ArticleAmerican journal of physiology. Cell physiology2009
Protein kinase D mediates synergistic expression of COX-2 induced by TNF-{alpha} and bradykinin in human colonic myofibroblasts.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Activation of the Piezo1 channel stimulates protein kinase D and migration in human aortic endothelial cells.American journal of physiology. Cell physiology · 2025Article
- Article
- Statins inhibit protein kinase D (PKD) activation in intestinal cells and prevent PKD1-induced growth of murine enteroids.American journal of physiology. Cell physiology · 2023Article
- Multifaceted Functions of Protein Kinase D in Pathological Processes and Human Diseases.Biomolecules · 2021Review
- Angiogenin regulates PKD activation and COX-2 expression induced by TNF-α and bradykinin in the colonic myofibroblast.Biochemical and biophysical research communications · 2020Article
- Protein kinase Cε regulates nuclear translocation of extracellular signal-regulated kinase, which contributes to bradykinin-induced cyclooxygenase-2 expression.Scientific reports · 2018Article
- Protein kinase D signaling in cancer: A friend or foe?Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Bradykinin stimulates protein kinase D-mediated colonic myofibroblast migration via cyclooxygenase-2 and heat shock protein 27.The Journal of surgical research · 2017Article
- TNF-α stimulates colonic myofibroblast migration via COX-2 and Hsp27.The Journal of surgical research · 2016Article
- Protein kinase D interacts with neuronal nitric oxide synthase and phosphorylates the activatory residue serine 1412.PloS one · 2014Article
- Isolation of primary myofibroblasts from mouse and human colon tissue.Journal of visualized experiments : JoVE · 2013Article
- TNF-α and LPA promote synergistic expression of COX-2 in human colonic myofibroblasts: role of LPA-mediated transactivation of upregulated EGFR.BMC gastroenterology · 2013Article
- Anti-melanin-concentrating hormone treatment attenuates chronic experimental colitis and fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- TNF-α induces upregulation of EGFR expression and signaling in human colonic myofibroblasts.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Serum concentrations of cyclooxygenase-2 in patients with systemic sclerosis: association with lower frequency of pulmonary fibrosis.Journal of clinical immunology · 2012Article
- Protein kinase D1 mediates synergistic MMP-3 expression induced by TNF-α and bradykinin in human colonic myofibroblasts.Biochemical and biophysical research communications · 2011Article
- TNF-α potentiates lysophosphatidic acid-induced COX-2 expression via PKD in human colonic myofibroblasts.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Protein kinase D signaling: multiple biological functions in health and disease.Physiology (Bethesda, Md.) · 2011Review
- Role of protein kinase D signaling in pancreatic cancer.Biochemical pharmacology · 2010Review
- Mechanistic insight into the ability of American ginseng to suppress colon cancer associated with colitis.Carcinogenesis · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Myofibroblasts have recently been identified as major mediators of tumor necrosis factor-alpha (TNF-alpha)-associated colitis, but the precise mechanism(s) involved remains incompletely understood. In particular, the possibility that TNF-alpha signaling cross talks with other proinflammatory mediators, including bradykinin (BK), has not been examined in these cells. Here we show that treatment of 18Co cells, a model of human colonic myofibroblasts, with BK and TNF-alpha induced striking synergistic COX-2 protein expression that was paralleled by increases in the levels of transcripts encoding COX-2 and microsomal prostaglandin E synthase 1 (mPGES-1) and by the production of PGE(2). COX-2 expression in 18Co cells treated with BK and TNF-alpha was prevented by the B(2) BK receptor antagonist HOE-140, the preferential protein kinase C (PKC) inhibitors Ro31-8220 and GF-109203X, and Gö-6976, an inhibitor of conventional PKCs and protein kinase D (PKD). In a parallel fashion, TNF-alpha, while having no detectable effect on the activation of PKD when added alone, augmented PKD activation induced by BK, as measured by PKD phosphorylation at its activation loop (Ser(744)) and autophosphorylation site (Ser(916)). BK-induced PKD activation was also inhibited by HOE-140, Ro31-8220, and Gö-6976. Transfection of 18Co cells with small interfering RNA targeting PKD completely inhibited the synergistic increase in COX-2 protein in response to BK and TNF-alpha, demonstrating, for the first time, a critical role of PKD in the pathways leading to synergistic expression of COX-2. Our results imply that cross talk between TNF-alpha and BK amplifies a PKD phosphorylation cascade that mediates synergistic COX-2 expression in colonic myofibroblasts. It is plausible that PKD increases COX-2 expression in colonic myofibroblasts to promote an inflammatory microenvironment that supports tumor growth.
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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.