Long Non-Coding RNA CASC2 Improves Diabetic Nephropathy by Inhibiting JNK Pathway

It's known that long non-coding RNA CASC2 overexpression inhibit the JNK pathway in some disease models, while JNK pathway activation exacerbates diabetic nephropathy. Therefore we speculate that long non-coding RNA CASC2 can improve diabetic nephropathy by inhibiting JNK pathway. Thus, our stu...

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Published inExperimental and clinical endocrinology & diabetes Vol. 127; no. 8; p. 533
Main Authors Yang, Huihui, Kan, Quan E, Su, Yong, Man, Hua
Format Journal Article
LanguageEnglish
Published Germany 01.09.2019
Subjects
Adolescent
Adult
Aged
Animals
Apoptosis
Cells, Cultured
Diabetic Nephropathies - metabolism
Diabetic Nephropathies - pathology
Female
Gene Expression Regulation
Humans
Male
Mice
Middle Aged
Mitogen-Activated Protein Kinase 8 - metabolism
Podocytes - metabolism
Podocytes - pathology
RNA, Long Noncoding - biosynthesis
Signal Transduction
Tumor Suppressor Proteins - biosynthesis
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Summary:It's known that long non-coding RNA CASC2 overexpression inhibit the JNK pathway in some disease models, while JNK pathway activation exacerbates diabetic nephropathy. Therefore we speculate that long non-coding RNA CASC2 can improve diabetic nephropathy by inhibiting JNK pathway. Thus, our study was carried out to investigate the involvement of CASC2 in diabetic nephropathy. We found that serum level of CASC2 was significantly lower in diabetic nephropathy patients than in normal people, and serum level of CASC2 showed no significant correlations with age, gender, alcohol consumption and smoking habits, but was correlated with course of disease. ROC curve analysis showed that serum level of CASC2 could be used to accurately predict diabetic nephropathy. Diabetes mellitus has many complications. This study also included a series of complications of diabetes, such as diabetic retinopathy, diabetic ketoacidosis, diabetic foot infections and diabetic cardiopathy, while serum level of CASC2 was specifically reduced in diabetic nephropathy. CASC2 expression level decreased, while JNK1 phosphorylation level increased in mouse podocyte cells treated with high glucose. CASC2 overexpression inhibited apoptosis of podocyte cells and reduced phosphorylation level of JNK1. We conclude that long non-coding RNA CASC2 may improve diabetic nephropathy by inhibiting JNK pathway.
ISSN:1439-3646
DOI:10.1055/a-0629-9958