ArticleCancer management and research2012
The bradykinin B(2) receptor induces multiple cellular responses leading to the proliferation of human renal carcinoma cell lines.
Article in Cancer management and research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 11 citations in OpenAlex.
- A modular map of Bradykinin-mediated inflammatory signaling network.Journal of cell communication and signaling · 2022Article
- Renin angiotensin system deregulation as renal cancer risk factor.Oncology letters · 2017Article
- Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells.Oncotarget · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe vasoactive peptide bradykinin (BK) acts as a potent growth factor for normal kidney cells, but there have been few studies on the role of BK in renal cell carcinomas. PURPOSE: In this study, we tested the hypothesis that BK also acts as a mitogen in kidney carcinomas, and explored the effects of BK in human renal carcinoma A498 cells.
methodsThe presence of mRNAs for BK B(1) and BK B(2) receptors in A498 cells was demonstrated by reverse transcription-polymerase chain reaction. To study BK signaling pathways, we employed fluorescent measurements of intracellular Ca(2+), measured changes in extracellular pH as a reflection of Na(+)/H(+) exchange (NHE) with a Cytosensor microphysiometer, and assessed extracellular signal-regulated kinase (ERK) activation by Western blotting.
resultsExposure to 100 nM of BK resulted in the rapid elevation of intracellular Ca(2+), caused a ≥30% increase in NHE activity, and a ≥300% increase in ERK phosphorylation. All BK signals were blocked by HOE140, a BK B(2) receptor antagonist, but not by a B(1) receptor antagonist. Inhibitor studies suggest that BK-induced ERK activation requires phospholipase C and protein kinase C activities, and is Ca(2+)/calmodulin-dependent. The amiloride analog 5-(N-methyl-N-isobutyl)-amiloride (MIA) blocked short-term NHE activation and inhibited ERK phosphorylation, suggesting that NHE is critical for ERK activation by BK. BK induced an approximately 40% increase in the proliferation of A498 cells as assessed by bromodeoxyuridine uptake. This effect was blocked by the ERK inhibitor PD98059, and was dependent on NHE activity.
conclusionWe conclude that BK exerts mitogenic effects in A498 cells via the BK B(2) receptor activation of growth-associated NHE and ERK.
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