IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells
Bone remodeling mediated by bone-forming osteoblasts (OBs) and bone-resorbing osteoclasts (OCs) maintains bone structure and function. Excessive OC activation leads to bone-destroying diseases such as osteoporosis and bone erosion of rheumatoid arthritis (RA). Differentiation of OCs from bone marrow...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-01-01
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| Series: | Journal of Pharmacological Sciences |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1347861322000822 |
| _version_ | 1811296259508535296 |
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| author | Yuto Otsuka Takao Kondo Hiromasa Aoki Yoh Goto Yohei Kawaguchi Yuko Waguri-Nagaya Ken Miyazawa Shigemi Goto Mineyoshi Aoyama |
| author_facet | Yuto Otsuka Takao Kondo Hiromasa Aoki Yoh Goto Yohei Kawaguchi Yuko Waguri-Nagaya Ken Miyazawa Shigemi Goto Mineyoshi Aoyama |
| author_sort | Yuto Otsuka |
| collection | DOAJ |
| description | Bone remodeling mediated by bone-forming osteoblasts (OBs) and bone-resorbing osteoclasts (OCs) maintains bone structure and function. Excessive OC activation leads to bone-destroying diseases such as osteoporosis and bone erosion of rheumatoid arthritis (RA). Differentiation of OCs from bone marrow cells (BMCs) is regulated by the bone microenvironment. The proinflammatory cytokine interleukin (IL)-1β reportedly enhances osteoclastogenesis and plays important roles in RA-associated bone loss. The present study investigated the effect of IL-1β on OC formation via microenvironmental cells. Treating mouse BMCs with IL-1β in the presence of receptor activator of NF-κB ligand and macrophage colony-stimulating factor increased the number of OCs. Real-time RT-PCR revealed increased expression of the IL-1β, IL-1RI, and IL-1RII genes in non-OCs compared with OCs. Removing CD45− cells which cannot differentiate into OCs, from mouse BMCs reduced the IL-1β–mediated enhancement of osteoclastogenesis. IL-1β treatment upregulated the expression of inducible nitric oxide synthase, insulin-like growth factor 2 (IGF2), and the chemokines stromal cell derived factor 1, C-X3-C motif ligand 1 (CX3CL1), and CXCL7 in non-OCs. Neutralizing antibodies against these chemokines and IGF2 suppressed osteoclastogenesis in the presence of IL-1β. These results suggest that IL-1β enhances osteoclastogenesis by upregulating IGF2 and chemokine expression in non-OCs. |
| first_indexed | 2024-04-13T05:45:53Z |
| format | Article |
| id | doaj.art-63db6e9ba3dd472e959d57338d484385 |
| institution | Directory Open Access Journal |
| issn | 1347-8613 |
| language | English |
| last_indexed | 2024-04-13T05:45:53Z |
| publishDate | 2023-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Pharmacological Sciences |
| spelling | doaj.art-63db6e9ba3dd472e959d57338d4843852022-12-22T02:59:57ZengElsevierJournal of Pharmacological Sciences1347-86132023-01-01151118IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cellsYuto Otsuka0Takao Kondo1Hiromasa Aoki2Yoh Goto3Yohei Kawaguchi4Yuko Waguri-Nagaya5Ken Miyazawa6Shigemi Goto7Mineyoshi Aoyama8Department of Pathobiology, Nagoya City University Graduate School of Pharmaceutical Sciences, 3-1 Tanabe-dori, Mizuho-ku, Nagoya 467-8603, JapanDepartment of Pathobiology, Nagoya City University Graduate School of Pharmaceutical Sciences, 3-1 Tanabe-dori, Mizuho-ku, Nagoya 467-8603, JapanDepartment of Pathobiology, Nagoya City University Graduate School of Pharmaceutical Sciences, 3-1 Tanabe-dori, Mizuho-ku, Nagoya 467-8603, JapanDepartment of Orthodontics, School of Dentistry, Aichi-Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, JapanDepartment of Glial Cell Biology, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan; Department of Orthopaedic Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, JapanDepartment of Orthopaedic Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, JapanDepartment of Orthodontics, School of Dentistry, Aichi-Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, JapanDepartment of Orthodontics, School of Dentistry, Aichi-Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, JapanDepartment of Pathobiology, Nagoya City University Graduate School of Pharmaceutical Sciences, 3-1 Tanabe-dori, Mizuho-ku, Nagoya 467-8603, Japan; Corresponding author.Bone remodeling mediated by bone-forming osteoblasts (OBs) and bone-resorbing osteoclasts (OCs) maintains bone structure and function. Excessive OC activation leads to bone-destroying diseases such as osteoporosis and bone erosion of rheumatoid arthritis (RA). Differentiation of OCs from bone marrow cells (BMCs) is regulated by the bone microenvironment. The proinflammatory cytokine interleukin (IL)-1β reportedly enhances osteoclastogenesis and plays important roles in RA-associated bone loss. The present study investigated the effect of IL-1β on OC formation via microenvironmental cells. Treating mouse BMCs with IL-1β in the presence of receptor activator of NF-κB ligand and macrophage colony-stimulating factor increased the number of OCs. Real-time RT-PCR revealed increased expression of the IL-1β, IL-1RI, and IL-1RII genes in non-OCs compared with OCs. Removing CD45− cells which cannot differentiate into OCs, from mouse BMCs reduced the IL-1β–mediated enhancement of osteoclastogenesis. IL-1β treatment upregulated the expression of inducible nitric oxide synthase, insulin-like growth factor 2 (IGF2), and the chemokines stromal cell derived factor 1, C-X3-C motif ligand 1 (CX3CL1), and CXCL7 in non-OCs. Neutralizing antibodies against these chemokines and IGF2 suppressed osteoclastogenesis in the presence of IL-1β. These results suggest that IL-1β enhances osteoclastogenesis by upregulating IGF2 and chemokine expression in non-OCs.http://www.sciencedirect.com/science/article/pii/S1347861322000822OsteoclastIL-1βChemokineIGF2Microenvironment |
| spellingShingle | Yuto Otsuka Takao Kondo Hiromasa Aoki Yoh Goto Yohei Kawaguchi Yuko Waguri-Nagaya Ken Miyazawa Shigemi Goto Mineyoshi Aoyama IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells Journal of Pharmacological Sciences Osteoclast IL-1β Chemokine IGF2 Microenvironment |
| title | IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells |
| title_full | IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells |
| title_fullStr | IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells |
| title_full_unstemmed | IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells |
| title_short | IL-1β promotes osteoclastogenesis by increasing the expression of IGF2 and chemokines in non-osteoclastic cells |
| title_sort | il 1β promotes osteoclastogenesis by increasing the expression of igf2 and chemokines in non osteoclastic cells |
| topic | Osteoclast IL-1β Chemokine IGF2 Microenvironment |
| url | http://www.sciencedirect.com/science/article/pii/S1347861322000822 |
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