Chymase 1 (CMA1), a gene known to be expressed in mast cells (MCs), is largely linked to immunity. However, the relationship between CMA1 and prognosis of multiple tumours and tumour-infiltrating lymphocytes (TILs) remains elusive. The differential expressions of CMA1 in different tumours and their corresponding normal tissues were evaluated exploring Tumour Immune Estimation Resource (TIMER) and Oncomine database; the correlation within expression level of CMA1 and outcome of cancer patients was evaluated Kaplan-Meier plotter and Gene Expression Profiling Interactive Analysis (GEPIA) database; the correlation between CMA1 and tumour immune cell infiltration was further investigated by TIMER; additionally, the correlation between CMA1 and gene signature pattern of immune infiltration were checked using TIMER and GEPIA. There were significant differences in CMA1 expression levels between gastric cancer (GC) tissues and adjacent normal tissues. The high expression of CMA1 was closed related to poor overall survival (OS) and progression-free survival (PFS) in patients with GC (OS HR = 1.50, = .00015; PFS HR = 1.33, = .016). Especially, in GC patients at N1, N2 and N3 stages, high CMA1 expression was correlated with poor OS and PFS, but not with NO ( = .15, .09). The expression of CMA1 was positively associated with the levels of infiltrated CD4+, CD8+ T cells, neutrophils, macrophages, and dendritic cells (DCs) in GC. Whereas, CMA1 expression was considerably associated with various immune markers. CMA1 is a key gene whose expression level is significantly correlated with GC prognosis and infiltration levels of CD8+, CD4+ T cells, neutrophils, macrophages, and DCs in GC. In addition, the expression of CMA1 may be involved in regulating tumour-associated macrophages (TAMs), dendritic cells, exhausted T cells and regulatory T cells in GC. It suggests that CMA1 could be utilized as a prognostic marker and a sign of immune infiltration in GC.
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http://dx.doi.org/10.1080/08916934.2020.1735371 | DOI Listing |
Int Immunopharmacol
December 2024
Department of Dermatology, The First Hospital of China Medical University, Shenyang, China; NHC Key Laboratory of Immunodermatology, Ministry of Education Key Laboratory of Immunodermatology, National Joint Engineering Research Center for Diagnosis and Treatment of Immunologic Skin Diseases, The First Hospital of China Medical University, Shenyang, China.
Background: Activation of the aryl hydrocarbon receptor (AhR) ameliorates LL-37-induced rosacea-like dermatitis in mice, whereas mast cells and cytokine overexpression are prominent features in rosacea skin.
Objective: To evaluate the potential mechanisms of AhR activation on autophagy and degranulation of mast cells in rosacea.
Methods: LL-37 treated mast cells were used to mimic rosacea.
Osteoarthritis Cartilage
January 2025
Department of Biomedical Engineering, Cleveland Clinic, Cleveland, OH, USA; Musculoskeletal Research Center, Cleveland Clinic, Cleveland, OH, USA; Department of Orthopaedic Surgery, Cleveland Clinic, Cleveland, OH, USA. Electronic address:
Objectives: Proteolytic cartilage extracellular matrix breakdown is a major mechanism of articular cartilage loss in osteoarthritis (OA) pathogenesis. We sought to determine the overlap of proteolytic peptides in matched knee OA cartilage and synovial fluid on a proteome-wide scale to increase the prospective biomarker repertoire and to attribute proteolytic cleavages to specific secreted proteases.
Design: Matched human knee OA cartilage and synovial fluid (n = 5) were analyzed by N-terminomics using Terminal Amine Isotopic Labeling of Substrates (TAILS), comprising labeling and enrichment of protein N-termini, high-resolution mass spectrometry and positional peptide mapping.
Heliyon
August 2024
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Unlabelled: Immune cells play a critical role in the transition from acute to chronic pain. However, the role of mast cells in pain remains under-investigated. Here, we demonstrated that the resolution of inflammatory pain is markedly delayed in mast-cell-deficient mice.
View Article and Find Full Text PDFMucosal Immunol
October 2024
Mary H Weiser Food Allergy Center, Michigan Medicine, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA; Department of Pathology, Michigan Medicine, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA. Electronic address:
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