox signaling and mitochondrial function in the heart during insulin resistant conditions, diet-induced obese insulin resistant (OLETF) rats (n=8/group) were treated with the AT1 blocker (ARB) Olmesartan for 6 weeks. Cardiac Nox2 protein expression increased 40% in OLETF compared to age-matched LETO rats while mRNA and protein expression of the H2O2-producing, Nox4, increased 40-100%. ARB treatment prevented the increase in Nox2 without altering Nox4. ARB treatment also normalized increased levels of protein and lipid oxidation (nitrotyrosine, 4-hydroxynonenal) and increased the redox-sensitive transcription factor, Nrf2, by 30%, and antioxidant enzymes (SOD, catalase, GPx) by 50-70%. Citrate synthase (CS) and succinate dehydrogenase (SDH) activities decreased 60-70% while cardiac succinate levels decreased 35% in OLETF compared to LETO suggesting that mitochondrial function in the heart is impaired during insulin resistance. ARB treatment normalized CS, SDH and succinate levels while increasing AMPK phosphorylation and normalizing AKT phosphorylation suggesting that AT1 activation impairs cellular metabolism in the diabetic heart. These data suggest that the cardiovascular complications associated with metabolic syndrome may be the consequence of oxidants produced as a consequence of AT1-mediated Nox2 activation that is associated with impaired redox signaling and mitochondrial activity, resulting in dysregulation of cellular metabolism in the heart. -
Document Type:

Reference

Product Catalog Number:

07-024
Product Catalog Name:

Anti-gp91-phox Antibody
Induction of ketosis in rats fed low-carbohydrate, high fat diets depends on the relative abundance of dietary fat and protein.
Low-carbohydrate/high-fat diets (LC-HFDs) in rodent models have been implicated with both weight loss and as therapeutic approach to treat neurological diseases. LC-HFDs are known to induce ketosis, however, systematic studies analyzing the impact of the macronutrient composition on ketosis induction and weight loss success are lacking. Methods: Male Wistar rats were pair-fed either a standard chow diet or one of 3 different LC-HFDs for 4 weeks, which only differed in the relative abundance of fat and protein (percentages of fat/protein in dry matter: LC-75/10; LC-65/20; LC-55/30). We subsequently measured body composition by NMR, analyzed blood chemistry and urine acetone content, evaluated gene expression changes of key ketogenic and gluconeogenic genes, and measured energy expenditure (EE) and locomotor activity (LA) during the first 4 days and after 3 weeks on the respective diets. Results: Compared to chow, rats fed with LC-75/10, LC-65/20 and LC-55/30 gained significantly less bodyweight. Reductions in body weight were mainly due to lower lean body mass and paralleled by significantly increased fat mass. Levels of β-hydroxybutyate were significantly elevated feeding LC-75/10 and LC-65/20 but decreased in parallel to reductions in dietary fat. Acetone was about 16-fold higher with LC-75/10, only (p<0.001). In contrast, rats fed with LC-55/30 were not ketotic. Serum FGF-21, hepatic mRNA expression of hydroxymethylglutaryl-CoA-lyase, PGC-1α and PGC-1β were increased with LC-75/10, only. Expression of PCK1 and glucose-6-phosphatase was down-regulated by 50-70% in LC-HF groups. Furthermore, EE and LA were significantly decreased in all groups fed with LC-HFDs after 3 weeks on the diets. Summary: In rats, the absence of dietary carbohydrates per se does not induce ketosis. LC-HFDs must be high in fat, but also low in protein contents to be clearly ketogenic. Independent of the macronutrient composition, LC-HFD-induced weight loss is not due to increased EE and LA.
Document Type:

Reference

Product Catalog Number:

EZRMFGF21-26K
Product Catalog Name:

Rat / Mouse FGF-21 ELISA Kit