RGD Reference Report - microRNA-9 and -29a regulate the progression of diabetic peripheral neuropathy via ISL1-mediated sonic hedgehog signaling pathway. - Rat Genome Database

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microRNA-9 and -29a regulate the progression of diabetic peripheral neuropathy via ISL1-mediated sonic hedgehog signaling pathway.

Authors: Sun, Qin  Zeng, Jun  Liu, Yang  Chen, JingYan  Zeng, Qing-Cui  Chen, Yan-Qiu  Tu, Li-Li  Chen, Ping  Yang, Fan  Zhang, Min 
Citation: Sun Q, etal., Aging (Albany NY). 2020 Jun 16;12(12):11446-11465. doi: 10.18632/aging.103230. Epub 2020 Jun 16.
RGD ID: 243065126
Pubmed: PMID:32544883   (View Abstract at PubMed)
PMCID: PMC7343507   (View Article at PubMed Central)
DOI: DOI:10.18632/aging.103230   (Journal Full-text)

In this study, we tested the hypothesis that overexpression of miR-9 and miR-29a may contribute to DPN development and progression. We performed a meta-analysis of miR expression profile studies in human diabetes mellitus (DM) and the data suggested that miR-9 and miR-29a were highly expressed in patients with DM, which was further verified in serum samples collected from 30 patients diagnosed as DM. Besides, ISL1 was confirmed to be a target gene of miR-9 and miR-29a. Lentivirus-mediated forced expression of insulin gene enhancer binding protein-1 (ISL1) activated the sonic hedgehog (SHH) signaling pathway, increased motor nerve conduction velocity and threshold of nociception, and modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage. However, lentivirus-mediated forced expression of miR-9 or miR-29a exacerbated DM and antagonized the beneficial effect of ISL1 on DPN. Collectively, this study revealed potential roles of miR-9 and miR-29a as contributors to DPN development through the SHH signaling pathway by binding to ISL1. Additionally, the results provided an experimental basis for the targeted intervention treatment of miR-9 and miR-29a.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR142Humandiabetes mellitus  IEP RNA:increased expression:blood:RGD 
MIR29AHumandiabetes mellitus exacerbatesISOMir29a (Rattus norvegicus)RNA:increased expression:sciatic nerve:RGD 
MIR29AHumandiabetes mellitus  IEP RNA:increased expression:blood:RGD 
MIR7-3Humandiabetes mellitus exacerbatesISOMir9 (Rattus norvegicus)RNA:increased expression:sciatic nerve:RGD 
Mir142Mousediabetes mellitus  ISOMIR142 (Homo sapiens)RNA:increased expression:blood:RGD 
Mir142Ratdiabetes mellitus  ISOMIR142 (Homo sapiens)RNA:increased expression:blood:RGD 
Mir29aMousediabetes mellitus exacerbatesISOMir29a (Rattus norvegicus)RNA:increased expression:sciatic nerve:RGD 
Mir29aRatdiabetes mellitus  ISOMIR29A (Homo sapiens)RNA:increased expression:blood:RGD 
Mir29aRatdiabetes mellitus exacerbatesIDA RNA:increased expression:sciatic nerve:RGD 
Mir29aMousediabetes mellitus  ISOMIR29A (Homo sapiens)RNA:increased expression:blood:RGD 
Mir7bMousediabetes mellitus exacerbatesISOMir9 (Rattus norvegicus)RNA:increased expression:sciatic nerve:RGD 
Mir9Ratdiabetes mellitus exacerbatesIDA RNA:increased expression:sciatic nerve:RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Mir29aRatnegative regulation of smoothened signaling pathway  IDA  RGD 
Mir9Ratnegative regulation of smoothened signaling pathway  IDA  RGD 
Isl1Ratpositive regulation of smoothened signaling pathway  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Isl1  (ISL LIM homeobox 1)
Mir142  (microRNA 142)
Mir29a  (microRNA 29a)
Mir9  (microRNA 9)

Genes (Mus musculus)
Mir142  (microRNA 142)
Mir29a  (microRNA 29a)
Mir7b  (microRNA 7b)

Genes (Homo sapiens)
MIR142  (microRNA 142)
MIR29A  (microRNA 29a)
MIR7-3  (microRNA 7-3)


Additional Information