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The asthma candidate gene NPSR1 mediates isoform specific downstream signalling. | LitMetric

AI Article Synopsis

  • Neuropeptide S Receptor 1 (NPSR1) is linked to asthma and allergy susceptibility, with two variants (NPSR1-A and NPSR1-B) showing different expressions in asthmatic airways.
  • This study investigated the downstream signaling properties of NPSR1-B compared to NPSR1-A through experiments on HEK-293 cells, revealing both isoforms activate similar pathways but differ in the strength of their signaling.
  • NPSR1-B showed lower overall signaling than NPSR1-A, except for a notable increase in the regulation of CD69, suggesting a potential specific role in asthma and allergy processes.

Article Abstract

Background: Neuropeptide S Receptor 1 (NPSR1, GPRA, GPR154) was first identified as an asthma candidate gene through positional cloning and has since been replicated as an asthma and allergy susceptibility gene in several independent association studies. In humans, NPSR1 encodes two G protein-coupled receptor variants, NPSR1-A and NPSR1-B, with unique intracellular C-termini. Both isoforms show distinct expression pattern in asthmatic airways. Although NPSR1-A has been extensively studied, functional differences and properties of NPSR1-B have not yet been clearly examined. Our objective was to investigate downstream signalling properties of NPSR1-B and functional differences between NPSR1-A and NPSR1-B.

Methods: HEK-293 cells transiently overexpressing NPSR1-A or NPSR1-B were stimulated with the ligand neuropeptide S (NPS) and downstream signalling effects were monitored by genome-scale affymetrix expression-arrays. The results were verified by NPS concentration-response and time series analysis using qRT-PCR, cAMP and Ca²⁺ assays, and cAMP/PKA, MAPK/JNK and MAPK/ERK pathway specific reporter assays.

Results: NPSR1-B signalled through the same pathways and regulated the same genes as NPSR1-A, but NPSR1-B yielded lower induction on effector genes than NPSR1-A, with one notable exception, CD69, a marker of regulatory T cells.

Conclusions: We conclude that NPSR1-B is regulating essentially identical set of genes as NPSR1-A, with few, but possibly important exceptions, and that NPSR1-A induces stronger signalling effects than NPSR1-B. Our findings suggest an isoform-specific link to pathogenetic processes in asthma and allergy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142248PMC
http://dx.doi.org/10.1186/1471-2466-11-39DOI Listing

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