2. Academic Validation
  3. Dental pulp stem cells accelerate wound healing through CCL2-induced M2 macrophages polarization

Dental pulp stem cells accelerate wound healing through CCL2-induced M2 macrophages polarization

  • iScience. 2023 Sep 24;26(10):108043. doi: 10.1016/j.isci.2023.108043.
Zi Yang 1,  Linsha Ma 1 2,  Conglin Du 1 2,  Jingsong Wang 1 2 3,  Chunmei Zhang 1 2,  Lei Hu 1 2 4,  Songlin Wang 1 2 3 5 6
Affiliations

Affiliations

  • 1 Salivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Beijing Laboratory of Oral Health and Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
  • 2 Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
  • 3 Department of Biochemistry and Molecular Biology, Capital Medical University School of Basic Medicine, Beijing, China.
  • 4 Department of Prosthodontics, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
  • 5 Laboratory for Oral and General Health Integration and Translation, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
  • 6 Research Units of Tooth Development and Regeneration, Chinese Academy of Medical Sciences, Beijing, China.
PMID: 37829207 DOI: 10.1016/j.isci.2023.108043
Abstract

The crosstalk between mesenchymal stem cells (MSCs) and the host immune function plays a key role in the efficiency of tissue regeneration and wound healing. However, the difference in immunological modulation and tissue regeneration function between MSCs from different sources remains unclear. Compared to PDLSCs, BMMSCs, and ADSCs, DPSCs exhibited greater tissue regeneration potential and triggered more M2 macrophages in vivo. DPSCs elicited the polarization of M2a macrophages by conditioned medium and transwell assay and exhibited higher expression levels of C-C motif chemokine ligand 2 (CCL2). Specific blocking of CCL2 could significantly inhibit the DPSCs-induced polarization of M2 macrophages. DPSCs promoted wound healing of the palatal mucosa and M2 macrophages polarization in vivo, which could be significantly impaired by CCL2-neutralized antibody. Our data indicate that DPSCs exert better tissue regeneration potential and immunoregulatory function by secreting CCL2, which can enhance MSCs-mediated tissue regeneration or wound healing.

Keywords

Cell biology; Immunology; Molecular biology.

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