ArticlePediatric research2022
Possible mechanism of CHI3L1 promoting tonsil lymphocytes proliferation in children with obstructive sleep apnea syndrome.
Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Abnormally high expression of CHI3L1 in peripheral blood mononuclear cells and serum and their potential diagnosis and prediction from lymphoma patients.Frontiers in immunology · 2025Article
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Overexpression of YKL40,IL-6, IL-8, TNF-α in tonsils and the role of YKL40 in childhood with obstructive sleep apnea syndrome.Scientific reports · 2024Article
- A simple preparation step to remove excess liquid lipids in white adipose tissue enabling improved detection of metabolites via MALDI-FTICR imaging MS.Histochemistry and cell biology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe typical characteristic of pediatric obstructive sleep apnea syndrome (OSAS) is systemic inflammation and adenotonsillar hypertrophy (ATH), but the inflammatory markers and mechanism of adenotonsillar proliferation are unclear.
methodsIHC, qPCR, and western blotting were used to identify the expression of CHI3L1 in the tonsils of children with OSAS. The primary tonsil lymphocytes (PTLCs) from children with OSAS were cultured and recombinant human CHI3L1 protein was added to culture media. After the stimulation with CHI3L1 protein of different concentrations and time points, lymphocyte proliferation was assessed by CCK-8 kits and flow cytometry. The activation of ERK1/2 and the effects on the proliferation of PTLCs were observed by western blotting.
resultsThe expression of CHI3L1 was higher in the OSAS group than in the PS group. CHI3L1 (100 ng/mmol for 24 h) resulted in a significant increase in the proliferation rate. The ERK1/2 activator (PMA) promoted the proliferation of PTLCs and inhibitor AG126 significantly inhibited proliferation.
conclusionsCHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways. This result indicates that CHI3L1 may play an important role in the pathogenesis of OSAS in children. Inhibition of CHI3L1 or ERK1/2 may be potential therapeutic targets for CHI3L1-induced proliferation in childhood OSAS. IMPACT: CHI3L1 may be an inflammatory marker in childhood OSAS. CHI3L1 can promote the proliferation of PTLCs in a concentration and time-dependent condition. CHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways.
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