ArticleAmerican journal of respiratory cell and molecular biology2006
PKCalpha mediates CCL18-stimulated collagen production in pulmonary fibroblasts.
Article in American journal of respiratory cell and molecular biology, 2006. 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, 38 citations in OpenAlex.
- Review
- Review
- Wild-type S100A3 and S100A13 restore calcium homeostasis and mitigate mitochondrial dysregulation in pulmonary fibrosis patient-derived cells.Frontiers in cell and developmental biology · 2023Article
- A multi-cellular molecular signaling and functional network map of C-C motif chemokine ligand 18 (CCL18): a chemokine with immunosuppressive and pro-tumor functions.Journal of cell communication and signaling · 2022Article
- CCL18 in the Progression of Cancer.International journal of molecular sciences · 2020Review
- Role of phospholipase D in bleomycin-induced mitochondrial reactive oxygen species generation, mitochondrial DNA damage, and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Sustained low peritoneal effluent CCL18 levels are associated with preservation of peritoneal membrane function in peritoneal dialysis.PloS one · 2017Article
- Epigenetic regulation of diacylglycerol kinase alpha promotes radiation-induced fibrosis.Nature communications · 2016Article
- Prostaglandin Transporter (PGT/SLCO2A1) Protects the Lung from Bleomycin-Induced Fibrosis.PloS one · 2015Article
- IFN-γ directly controls IL-33 protein level through a STAT1- and LMP2-dependent mechanism.The Journal of biological chemistry · 2014Article
- Impact of endobronchial allergen provocation on macrophage phenotype in asthmatics.BMC immunology · 2014Article
- Interleukin-33 potentiates bleomycin-induced lung injury.American journal of respiratory cell and molecular biology · 2013Article
- Thrombin induces epithelial-mesenchymal transition via PAR-1, PKC, and ERK1/2 pathways in A549 cells.Experimental lung research · 2013Article
- Segmental allergen challenge enhances chitinase activity and levels of CCL18 in mild atopic asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2013Article
- Cytokines in chronic respiratory diseases.F1000 biology reports · 2013Article
- Molecular and cellular mechanisms of pulmonary fibrosis.Fibrogenesis & tissue repair · 2012Article
- Full-length IL-33 promotes inflammation but not Th2 response in vivo in an ST2-independent fashion.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Regulation of pulmonary inflammation and fibrosis through expression of integrins alphaVbeta3 and alphaVbeta5 on pulmonary T lymphocytes.Arthritis and rheumatism · 2009Article
- PKCdelta mediates thrombin-augmented fibroblast-mediated collagen gel contraction.Biochemical and biophysical research communications · 2008Article
- Macrophages produce TGF-beta-induced (beta-ig-h3) following ingestion of apoptotic cells and regulate MMP14 levels and collagen turnover in fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A CC chemokine, CCL18, has been previously reported to stimulate collagen production in pulmonary fibroblasts. This study focused on the role of protein kinase C (PKC) in the profibrotic signaling activated by CCL18 in pulmonary fibroblasts. Of the three PKC isoforms that are predominantly expressed in fibroblasts (PKCalpha, PKCdelta, and PKCepsilon), two isoforms (PKCdelta and PKCepsilon) have been implicated in profibrotic intracellular signaling. The role of PKCalpha-mediated signaling in the regulation of collagen production remains unclear. In this study, PKCalpha was found mostly in the cytoplasm, whereas PKCdelta and PKCepsilon were found mostly in the nucleus of cultured primary pulmonary fibroblasts. In response to stimulation with CCL18, PKCalpha but not PKCdelta or PKCepsilon underwent rapid (within 5-10 min) transient phosphorylation and nuclear translocation. Inhibition with dominant-negative mutants of PKCalpha and ERK2, but not PKCdelta or PKCepsilon, abrogated CCL18-stimulated ERK2 phosphorylation and collagen production. The effect of CCL18 on collagen production and the activity of collagen promoter reporter constructs were also abrogated by a selective pharmacologic inhibitor of PKCalpha Gö6976. Stimulation of fibroblasts with CCL18 caused an increase in intracellular calcium concentration. Consistent with the known calcium dependence of PKCalpha signaling, blocking of the calcium signaling with the intracellular calcium-chelating agent BAPTA led to abrogation of PKCalpha nuclear translocation, ERK2 phosphorylation, and collagen production. These observations suggest that in primary pulmonary fibroblasts, PKCalpha but not PKCdelta or PKCepsilon mediate the profibrotic effect of CCL18. PKCalpha may therefore become a viable target for future antifibrotic therapies.
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