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Generation and Labeling of Murine Bone Marrow-derived Dendritic Cells with Qdot Nanocrystals for Tracking Studies

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Bone marrow-derived NGFR-positive dendritic cells regulate arterial remodeling.

Shinichiro Takashima¹, Soichiro Usui¹, Shintaro Matsuura²

¹Department of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.

American Journal of Physiology. Cell Physiology

|January 2, 2025

Summary

Bone marrow-derived Nerve Growth Factor Receptor-positive (NGFR+) dendritic cells (DCs) suppress arteriosclerosis by undergoing apoptosis and promoting anti-inflammatory macrophages. Insufficient NGFR+ cell increase in acute coronary syndrome patients predicts future lesion progression.

Keywords:

apoptosis arterial remodeling bone marrow dendritic cells nerve growth factor receptor

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Culture of myeloid dendritic cells from bone marrow precursors

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Published on: July 25, 2008

Area of Science:

Cardiovascular Biology
Immunology
Cell Biology

Background:

Bone marrow's role in arteriosclerosis pathogenesis is under investigation.
Nerve Growth Factor Receptor (NGFR) is present in bone marrow stromal cells, peripheral blood, and coronary arteries.
NGFR-positive (NGFR+) cells are hypothesized to influence arterial remodeling.

Purpose of the Study:

To investigate the role of bone marrow-derived NGFR+ cells in arterial remodeling and arteriosclerosis.
To determine the impact of NGFR+ cells on smooth muscle cell proliferation and inflammation in the neointima.
To assess the clinical relevance of NGFR+ peripheral mononuclear cells (MNCs) in acute coronary syndrome (ACS).

Main Methods:

Utilized mouse models with bone marrow-specific NGFR+ cell depletion and NGFR knockout.
Analyzed human peripheral blood mononuclear cells (MNCs) and cells within arterial lesions.
Quantified neointimal formation, smooth muscle cell (SMC) proliferation, and macrophage accumulation.
Measured interleukin-10 (IL-10) secretion and assessed NGFR+ MNCs in ACS patients.

Main Results:

Depletion or knockout of bone marrow NGFR+ cells led to increased neointimal formation and SMC proliferation.
Bone marrow-derived NGFR+ cells accumulated in the neointima, underwent apoptosis, and promoted anti-inflammatory M2 macrophages.
NGFR+ cells secreted IL-10, inhibiting SMC proliferation, and their numbers increased post-ACS onset.
Insufficient NGFR+ peripheral MNC increase in ACS was an independent risk factor for intimal progression.

Conclusions:

Bone marrow-derived NGFR+ dendritic cells (DCs) act as suppressors of arteriosclerosis.
NGFR+ DCs inhibit neointimal progression via apoptosis and by promoting an anti-inflammatory environment.
Reduced mobilization of NGFR+ MNCs in ACS patients indicates a higher risk for future arterial lesion progression.