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TP73-AS1 Regulates MPP+-Induced Cell Inflammation and Apoptosis in SH-SY5Y Cells.

Xue Zhang1,2, Li Xue3, Haiyan Li2

  • 1Department of Neurology, Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.

Degenerative Neurological and Neuromuscular Disease
|September 12, 2025
PubMed
Summary

Long non-coding RNA TP73-AS1 is upregulated in Parkinson's disease (PD), promoting apoptosis and inflammation. Reducing TP73-AS1 expression offers a protective effect and may serve as a diagnostic marker for PD.

Keywords:
TP73-AS1apoptosishigh-throughput sequencinginflammationlong non-coding RNA

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Parkinson's disease (PD) pathogenesis involves complex genetic and molecular mechanisms.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in neurodegenerative diseases.
  • The specific involvement of TP73-AS1 in PD remains largely unexplored.

Purpose of the Study:

  • To investigate the role of lncRNA TP73-AS1 in the pathogenesis of Parkinson's disease.
  • To explore TP73-AS1 as a potential diagnostic biomarker for PD.
  • To elucidate the functional impact of TP73-AS1 on apoptosis and inflammation in PD.

Main Methods:

  • Analysis of lncRNA expression profiles in peripheral blood from early-onset PD, late-onset PD, and healthy controls using Illumina HiSeq2500.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) to specifically assess TP73-AS1 expression.
  • In vitro studies using SH-SY5Y cells treated with MPP+ to evaluate the functional role of TP73-AS1, apoptosis markers (Cleaved caspase-3, Bcl-2, Bax), inflammatory cytokines (IL-16, IL-6), and alpha-synuclein (α-SYN) via flow cytometry, Western blot, and immunofluorescence.

Main Results:

  • Significant differential expression of numerous lncRNAs was observed in both early-onset and late-onset PD patients compared to controls.
  • TP73-AS1 expression was significantly increased in MPP+-treated SH-SY5Y cells, correlating with elevated apoptosis markers (Cleaved caspase-3, increased Bax/Bcl-2 ratio) and inflammatory cytokines (IL-16, IL-6).
  • Reduction of TP73-AS1 expression led to decreased apoptosis, inflammation, and α-SYN levels, demonstrating a protective effect against PD pathogenesis.

Conclusions:

  • TP73-AS1 plays a significant role in promoting apoptosis and inflammation, contributing to the pathogenesis of Parkinson's disease.
  • TP73-AS1 may serve as a potential therapeutic target for PD treatment.
  • The findings suggest TP73-AS1 as a promising molecular marker for early PD diagnosis.