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PubMed Central
Other literature type . 2020
Data sources: PubMed Central
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Journal of Translational Medicine
Article . 2020
Data sources: DOAJ
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microRNA-128 mediates CB1 expression and regulates NF-KB/p-JNK axis to influence the occurrence of diabetic bladder disease.

Authors: Xin Gou; Jing Wu; Mingqing Huang; Yuting Weng; Tongxin Yang; Tao Chen; Guiqing Li; +1 Authors

microRNA-128 mediates CB1 expression and regulates NF-KB/p-JNK axis to influence the occurrence of diabetic bladder disease.

Abstract

Diabetic bladder disease is common complications of diabetes, its symptoms are diverse, can be due to different stages. In this study we investigate the mechanism of miR-128 targeting CB1 expression to mediate the occurrence of diabetic bladder disease.Bioinformatics analysis predicts related regulatory factors of miR-128 in diabetic bladder disease. Models of diabetic bladder lesions were constructed in male SD rats by intraperitoneal injection of streptozotocin at 65 mg/kg body weight. The expression of miR-128 and CB1 mRNA in bladder tissues of each group was detected by RT-qPCR, and CB1, NF-KB, p-JNK and Bcl2 protein expression was detected by Western Blotting. We tested the function of the bladder by urodynamics, detected the pathological characteristics of the bladder tissue by HE staining, and verified the targeting relationship between miR-128 and CB1 through the prediction of the biological website, dual luciferase reporter gene assay and RIP.miR-128 was highly expressed in the bladder tissue of diabetic rats. Inhibition of miR-128 could improve the occurrence of diabetic bladder lesions in rats. miR-128 could target the inhibition of CB1 expression, and high expression of CB1 could antagonize miR-128 against diabetic bladder. In the diabetic bladder, miR-128 can regulate the expression of NF-KB and p-JNK through CB1 and affect the level of apoptosis. miR-128 regulates NF-KB/p-JNK through CB1, thus affecting the occurrence of diabetic bladder disease.The high expression of miR-128 can down-regulate the expression of CB1, promote the activation of NF-KB and p-JNK, increase the level of apoptosis and promote the occurrence of diabetic bladder disease.

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Keywords

Male, Research, Diabetes, R, NF-kappa B, Urinary Bladder Diseases, Apoptosis, P-JNK, CB1, Diabetes Mellitus, Experimental, Rats, Rats, Sprague-Dawley, MicroRNAs, Receptor, Cannabinoid, CB1, Medicine, Animals, NF-KB, microRNA-128, Bladder disease, Signal Transduction

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
2
Average
Average
Average
Green
gold