ArticleInflammation2003
Bradykinin stimulates MMP-2 production in guinea pig tracheal smooth muscle cells.
Article in Inflammation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- KLK12 Regulates MMP-1 and MMP-9 via Bradykinin Receptors: Biomarkers for Differentiating Latent and Active Bovine Tuberculosis.International journal of molecular sciences · 2022Article
- Matrix metalloproteinases: Expression, regulation and role in the immunopathology of tuberculosis.Cell proliferation · 2019Review
- Cardiac kallikrein-kinin system is upregulated in chronic volume overload and mediates an inflammatory induced collagen loss.PloS one · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The implication of bradykinin (BK) receptors in the release of the matrix metalloproteinase-2 (MMP-2; gelatinase A) was studied in guinea pig tracheal smooth muscle cells (GP-TSMC). Bradykinin (10(-8)-10(-4) M) induced a time- and concentration-dependent upregulation of MMP-2 production from cultured GP-TSMC. Pretreatment of the GP-TSMC with the bradykinin B2 receptor (BKB2-R) antagonist Hpp-HOE-140 (Hpp-D-Arg0-Hyp3-Thi5-D-Tic7-Oic8-BK; 10(-8)-10(-4) M) significantly inhibited the BK-stimulated upregulation of MMP-2 in GP-TSMC in a concentration-related manner. Conversely, GP-TSMC pretreated with the selective bradykinin B1 receptor (BKB1-R) antagonist R-954 (Ac-Om[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9BK; 10(-8)-10(-4) M) did not show any change in the response to BK. Moreover, the selective BKB2-R agonist Lys0BK (kallidin; 10(-8)-10(-4) M) stimulated whereas the selective BKB1-R agonist desArg9BK (DBK; 10(-8)-10(-4) M) had no effect on MMP-2 release from GP-TSMC. Further, the nonselective cyclooxygenase (COX) enzyme inhibitor indomethacin (IND; 10(-5) M), the glucocorticosteroid dexamethasone (DEX; 1 ng/mL) and the protein synthesis inhibitors, cycloheximide (CHX; 10(-6) M) and actinomycin D (ACT-D; 10(-8) M) also inhibited BK-induced MMP-2 release from GP-TSMC. These results provide the first evidence for the involvement of BK in the release of MMP-2 from airway smooth muscle cells through activation of the BKB2-R. Such response is mostly mediated by the induction of COX and the subsequent production of endogenous prostaglandins (PGs). It could therefore be suggested that MMP-2 might play a role in the process of airway remodeling.
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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.