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Category:2012 albumsHypoxia upregulates C-peptide in pancreatic beta-cells by modulating the JAK/STAT3 pathway.
Hypoxia-induced diabetes and abnormal glucose metabolism are common in patients with end-stage renal disease. Hypoxia-inducible factor (HIF)-1alpha is a master regulator of cellular response to hypoxia. The aim of this study is to determine whether C-peptide, a marker of beta-cell function, is regulated by HIF-1alpha under hypoxia. beta-cell-specific HIF-1alpha transgenic mice were generated to examine the direct effect of HIF-1alpha on C-peptide expression. Studies of primary cultured islets revealed that islet-specific overexpression of HIF-1alpha increased mRNA and protein levels of C-peptide. In contrast, HIF-1alpha knockout islets exhibited reduced C-peptide expression. In addition, HIF-1alpha overexpression enhanced phosphorylation of STAT3 and activation of its target gene BCL2 under hypoxia, and the increase in C-peptide expression was abrogated by a pharmacological inhibitor of JAK/STAT3 signaling. Taken together, these results indicate that C-peptide expression is upregulated by HIF-1alpha under hypoxia through the JAK/STAT3 signaling pathway./**
* @fileoverview Detect file type from file extension
* @author NHN FE Development Lab
*/
'use strict';
let reader = require('../reader');
module.exports = class {
/**
* detectFileType
* @return {Promise}
*/
static detectFileType(filepath) {
return new Promise((resolve, reject) => {
reader.load(filepath, (err, module) => {
if (err) {
return reject(err);
}
if (module be359ba680
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