ArticleScientific reports2022
Promotion of the inflammatory response in mid colon of complement component 3 knockout mice.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Bioinformatics analysis of proteins in the complement and coagulation cascades in colon cancer: Discovering the potential biomarker SERPINA1.Oncology letters · 2026Article
- Serum proteomics in paediatric inflammatory bowel disease from a case-control study: biomarker discovery and ulcerative colitis-Crohn's disease differentiation.EBioMedicine · 2026Article
- Therapeutic potency and the related mechanism of deinoxanthin in experimental animal and cell models of periodontitis.Scientific reports · 2026Article
- Dual roles of complement in ulcerative colitis: insights from clinical studies and animal research.European journal of medical research · 2025Review
- The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025Review
- Targeting the complement-mTOR-autophagy axis: the role of apolipoprotein E in depression.BMC biology · 2025Article
- Novel Therapeutic Effects ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Novel Role of theInternational journal of molecular sciences · 2024Article
- Complement C3-Deficiency-Induced Constipation in FVB/N-C3International journal of molecular sciences · 2023Article
- Identification of Novel Core Genes Involved in Malignant Transformation of Inflamed Colon Tissue Using a Computational Biology Approach and Verification in Murine Models.International journal of molecular sciences · 2023Article
- Protective Effects ofAntioxidants (Basel, Switzerland) · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- Dysregulation of the Enteric Nervous System in the Mid Colon of Complement Component 3 Knockout Mice with Constipation Phenotypes.International journal of molecular sciences · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To determine whether complement component 3 (C3) deficiency affects its receptor downstream-mediated inflammatory response, the current study was undertaken to measure alterations in the inducible nitric oxide synthase (iNOS)‑mediated cyclooxygenase‑2 (COX‑2) induction pathway, inflammasome pathway, nuclear factor-κB (NF-κB) activation, and inflammatory cytokine expressions in the mid colon of C3 knockout (KO) mice. Significant enhancement was observed in expressions of key components of the iNOS‑mediated COX‑2 induction pathway, and in the phosphorylation of mitogen‑activated protein (MAP) kinase members. A similar pattern of increase was also observed in the expression levels of inflammasome proteins in C3 KO mice. Moreover, compared to WT mice, C3 KO mice showed remarkably enhanced phosphorylation of NF-κB and Inhibitor of κB-α (IκB-α), which was reflected in entirety as increased expressions of Tumor necrosis factor (TNF), IL-6 and IL-1α. However, the levels of E-cadherin, tight junction channels and ion channels expressions were lower in the C3 KO mice, although myeloperoxidase (MPO) activity for neutrophils was slightly increased. Taken together, results of the current study indicate that C3 deficiency promotes inflammatory responses in the mid colon of C3 KO mice through activation of the iNOS‑mediated COX‑2 induction pathway, Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC)-inflammasome pathway and NF-κB signaling pathway, and the enhancement of inflammatory cytokine expressions.
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