TP73-AS1 Regulates MPP+-Induced Cell Inflammation and Apoptosis in SH-SY5Y Cells
Among early-onset PD patients, 59 lncRNAs were significantly upregulated, and 57 lncRNAs were significantly downregulated compared to the control group. Similarly, late-onset PD patients showed 70 upregulated lncRNAs and 77 downregulated lncRNAs with statistical significance compared to the control group. In vitro studies indicated a significant increase in lncRNA TP73-AS1 expression in the MPP+-treated group in contrast with the control group (<i>P</i> < 0.001). Furthermore, the MPP+-treated group displayed elevated levels of Cleaved caspase-3, IL-16, as well as IL-6 (<i>P</i> < 0.001). Conversely, Bcl-2 expression decreased, Bax expression increased, and the Bax/Bcl-2 expression ratio demonstrated an increase (<i>P</i> < 0.001). Reducing lncRNA TP73-AS1 resulted in decreased apoptosis and inflammation, along with a decrease in α-SYN expression (<i>P</i> < 0.001). Notably, the absence of TP73-AS1 showed a protective effect against PD, suggesting it to be a potential target for the treatment of PD. These findings suggest that TP73-AS1 may serve as a potential molecular marker for the early diagnosis of PD, providing a new perspective for understanding the regulatory mechanisms of inflammation and apoptosis in PD.
Authors
- Anmu Xie (ORCID: https://orcid.org/0000-0003-2591-467X)
- Kaixin Dou (ORCID: https://orcid.org/0000-0002-6677-3511)
- Haiyan Li (ORCID: https://orcid.org/0000-0002-7423-2715)
- Xue Li (ORCID: https://orcid.org/0000-0001-9247-0584)
- Xue Zhang (ORCID: https://orcid.org/0000-0002-5782-2174)
- Xiaolong Yu (ORCID: https://orcid.org/0000-0001-6505-8914)
Institutions
- Qingdao University (CN)
- Affiliated Hospital of Qingdao University (CN)
- Qingdao Municipal Hospital (CN)
- Qingdao Eighth People's Hospital (CN)
Publication Details
- Journal
- Degenerative Neurological and Neuromuscular Disease
- Published
- 2025-09-01
- DOI
- https://doi.org/10.2147/dnnd.s539895
- Primary Topic
- RNA regulation and disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Qingdao