ArticleFree radical biology & medicine2014
Upregulation of cannabinoid receptor-1 and fibrotic activation of mouse hepatic stellate cells during Schistosoma J. infection: role of NADPH oxidase.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Unveiling the toxic effects of perfluorooctanoic acid on osteoblast function and extracellular matrix deposition using 2D and 3D models.Cell death discovery · 2026Article
- TIGIT impairs NK cell antifibrotic activity through the IFNγ-IFI30 axis in schistosomiasis-induced liver fibrosis.Frontiers in immunology · 2026Article
- NLRP3 inflammasome inhibition decreasesInfection and immunity · 2024Article
- Review
- Inflammation and Nitro-oxidative Stress as Drivers of Endocannabinoid System Aberrations in Mood Disorders and Schizophrenia.Molecular neurobiology · 2022Review
- Trickle infection withFrontiers in immunology · 2022Article
- Article
- Schistosome eggs stimulate reactive oxygen species production to enhance M2 macrophage differentiation and promote hepatic pathology in schistosomiasis.PLoS neglected tropical diseases · 2021Article
- Endocannabinoid System and Its Regulation by Polyunsaturated Fatty Acids and Full Spectrum Hemp Oils.International journal of molecular sciences · 2021Review
- Release and Actions of Inflammatory Exosomes in Pulmonary Emphysema: Potential Therapeutic Target of Acupuncture.Journal of inflammation research · 2021Article
- Downregulation of the CB1-Mediated Endocannabinoid Signaling Underlies D-Galactose-Induced Memory Impairment.Frontiers in molecular neuroscience · 2020Article
- The role of microRNAs in the pathogenesis, grading and treatment of hepatic fibrosis in schistosomiasis.Parasites & vectors · 2019Review
- Cannabinoid receptor-1 antagonism: a new perspective on treating a murine schistosomal liver fibrosis model.Memorias do Instituto Oswaldo Cruz · 2019Article
- Modulation of the Oxidative Stress and Lipid Peroxidation by Endocannabinoids and Their Lipid Analogues.Antioxidants (Basel, Switzerland) · 2018Review
- Article
- NLRP3 inflammasome activation results in liver inflammation and fibrosis in mice infected with Schistosoma japonicum in a Syk-dependent manner.Scientific reports · 2017Article
- Targeting cannabinoid signaling for peritoneal dialysis-induced oxidative stress and fibrosis.World journal of nephrology · 2017Review
- Therapeutic Potential of Novel Twin Compounds Containing Tetramethylpyrazine and Carnitine Substructures in Experimental Ischemic Stroke.Oxidative medicine and cellular longevity · 2017Article
- Activation of NLRP3 inflammasomes in mouse hepatic stellate cells during Schistosoma J. infection.Oncotarget · 2016Article
- Modulation of cellular redox homeostasis by the endocannabinoid system.Open biology · 2016Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The endocannabinoid system (CS) has been implicated in the development of hepatic fibrosis such as schistosomiasis-associated liver fibrosis (SSLF). However, the mechanisms mediating the action of the CS in hepatic fibrosis are unclear. The present study hypothesized that Schistosoma J. infection upregulates cannabinoid receptor 1 (CB1) due to activation of NADPH oxidase leading to a fibrotic phenotype in hepatic stellate cells (HSCs). The SSLF model was developed by infecting mice with Schistosoma J. cercariae in the skin, and HSCs from control and infected mice were then isolated, cultured, and confirmed by analysis of HSC markers α-SMA and desmin. CB1 significantly increased in HSCs isolated from mice with SSLF, which was accompanied by a greater expression of fibrotic markers α-SMA, collagen I, and TIMP-1. CB1 upregulation and enhanced fibrotic changes were also observed in normal HSCs treated with soluble egg antigen (SEA) from Schistosoma J. Electron spin resonance (ESR) analysis further demonstrated that superoxide (O2(-)) production was increased in infected HSCs or normal HSCs stimulated with SEA. Both Nox4 and Nox1 siRNA prevented SEA-induced upregulation of CB1, α-SMA, collagen I, and TIMP-1 by inhibition of O2(-) production, while CB1 siRNA blocked SEA-induced fibrotic changes without effect on O2(-) production in these HSCs. Taken together, these data suggest that the fibrotic activation of HSCs on Schistosoma J. infection or SEA stimulation is associated with NADPH oxidase-mediated redox regulation of CB1 expression, which may be a triggering mechanism for SSLF.
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