ArticleInflammation2019
CTGF Triggers Rat Astrocyte Activation and Astrocyte-Mediated Inflammatory Response in Culture Conditions.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.Cell cycle (Georgetown, Tex.) · 2026Article
- CTGF: The remodeler of the tumor immune microenvironment (Review).Oncology reports · 2026Review
- Advances in the role of astrocytes in glioma progression and therapy.Acta pharmacologica Sinica · 2026Review
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Metabolic-driven analytics of traumatic brain injury and neuroprotection by ethyl pyruvate.Journal of neuroinflammation · 2024Article
- Proteomic and transcriptomic profiling of brainstem, cerebellum and olfactory tissues in early- and late-phase COVID-19.Nature neuroscience · 2024Article
- The effect of dietary omega-6 fatty acid enrichment in rodent models of military-relevant acute traumatic psychological stress and traumatic brain injury.Frontiers in microbiomes · 2024Article
- Distinct developmental and degenerative functions of SARM1 require NAD+ hydrolase activity.PLoS genetics · 2022Article
- TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications.Biomedicines · 2022Review
- Role of RGC-32 in multiple sclerosis and neuroinflammation - few answers and many questions.Frontiers in immunology · 2022Review
- Neuroinflammation of traumatic brain injury: Roles of extracellular vesicles.Frontiers in immunology · 2022Review
- Transcriptomic profiling of high- and low-spiking regions reveals novel epileptogenic mechanisms in focal cortical dysplasia type II patients.Molecular brain · 2021Article
- Reactive Astrocytes in Central Nervous System Injury: Subgroup and Potential Therapy.Frontiers in cellular neuroscience · 2021Review
- Niche Cells Crosstalk In Neuroinflammation After Traumatic Brain Injury.International journal of biological sciences · 2021Review
- RGC-32 Regulates Generation of Reactive Astrocytes in Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2020Article
- Connective Tissue Growth Factor: From Molecular Understandings to Drug Discovery.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To improve clinical outcomes for patients with traumatic brain injury (TBI), it is necessary to explore the mechanism of traumatic brain injury (TBI)-induced neuroinflammation. Connective tissue growth factors (CTGF) have been reported to be involved in the process of inflammatory response or tissue repair, whereas whether and how CTGF participates in the astrocyte-mediated inflammation after TBI remains unclear. In the present study, the TBI-induced activation of astrocytes and augmentation of inflammatory response were simulated by stimulating rat astrocytes with TGF-β1 or CTGF in cultured conditions. TGF-β1 and CTGF both upregulated the expression of GFAP in astrocytes and facilitated the production of inflammatory cytokines and chemokines. Activation of astrocytes by CTGF is in an autocrine manner. According to the results of Boyden chamber assay, CTGF enhanced the recruitment of peripheral blood mononuclear cells (PBMCs) by reactive astrocytes. Besides, CTGF-mediated activation of astrocytes and augmentation of inflammatory response can be terminated by the inhibitor of ASK1 or p38 and JNK. Thus, our data suggested that CTGF could activate astrocytes in an autocrine manner and promote astrocyte-mediated inflammatory response by triggering the ASK1-p38/JNK-NF-κB/AP-1 pathways in astrocytes. Collectively, our study provided evidence that astrocyte-secreted CTGF serves as an amplifier of neuroinflammatory and could be a potential target for alleviating TBI-induced inflammation.
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Registered trials
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.