SCIENTIFIC HUB

Follow the evidence.

SCIENTIFIC LITERATURE · MED

Low Level of Autophagy-Related Gene 10 (ATG10) Expression in the 6-Hydroxydopamine Rat Model of Parkinson's Disease

Iran Biomed J · 2017-07-23

DOI: 10.22034/ibj.22.1.15PMID: 28734275

Open accessresearch-article; Journal ArticleOriginal source ↗

Research overview

The text below is the source article’s original abstract under a verified reuse license. cc by

BackgroundAutophagy is a mechanism disassembling the damaged organelles from the cell. This study attempted to examine the expression of several autophagy-related genes in Parkinson’s disease (PD) rat model.MethodsThe male Wistar rats were divided into three groups as control, sham, and lesion. In the latter group, the PD rat model was induced by the injection of 6-hydroxydopamine in the striatum. The behavioral test was conducted one (baseline) and four weeks after the surgery through apomorphine hydrochloride. Then the RT-PCR technique was employed to evaluate the expressions of p62/SQSTM, autophagy-related genes (ATG)5, ATG12, ATG16L1, ATG10, as well as GAPDH and LC3.ResultsBy injecting apomorphine, the striatal lesion group showed a significant contralateral rotation at fourth week as compared to the baseline. The examination of p62, ATG5, ATG12, ATG16L1, and LC3 expressions using RT-PCR revealed that p62, ATG5, ATG12, LC3, and ATG16L1 were expressed in the substantia nigra of PD rat model, while ATG10 was not expressed.ConclusionATG10 expression is necessary for the initiation of autophagy. Thus, these results show that autophagy deregulation occurs in the initiation stages of the process in the rat model of PD.

Scientific assessment

01

Research question

Assess the question within the original study’s scope.

02

Methods & sample

Check the source article for study design and sample details.

03

Key findings

An editorially approved findings summary is not yet published for this record.

04

Limitations

Generalizability, bias and clinical meaning require separate assessment.

Methods, samples and clinical conclusions are not inferred from bibliographic metadata.