ArticleBone research2023
Mobilization of monocytic myeloid-derived suppressor cells is regulated by PTH1R activation in bone marrow stromal cells.
Article in Bone research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Mechanisms of systemic immune modulation in tumor development: Interactions across lymph nodes, bone marrow, and blood.Cancer metastasis reviews · 2026Review
- Clinical guidance on evaluation and management of bone fragility in patients with monoclonal gammopathy of undetermined significance (MGUS): an IOF position statement.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- Decoding the Role of MDSCs in Bone Metastasis: Multicellular Interactions and Clinical Implications.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Human Adipose Stem Cells Engineered to Express Carboxylesterase Confer Anti-Tumoral Efficacy of Irinotecan in Castration-Resistant Prostate Cancer Bone Metastasis Growth and Osteolysis.The world journal of men's health · 2026Article
- Digital spatial profiling of α-PD-1 treated breast cancer bone metastases reveals region-specific signaling and enrichment of immune-suppressive markers.Journal of bone oncology · 2026Article
- Splenic PD-L1Research (Washington, D.C.) · 2026Article
- Systemic chemotherapy in metastatic TNBC polarizes effector T cell differentiation.Cancer cell international · 2025Article
- Seizure evolution in a mouse model of West syndrome involves complex and time-dependent synapse remodeling, gliosis and alterations in lipid metabolism.PLoS biology · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
Myeloid-derived suppressor cells (MDSCs) are bone marrow (BM)-derived immunosuppressive cells in the tumor microenvironment, but the mechanism of MDSC mobilization from the BM remains unclear. We investigated how BM stromal cell activation by PTH1R contributes to MDSC mobilization. PTH1R activation by parathyroid hormone (PTH) or PTH-related peptide (PTHrP), a tumor-derived counterpart, mobilized monocytic (M-) MDSCs from murine BM without increasing immunosuppressive activity. In vitro cell-binding assays demonstrated that α4β1 integrin and vascular cell adhesion molecule (VCAM)-1, expressed on M-MDSCs and osteoblasts, respectively, are key to M-MDSC binding to osteoblasts. Upon PTH1R activation, osteoblasts express VEGF-A and IL6, leading to Src family kinase phosphorylation in M-MDSCs. Src inhibitors suppressed PTHrP-induced MDSC mobilization, and Src activation in M-MDSCs upregulated two proteases, ADAM-17 and MMP7, leading to VCAM1 shedding and subsequent disruption of M-MDSC tethering to osteoblasts. Collectively, our data provide the molecular mechanism of M-MDSC mobilization in the bones of tumor hosts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.