ArticleMolecular pathology : MP2001
The control of ccn2 (ctgf) gene expression in normal and scleroderma fibroblasts.
Article in Molecular pathology : MP, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Recent advances on Hippo-YAP pathway in skin diseases.Frontiers in immunology · 2025Review
- Cysteine-rich domain of type III collagen N-propeptide inhibits fibroblast activation by attenuating TGFβ signaling.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- The Role of Increased Connective Tissue Growth Factor in the Pathogenesis of Oral Submucous Fibrosis and its Malignant Transformation-An Immunohistochemical Study.Head and neck pathology · 2021Article
- Concurrent YAP/TAZ and SMAD signaling mediate vocal fold fibrosis.Scientific reports · 2021Article
- CCN2/CTGF promotor activity in the developing and adult mouse eye.Cell and tissue research · 2021Article
- Proximal tubule LPA1 and LPA2 receptors use divergent signaling pathways to additively increase profibrotic cytokine secretion.American journal of physiology. Renal physiology · 2021Article
- Verteporfin treatment controls morphology, phenotype, and global gene expression for cells of the human nucleus pulposus.JOR spine · 2020Article
- HIF-hypoxia signaling in skeletal muscle physiology and fibrosis.Journal of cell communication and signaling · 2020Review
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- Hepatocyte nuclear factor 4α negatively regulates connective tissue growth factor during liver regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Quantitative relationships between SMAD dynamics and target gene activation kinetics in single live cells.Scientific reports · 2019Article
- Development of Normal and Cleft Palate: A Central Role for Connective Tissue Growth Factor (CTGF)/CCN2.Journal of developmental biology · 2018Review
- MEKK1, JNK, and SMAD3 mediate CXCL12-stimulated connective tissue growth factor expression in human lung fibroblasts.Journal of biomedical science · 2018Article
- Article
- Transforming growth factor β1 regulates the expression of CCN2 in human keratinocytes via Smad-ERK signalling.International wound journal · 2017Article
- Low-power laser irradiation inhibits arecoline-induced fibrosis: an in vitro study.International journal of oral science · 2017Article
- Antioxidants and NOX1/NOX4 inhibition blocks TGFβ1-induced CCN2 and α-SMA expression in dermal and gingival fibroblasts.PloS one · 2017Article
- Ageing in the musculoskeletal system.Acta orthopaedica · 2016Review
- Nanolayered siRNA delivery platforms for local silencing of CTGF reduce cutaneous scar contraction in third-degree burns.Biomaterials · 2016Article
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Although the role of transforming growth factor beta (TGFbeta) in initiating fibrosis is well established, the role that TGFbeta plays in maintaining fibrosis is unclear. The gene encoding connective tissue growth factor (ccn2; ctgf), which promotes fibrosis, is not normally expressed in dermal fibroblasts unless TGFbeta is present. However, in dermal fibroblasts cultured from lesional areas of scleroderma, ccn2 (ctgf) is expressed constitutively. The contribution of several elements in the ccn2 (ctgf) promoter to basal and TGFbeta induced ccn2 (ctgf) expression in normal and scleroderma fibroblasts has been investigated. A functional SMAD binding site in the ccn2 (ctgf) promoter that is necessary for the TGFbeta mediated induction of this gene has been identified. The previously termed TGFbeta responsive enhancer (TGFbetaRE) in the ccn2 (ctgf) promoter has been found to be necessary for basal promoter activity in normal fibroblasts. The SMAD element is not necessary for the high ccn2 (ctgf) promoter activity seen in scleroderma fibroblasts. However, mutation of the previously termed TGFbetaRE reduces ccn2 (ctgf) promoter activity in scleroderma fibroblasts to that seen in normal fibroblasts. Thus, the maintenance of the scleroderma phenotype, as assessed by a high degree of ccn2 (ctgf) promoter activity, appears to be relatively independent of SMAD action and seems to reflect increased basal promoter activity.
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Registered trials
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