Biology subjects

Miyamoto, J. G.

Publications and source records attributed to Miyamoto, J. G..

3 recordsLinked to original sources

bioRxiv2026

Single-cell proteomics maps circulating monocyte dynamics in advanced head and neck squamous cell carcinoma

It remains unclear whether metastatic progression in head and neck squamous cell carcinoma (HNSCC) is accompanied by functional remodeling of circulating immune cells at the proteome level. To address this question, we applied single-cell proteomics (SCP) to cryopreserved peripheral blood mononuclear cells (PBMCs) from three patients with HNSCC representing distinct stages of metastatic progression and two healthy donors. Proteomic analysis of 619 individual PBMCs resolved major immune cell populations, with up to 1,638 proteins quantified per cell. Trajectory inference, clustering, and differential abundance analyses revealed proteomic remodeling associated with disease progression, with the most pronounced changes occurring within a monocyte cluster composed exclusively of cells from patients with nodal metastasis. This population showed increased abundance of interferon-related proteins, HLA molecules, and myeloid immunoregulatory signatures, consistent with an activated, interferon-associated monocyte state. In parallel, lymphocytes showed reduced coordinated abundance of proteins associated with activation, cytotoxicity, and degranulation, consistent with altered cytotoxic effector programs across disease stages. Overall, these findings reveal distinct proteomic states in circulating monocytes and lymphocytes associated with HNSCC progression and identify selective remodeling of the monocyte compartment in nodal metastatic disease.

cancer biology↗

bioRxiv2025

Single-cell proteomics workflow for characterizing heterogeneous cell populations in saliva and tear fluid

Single-cell proteomics (SCP) has advanced considerably but still is largely limited to homogeneous populations and distant from clinical applicability. We present an SCP workflow for assessing the cellular heterogeneity in saliva and tear fluid. Initially, benchmarks were established using a standard HeLa digestion curve, resulting in more than 5,463 protein groups (PGs) at 50 pg. For single HeLa cells, the workflow was improved to minimize contamination and increase quantitative performance, reaching a maximum of 3,785 PGs per single cell. Following, SCP was benchmarked across heterogenous populations of saliva and tear fluid, collected from 10 healthy individuals. By improving cell isolation, contamination control, and DIA-based search and quantitation, single cells from saliva (n=110) and tear fluid (n=149), with average diameters of 8 and 11 {micro}m, respectively, yielded a maximum of 700 PGs per single cell. Downstream analysis indicated overrepresented protein functions, distinct cluster markers and twenty-three validated therapeutic targets identified from single-cell data. Taken together, this study demonstrates the robustness of our SCP workflow applied to biofluids, driving the discovery of biomarkers and therapeutic targets in complex microenvironments.

molecular biology↗

bioRxiv2022

ArtinM Cytotoxicity in B cells derived from Non-Hodgkins Lymphoma is regulated by CD45 phosphatase activity and Src family kinases

Receptors on the immune cell surface have a variety of glycans that may account for the immunomodulation induced by lectins, which have a carbohydrate recognition domain (CRD) that binds to monosaccharides or oligosaccharides in a specific manner. ArtinM, a D-mannose-binding lectin obtained from Artocarpus heterophyllus, has affinity for the N-glycans core. Immunomodulation by ArtinM toward the Th1 phenotype occurs via its interaction with TLR2/CD14 N-glycans on antigen-presenting cells, as well as recognition of CD3{gamma} N-glycans on murine CD4+ and CD8+ T cells. ArtinM exerts a cytotoxic effect on Jurkat human leukemic T cell line and human myeloid leukemia cell line (NB4). The current study evaluated the effects of ArtinM on murine and human B cells derived from non-Hodgkins lymphoma. We found that murine B cells are recognized by ArtinM via the CRD, and the ArtinM stimulus did not augment the proliferation rate or production of IL-2. However, murine B cells incubation with ArtinM augmented the rate of apoptosis, and this cytotoxic effect of ArtinM was also seen in human B cell lines sourced from non-Hodgkins lymphoma Raji cell line. This cytotoxic effect was inhibited by the phosphatase activity of CD45 on Lck, and the protein kinases of the Src family contribute to cell death triggered by ArtinM.

cell biology↗