title: miR-194 Promotes burn-induced hyperglycemia via attenuating IGF-IR expression.
abstract: Hyperglycemia is one of the most important clinical features of burn patients. Previous reports had demonstrated that miRNA was involved in regulating glucose metabolism in various diseases such as diabetes and obesity. Our current study discovered the relationship between miR-194 and hyperglycemia in burn rats via suppressing insulin-like growth factor 1 receptor (IGF-IR). We found that the fasting blood glucose was significantly increased in rats of the burn group, and protein expression of IGF-IR was attenuated in response to burn injury. Similar to the results of animal experiments, miR-194 expression was significantly elevated and IGF-IR protein level was suppressed in L6 cells treated with serum from burn rats compared with those treated by serum from sham rats. However, IGF-IR mRNA level was comparable between burn and sham rats, suggesting that IGF-IR may be downregulated at the translation level. Further experiments revealed that miR-194 was significantly increased in burn rats compared with sham rats using miRNA array and real-time polymerase chain reaction (PCR) assay. And IGF-IR protein expression was reduced in L6 cells transfected with miR-194 plasmid. Insulin-like growth factor 1 receptor expression was also repressed and fasting blood glucose was increased in rats injected with miR-194 plasmid. In general, we have identified a novel function of miR-194 in modulating burn-induced hyperglycemia via suppressing the expression of IGF-IR.
authors.affiliation: Department of Burn and Plastic Surgery, The First Affiliated Hospital to PLA General Hospital, Beijing, China.
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Yu
authors.forename: Jiake
authors.initials: J
authors.lastname: Chai
authors.forename: Haijun
authors.initials: H
authors.lastname: Zhang
authors.forename: Wanli
authors.initials: W
authors.lastname: Chu
authors.forename: Lingying
authors.initials: L
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Ma
authors.forename: Hongjie
authors.initials: H
authors.lastname: Duan
authors.forename: Bailing
authors.initials: B
authors.lastname: Li
authors.forename: Dawei
authors.initials: D
authors.lastname: Li
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000737:chemistry; D002056:Burns / Q000150:complications* / Q000378:metabolism; D005786:Gene Expression Regulation; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism*; D008297:Male; D035683:MicroRNAs / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism; D010957:Plasmids / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017526:Receptor, IGF Type 1 / Q000378:metabolism*; D013977:Tibia / Q000473:pathology; D014162:Transfection
chemical_list: D001786:Blood Glucose; C551975:MIRN194 microRNA, rat; D035683:MicroRNAs; D012333:RNA, Messenger; D017526:Receptor, IGF Type 1