Academic Journal
Decrease of NAD+ Inhibits the Apoptosis of OLP T Cells via Inducing Mitochondrial Fission
| Title: | Decrease of NAD+ Inhibits the Apoptosis of OLP T Cells via Inducing Mitochondrial Fission |
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| Authors: | Zhang ZY, Wang F, Zhou G |
| Source: | Journal of Inflammation Research, Vol Volume 18, Pp 1091-1106 (2025) |
| Publisher Information: | Dove Medical Press, 2025. |
| Publication Year: | 2025 |
| Collection: | LCC:Pathology LCC:Therapeutics. Pharmacology |
| Subject Terms: | mitochondria, nicotinamide adenine dinucleotide, t cells, oral lichen planus, Pathology, RB1-214, Therapeutics. Pharmacology, RM1-950 |
| More Details: | Zhuo-Yu Zhang,1 Fang Wang,1,2 Gang Zhou1,3 1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, People’s Republic of China; 2Center for Cariology, Endodontics and Periodontics, Optical Valley Branch, School & Hospital of Stomatology, Wuhan University, Wuhan, People’s Republic of China; 3Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan, People’s Republic of ChinaCorrespondence: Fang Wang, Center for Cariology, Endodontics and Periodontics, Optical Valley Branch, School & Hospital of Stomatology, Wuhan University, Wuhan, People’s Republic of China, Email wangfang-nm@whu.edu.cn Gang Zhou, Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan, People’s Republic of China, Email zhougang@whu.edu.cnPurpose: Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease involving T cells. Mitochondrial fission plays a crucial role in T cell fate through structural remodeling. Nicotinamide adenine dinucleotide (NAD+) regulates mitochondrial remodeling and function. This study explored the role of NAD+ in modulating mitochondrial fission and apoptosis in T cells under the OLP immune-inflammatory environment.Patients and Methods: T cells and plasma were isolated from peripheral blood. Mitochondrial morphology was characterized by transmission electron microscopy and Mito-Tracker staining. OLP plasma-exposed Jurkat T cells were infected with the Drp1 shRNA virus to investigate the role of mitochondrial fission in OLP T cell apoptosis. OLP T cells and OLP plasma-exposed Jurkat T cells were treated with either β-nicotinamide mononucleotide (an NAD+ synthesis precursor) or FK866 (an NAD+ synthesis inhibitor) to assess the effect of NAD+ regulation on mitochondrial remodeling and T cell apoptosis.Results: OLP T cells exhibited fragmented mitochondria with elevated dynamin-related protein 1 (Drp1) and reduced mitofusin 2 (Mfn2) expression, accompanied by decreased apoptosis. Drp1 knockdown in OLP plasma-exposed Jurkat T cells increased apoptosis and reduced proliferation. NAD+ levels were reduced in both OLP T cells and OLP plasma-treated Jurkat T cells, leading to enhanced mitochondrial fission, decreased mitochondrial membrane potential (MMP) and respiration function, and reduced apoptosis rate. β-nicotinamide mononucleotide supplementation restored NAD+ levels, suppressed mitochondrial fission, improved MMP, and promoted apoptosis in these cells.Conclusion: Reduced NAD+ levels in OLP T cells enhanced mitochondrial fission and contributed to decreased apoptosis. NAD+ supplementation mitigated these effects, suggesting a potential therapeutic strategy for restoring T cell homeostasis in OLP.Keywords: mitochondria, nicotinamide adenine dinucleotide, T cells, oral lichen planus |
| Document Type: | article |
| File Description: | electronic resource |
| Language: | English |
| ISSN: | 1178-7031 |
| Relation: | https://www.dovepress.com/decrease-of-nad-inhibits-the-apoptosis-of-olp-t-cells-via-inducing-mit-peer-reviewed-fulltext-article-JIR; https://doaj.org/toc/1178-7031 |
| Access URL: | https://doaj.org/article/0e56f2a33cb54a87a4758f1775294f76 |
| Accession Number: | edsdoj.0e56f2a33cb54a87a4758f1775294f76 |
| Database: | Directory of Open Access Journals |
| ISSN: | 11787031 |
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| Published in: | Journal of Inflammation Research |
| Language: | English |