ArticlePloS one2016
C5a Induces the Synthesis of IL-6 and TNF-α in Rat Glomerular Mesangial Cells through MAPK Signaling Pathways.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
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- Action of the Terminal Complement Pathway on Cell Membranes.The Journal of membrane biology · 2025Review
- A comprehensive assessment of smokeless tobacco (Shammah) extract: unraveling the effects on hematological parameters, antioxidant defense mechanisms, and organ health in rats.Journal of molecular histology · 2025Article
- The Complement System.Advances in experimental medicine and biology · 2025Review
- The Effect and Mechanism of Fufang Banbianlian Injection in the Treatment of Mesangial Proliferative Glomerulonephritis.Combinatorial chemistry & high throughput screening · 2025Article
- Identification of key extracellular proteins as the potential biomarkers in thyroid eye disease.PloS one · 2025Article
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- In Vivo Pharmacodynamic Method to Assess Complement C5a Receptor Antagonist Efficacy.ACS pharmacology & translational science · 2022Article
- Aqueous Extract and Polysaccharide of Aconiti Lateralis Radix Induce Apoptosis and G0/G1 Phase Cell Cycle Arrest by PI3K/AKT/mTOR Signaling Pathway in Mesangial Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Protective role of host complement system inFrontiers in immunology · 2022Article
- Complement C5 inhibition protects against hemolytic anemia and acute kidney injury in anthrax peptidoglycan-induced sepsis in baboons.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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- A novel potential target of IL-35-regulated JAK/STAT signaling pathway in lupus nephritis.Clinical and translational medicine · 2021Article
- Network Pharmacology-Based Dissection of the Anti-diabetic Mechanism ofFrontiers in pharmacology · 2020Article
- An experimental study of exenatide effects on renal injury in diabetic rats1.Acta cirurgica brasileira · 2019Article
- Effects of Qi Teng Xiao Zhuo granules on circRNA expression profiles in rats with chronic glomerulonephritis.Drug design, development and therapy · 2019Article
- Pseudane-VII Isolated from Pseudoalteromonas sp. M2 Ameliorates LPS-Induced Inflammatory Response In Vitro and In Vivo.Marine drugs · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response has been reported to contribute to the renal lesions in rat Thy-1 nephritis (Thy-1N) as an animal model of human mesangioproliferative glomerulonephritis (MsPGN). Besides C5b-9 complex, C5a is also a potent pro-inflammatory mediator and correlated to severity of various nephritic diseases. However, the role of C5a in mediating pro-inflammatory cytokine production in rats with Thy-1N is poorly defined. In the present studies, the levels of C5a, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were first determined in the renal tissues of rats with Thy-1N. Then, the expression of IL-6 and TNF-α was detected in rat glomerular mesangial cells (GMC) stimulated with our recombinant rat C5a in vitro. Subsequently, the activation of mitogen-activated protein kinase (MAPK) signaling pathways (p38 MAPK, ERK1/2 and JNK) and their roles in the regulation of IL-6 and TNF-α production were examined in the GMC induced by C5a. The results showed that the levels of C5a, IL-6 and TNF-α were markedly increased in the renal tissues of Thy-1N rats. Rat C5a stimulation in vitro could up-regulate the expression of IL-6 and TNF-α in rat GMC, and the activation of MAPK signaling pathways was involved in the induction of IL-6 and TNF-α. Mechanically, p38 MAPK activation promoted IL-6 production, while either ERK1/2 or JNK activation promoted TNF-α production in the GMC with exposure to C5a. Taken together, these data implicate that C5a induces the synthesis of IL-6 and TNF-α in rat GMC through the activation of MAPK signaling pathways.
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