Anti-REG3G polyclonal antibody

Introduction: The Reg genes play a major role in the regeneration of various tissues; however, no reports have been published regarding expression of the Reg3G gene in skeletal muscle. In this study we investigated the expression of the Reg3G gene in regeneration of rat skeletal muscle and injured nerves. Methods: We used 3 experimental models of muscle and nerve injury. RT-PCR and Western blot analysis were performed for detection of Reg3G in regenerating muscle and nerve. Results: We found transcriptional activation of the Reg3G gene in the soleus and extensor digitorum longus muscles and in their corresponding nerves after both muscle and nerve injury in different time periods, respectively. Conclusions: The results suggest that the Reg3G gene plays a major role in communication between injured axons and muscle and may play a significant role in skeletal muscle and peripheral nerve regeneration. Muscle Nerve49: 61-68, 2014

Nonalcoholic fatty liver disease (NAFLD) and obesity are characterized by altered gut microbiota, inflammation, and gut barrier dysfunction. Here, we investigated the role of mucin-2 (Muc2) as the major component of the intestinal mucus layer in the development of fatty liver disease and obesity. We studied experimental fatty liver disease and obesity induced by feeding wild-type and Muc2-knockout mice a high-fat diet (HFD) for 16 wk. Muc2 deficiency protected mice from HFD-induced fatty liver disease and obesity. Compared with wildtype mice, after a 16-wk HFD, Muc2-knockout mice exhibited better glucose homeostasis, reduced inflammation, and upregulated expression of genes involved in lipolysis and fatty acid beta-oxidation in white adipose tissue. Compared with wild-type mice that were fed the HFD as well, Muc2-knockout mice also displayed higher intestinal and plasma levels of IL-22 and higher intestinal levels of the IL-22 target genes Reg3b and Reg3g. Our findings indicate that absence of the intestinal mucus layer activates the mucosal immune system. Higher IL-22 levels protect mice from diet-induced features of the metabolic syndrome.