2018
DOI: 10.1007/s12035-018-1047-3
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MiR-34a Regulates Axonal Growth of Dorsal Root Ganglia Neurons by Targeting FOXP2 and VAT1 in Postnatal and Adult Mouse

Abstract: Hyperglycemia impairs nerve fibers of dorsal root ganglia (DRG) neurons, leading to diabetic peripheral neuropathy (DPN). However, the molecular mechanisms underlying DPN are not fully understood. Using a mouse model of type II diabetes (db/db mouse), we found that microRNA-34a (miR-34a) was over-expressed in DRG, sciatic nerve, and foot pad tissues of db/db mice. In vitro, high glucose significantly upregulated miR-34a in postnatal and adult DRG neurons, which was associated with inhibition of axonal growth. … Show more

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Cited by 25 publications
(19 citation statements)
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“…miRs are enriched in the axon (8) and can locally regulate axonal protein levels, leading to changes of axonal function (9). In vitro studies have demonstrated that alteration of axonal miR levels by high glucose (HG) in axons of DRG neurons inhibits axonal growth through changes of miR target proteins (10,11). Accordingly, using in vitro and in vivo approaches, the present study tested the hypothesis that exosomes derived from hyperglycemic Schwann cells communicate with axons of DRG neurons to promote development of DPN via alteration of axonal miRs and their putative target proteins.…”
mentioning
confidence: 99%
“…miRs are enriched in the axon (8) and can locally regulate axonal protein levels, leading to changes of axonal function (9). In vitro studies have demonstrated that alteration of axonal miR levels by high glucose (HG) in axons of DRG neurons inhibits axonal growth through changes of miR target proteins (10,11). Accordingly, using in vitro and in vivo approaches, the present study tested the hypothesis that exosomes derived from hyperglycemic Schwann cells communicate with axons of DRG neurons to promote development of DPN via alteration of axonal miRs and their putative target proteins.…”
mentioning
confidence: 99%
“…In order to reverse the neuropathic deficits associated with DN, another strategy involves the activation of axonal regeneration, which has shown promising results in in vitro and in vivo DN models (78)(79)(80). PNS neurons are capable of long-distance axonal regeneration (81).…”
Section: Roles Of Mirnas In the Neurovascular Dysfunction Of Diabeticmentioning
confidence: 99%
“…′ UTR region of forkhead box protein P2 and vesicle amine transport 1, leading to a reduction in axonal growth (79). Hyperglycemia down-regulates miR-146a, which is involved in the reduction of axonal outgrowth and apoptosis of DRG neurons (78,82).…”
Section: Roles Of Mirnas In the Neurovascular Dysfunction Of Diabeticmentioning
confidence: 99%
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“…Moreover, epigenetic inactivation of miR-34a by aberrant expression levels can be found in 18% of NHLs (18). Bioinformatic target prediction combined with functional analyses has revealed that the oncogene C-MYC mRNA can be regulated by miR-34a (19), and acts via post-transcriptional control of the transcription factor forkhead box (Fox) protein family, especially Foxp1 which is a hematopoietic oncoprotein overexpressed in DLBCL (20,21). Therefore, the C-MYC/miR-34a pathway may be closely related to the occurrence and development of DLBCL.…”
Section: Mrna Expression Profile Analysis Reveals a C-myc/mir-34a Patmentioning
confidence: 99%