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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
vtRNA1-1/p62 regulates macrophages autophagy in ankylosing spondylitis
Minxin Jiang1, Jianping Ni1, Xueying Yu1
1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China; The Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.
Abstract:
This research aims to investigate the role and mechanisms of the vtRNA1-1/p62 molecular axis in the regulation of autophagy in AS, with the goal of identifying novel diagnostic and therapeutic targets for AS. Clinical sample analysis revealed that the transcription levels of vtRNA1-1 and p62 decreased in the peripheral blood mononuclear cells (PBMCs) of the AS group; conversely, the levels of canonical autophagy-related genes (ATG3, ATG5) and inflammatory factors (TNF-α) significantly increased. Correlation analysis revealed that vtRNA1-1 levels were positively associated with p62 but were inversely associated with ATG3, ATG5, and TNF-α. In vitro cell experiments demonstrated that vtRNA1-1 depletion reduced p62 expression while increasing ATG3, ATG5, and LC3B levels. Computational modeling further confirmed significant interactions between vtRNA1-1 and p62. Notably, vtRNA1-1 and p62 demonstrated unique diagnostic value for AS, with their combination showing even greater diagnostic significance. This study innovatively links noncoding RNA regulatory networks with autophagy homeostasis imbalance, revealing that vtRNA1-1 may regulate macrophage autophagy through p62, thereby participating in the molecular pathogenesis of AS.
Insights
This study reveals that decreased vtRNA1-1 and p62 levels are linked to autophagy dysfunction and inflammation in AS patients. This vtRNA1-1/p62 axis offers potential new diagnostic and therapeutic strategies for AS.
Area of Science:
- Molecular Biology
- Cell Biology
- Immunology
Background:
- Autophagy plays a critical role in cellular homeostasis.
- Imbalances in autophagy are implicated in various diseases, including AS.
- The molecular mechanisms regulating autophagy in AS require further elucidation.
Purpose of the Study:
- To investigate the role of the vtRNA1-1/p62 molecular axis in regulating autophagy in AS.
- To identify novel diagnostic and therapeutic targets for AS based on this axis.
- To explore the link between noncoding RNA networks, autophagy, and AS pathogenesis.
Main Methods:
- Analysis of clinical samples (PBMCs) from AS patients and controls.
- In vitro cell experiments involving vtRNA1-1 depletion.
- Computational modeling to assess molecular interactions.
- Measurement of gene and protein expression levels (vtRNA1-1, p62, ATG3, ATG5, LC3B, TNF-α).
Main Results:
- AS patients showed decreased vtRNA1-1 and p62 levels, with increased ATG3, ATG5, and TNF-α in PBMCs.
- vtRNA1-1 levels positively correlated with p62 but inversely with ATG3, ATG5, and TNF-α.
- vtRNA1-1 depletion in vitro reduced p62 and increased ATG3, ATG5, and LC3B.
- vtRNA1-1 and p62 demonstrated diagnostic value for AS, individually and in combination.
Conclusions:
- The vtRNA1-1/p62 axis is a key regulator of autophagy in AS.
- vtRNA1-1 may modulate macrophage autophagy via p62, contributing to AS pathogenesis.
- The vtRNA1-1/p62 axis represents a promising target for AS diagnostics and therapeutics.
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