Abstract:
:Neuropathic pain represents one of the most common complications associated with diabetes mellitus (DM) that impacts quality of life. Accumulating studies have highlighted the involvement of miRNAs in DM. Thus, the current study aimed to investigate the roles of miR-155 in diabetic peripheral neuropathy (DPN). In vitro DPN models were established using rat Schwann cells (SCs) by treatment with 5.5 mM glucose. Gain- or loss-of-function studies were conducted to determine the effect of miR-155 on Nrf2, cellular function, reactive oxygen species and inflammation. Rat DNP models were established by streptozotocin injection and damage of sciatic nerve. Next, miR-155 antagomir or agomir was employed to investigate the effects associated with miR-155 on motor and sciatic nerve conduction velocity (MNCV, SNCV), angiogenesis and inflammatory response in vivo. Nrf2 was identified to be a target of miR-155 by dual-luciferase reporter gene assay. Silencing of miR-155 or restoration of Nrf2 promoted cell proliferation, inhibited apoptosis and alleviated inflammation in vitro. miR-155 antagomir-induced inhibition increased MNCV and SNCV, strengthened angiogenesis and alleviated inflammation in DPN rats. Additionally, the effects exerted by miR-155 were reversed when Nrf2 was restored both in vitro and in vivo. Taken together, the key findings of our study provide evidence indicating that miR-155 targeted and suppressed Nrf2 in DPN. miR-155 silencing was found to alleviate sciatic nerve injury in DPN, highlighting its potential as a therapeutic target for DPN.
journal_name
J Mol Endocrinoljournal_title
Journal of molecular endocrinologyauthors
Chen J,Li C,Liu W,Yan B,Hu X,Yang Fdoi
10.1530/JME-19-0067subject
Has Abstractpub_date
2019-10-01 00:00:00pages
227-238issue
3eissn
0952-5041issn
1479-6813pii
JME-19-0067.R1journal_volume
63pub_type
杂志文章abstract::Using the fluorescent indicators 2',7'-bis(2-carboxyethyl)-5'-(6')-carboxyfluorescein and Oxonol V to monitor intracellular pH (pHi) and cell membrane potential respectively, we have investigated the involvement of H(+)-dependent ATPase and H(+)-dependent K+ channels in the recovery of the rat thyroid cell strain FRTL...
journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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