RGD Reference Report - RNA-binding protein HuR suppresses senescence through Atg7 mediated autophagy activation in diabetic intervertebral disc degeneration. - Rat Genome Database

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RNA-binding protein HuR suppresses senescence through Atg7 mediated autophagy activation in diabetic intervertebral disc degeneration.

Authors: Shao, Zhenxuan  Ni, Libin  Hu, Sunli  Xu, Tianzhen  Meftah, Zaher  Yu, Zupo  Tian, Naifeng  Wu, Yaosen  Sun, Liaojun  Wu, Aimin  Pan, Zongyou  Chen, Linwei  Gao, Weiyang  Zhou, Yifei  Zhang, Xiaolei  Wang, Xiangyang 
Citation: Shao Z, etal., Cell Prolif. 2021 Feb;54(2):e12975. doi: 10.1111/cpr.12975. Epub 2020 Dec 28.
RGD ID: 407571673
Pubmed: PMID:33372336   (View Abstract at PubMed)
PMCID: PMC7848958   (View Article at PubMed Central)
DOI: DOI:10.1111/cpr.12975   (Journal Full-text)


OBJECTIVES: Diabetes is a risk factor for intervertebral disc degeneration (IVDD). Studies have demonstrated that diabetes may affect IVDD through transcriptional regulation; however, whether post-transcriptional regulation is involved in diabetic IVDD (DB-IVDD) is still unknown. This study was performed to illustrate the role of HuR, an RNA-binding protein, in DB-IVDD development and its mechanism.
MATERIALS AND METHODS: The expression of HuR was evaluated in nucleus pulposus (NP) tissues from diabetic IVDD patients and in high glucose-treated NP cells. Senescence and autophagy were assessed in HuR over-expressing and downregulation NP cells. The mRNAs that were regulated by HuR were screened, and immunoprecipitation was applied to confirm the regulation of HuR on targeted mRNAs.
RESULTS: The results showed that the expression of HuR was decreased in diabetic NP tissues and high glucose-treated NP cells. Downregulation of HuR may lead to increased senescence in high glucose-treated NP cells, while autophagy activation attenuates senescence in HuR deficient NP cells. Mechanistic study showed that HuR prompted Atg7 mRNA stability via binding to the AU-rich elements. Furthermore, overexpression of Atg7, but not HuR, may ameliorate DB-IVDD in rats in vivo.
CONCLUSIONS: In conclusion, HuR may suppress senescence through autophagy activation via stabilizing Atg7 in diabetic NP cells; while Atg7, but not HuR, may serve as a potential therapeutic target for DB-IVDD.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ATG7Humandegenerative disc disease amelioratesISOAtg7 (Rattus norvegicus) RGD 
Atg7Ratdegenerative disc disease amelioratesIDA  RGD 
Atg7Mousedegenerative disc disease amelioratesISOAtg7 (Rattus norvegicus) RGD 
ELAVL1Humandegenerative disc disease  ISOElavl1 (Rattus norvegicus)associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 
ELAVL1Humandegenerative disc disease  IEP associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 
Elavl1Mousedegenerative disc disease  ISOElavl1 (Rattus norvegicus)associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 
Elavl1Mousedegenerative disc disease  ISOELAVL1 (Homo sapiens)associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 
Elavl1Ratdegenerative disc disease  ISOELAVL1 (Homo sapiens)associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 
Elavl1Ratdegenerative disc disease  IEP associated with diabetes mellitus and protein:decreased expression:nucleus pulposusRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  

Objects Annotated

Genes (Rattus norvegicus)
Atg7  (autophagy related 7)
Elavl1  (ELAV like RNA binding protein 1)

Genes (Mus musculus)
Atg7  (autophagy related 7)
Elavl1  (ELAV like RNA binding protein 1)

Genes (Homo sapiens)
ATG7  (autophagy related 7)
ELAVL1  (ELAV like RNA binding protein 1)


Additional Information