ArticleJournal of cellular and molecular medicine2018
C5aR1 interacts with TLR2 in osteoblasts and stimulates the osteoclast-inducing chemokine CXCL10.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Effect of C5a Receptor Antagonist on the Osteogenic Differentiation of Dental Pulp Stem Cells.Clinical and experimental dental research · 2026Article
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Complement Proteins C1q-C5 as Context‑Dependent Regulators of Osteoblast Function and Fracture Healing: A Systematic Review.Orthopedic reviews · 2026Article
- The Crosstalk Between Sepsis-Associated Encephalopathy and Alzheimer's Disease: Identifying Potential Biomarkers and Therapeutic Targets for Cognition.Molecular neurobiology · 2025Article
- Subchondral osteoclasts and osteoarthritis: new insights and potential therapeutic avenues.Acta biochimica et biophysica Sinica · 2024Review
- Blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner.Cell death & disease · 2024Article
- Article
- Effects of circulating inflammatory proteins on osteoporosis and fractures: evidence from genetic correlation and Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Inhibition of C5AR1 impairs osteoclast mobilization and prevents bone loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- C3a-C3aR signaling is a novel modulator of skeletal homeostasis.Bone reports · 2023Article
- Novel insight into the underlying dysregulation mechanisms of immune cell-to-cell communication by analyzing multitissue single-cell atlas of two COVID-19 patients.Cell death & disease · 2023Article
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Functional and Expressional Analyses Reveal the Distinct Role of Complement Factor I in Regulating Complement System Activation during GCRV Infection inInternational journal of molecular sciences · 2022Article
- Increased Levels of C5a in Gingival Crevicular Fluid and Saliva of Patients with Periodontal Disease.Pathogens (Basel, Switzerland) · 2022Article
- Protein tyrosine phosphatases in skeletal development and diseases.Bone research · 2022Review
- Identification of TLR2 as a Key Target in Neuroinflammation in Vascular Dementia.Frontiers in genetics · 2022Article
- The role of C5a-C5aR1 axis in bone pathophysiology: A mini-review.Frontiers in cell and developmental biology · 2022Review
- Complement receptor C5aR1 on osteoblasts regulates osteoclastogenesis in experimental postmenopausal osteoporosis.Frontiers in endocrinology · 2022Article
- Functional Identification of Complement Factor D and Analysis of Its Expression during GCRV Infection in Grass Carp (International journal of molecular sciences · 2021Article
- Enhancement of innate and adaptive anti-tumor immunity by serum obtained from vascular photodynamic therapy-cured BALB/c mouse.Cancer immunology, immunotherapy : CII · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anaphylatoxin C5a is generated upon activation of the complement system, a crucial arm of innate immunity. C5a mediates proinflammatory actions via the C5a receptor C5aR1 and thereby promotes host defence, but also modulates tissue homeostasis. There is evidence that the C5a/C5aR1 axis is critically involved both in physiological bone turnover and in inflammatory conditions affecting bone, including osteoarthritis, periodontitis, and bone fractures. C5a induces the migration and secretion of proinflammatory cytokines of osteoblasts. However, the underlying mechanisms remain elusive. Therefore, in this study we aimed to determine C5a-mediated downstream signalling in osteoblasts. Using a whole-genome microarray approach, we demonstrate that C5a activates mitogen-activated protein kinases (MAPKs) and regulates the expression of genes involved in pathways related to insulin, transforming growth factor-β and the activator protein-1 transcription factor. Interestingly, using coimmunoprecipitation, we found an interaction between C5aR1 and Toll-like receptor 2 (TLR2) in osteoblasts. The C5aR1- and TLR2-signalling pathways converge on the activation of p38 MAPK and the generation of C-X-C motif chemokine 10, which functions, among others, as an osteoclastogenic factor. In conclusion, C5a-stimulated osteoblasts might modulate osteoclast activity and contribute to immunomodulation in inflammatory bone disorders.
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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.