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E3 Ubiquitin Ligase March1 Facilitates OX40L Expression in Allergen-Stimulated Dendritic Cells Through Mediating the Ubiquitination of HDAC11. | LitMetric

AI Article Synopsis

  • The study investigates the role of membrane-associated RING-CH 1 (March1) in asthma, highlighting its interaction with HDAC11 and OX40 ligand (OX40L) in dendritic cells (DCs) from asthmatic patients.
  • Results showed that both March1 and OX40L levels were elevated in asthmatic DCs, while HDAC11 levels were decreased, indicating a potential pathway affecting asthma pathology.
  • The findings suggest that March1 promotes OX40L expression by inducing the degradation of HDAC11, which normally represses OX40L, thereby revealing a complex regulatory mechanism involved in asthma.

Article Abstract

Background: It was demonstrated that membrane-associated RING-CH 1 (March 1) might play an important role in the pathogenesis of asthma.

Methods: The levels of mRNA and protein were measured by qRT-PCR and Western blot, respectively. Immunofluorescence assay was used to determine whether March1 co-locates with HDAC11. Co-immunoprecipitation was performed to examine the combination of proteins. Moreover, luciferase assay was used to measure the promoter activity of genes.

Results: The mRNA and protein levels of both March1 and OX40 ligand (OX40L) were increased in the dendritic cells (DCs) from asthmatic children and asthmatic animals. Histone deacetylase 11 (HDAC11) protein was decreased in the DCs from asthmatic children and asthmatic model. Increasing of March1 or decreasing of March1 only affect the expression of HDAC11 in protein level. Besides, increasing of HDAC11 could inhibit OX40L expression, and decreasing of HDAC11 promoted OX40L expression in house dust mites (HDMs)-treated DCs. Increasing of HDAC11 notably reversed the promotion of March1 to OX40L expression. Our data further proved that March1 reduced the protein level of HDAC11 through inducing ubiquitination and degradation. HDAC11 combined with krüppel-like factor 4 (KLF4) to decrease the activity of OX40L gene promoter, thus to downregulate the level of OX40L.

Conclusion: Overall, our data showed that HDAC11 promoted KLF4-dependent OX40L decreasing. However, March1 promoted OX40L expression through enhancing the ubiquitination and degradation of HDAC11 and subsequent blocking the inhibition of HDAC11 to OX40L.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8352640PMC
http://dx.doi.org/10.2147/JAA.S318104DOI Listing

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