ArticleThe Journal of allergy and clinical immunology2023
C1 inhibitor and prolylcarboxypeptidase modulate prekallikrein activation on endothelial cells.
Article in The Journal of allergy and clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Bradykinin contributes to vasogenic edema in murine experimental cerebral malaria.The Journal of clinical investigation · 2026Article
- Therapeutic Targeting of the Bradykinin B2 Receptor in Immunological and Vascular Diseases: Insights from Kinin Biology to Clinical Outcomes.Clinical reviews in allergy & immunology · 2026Review
- Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture.Molecules (Basel, Switzerland) · 2024Article
- Is there a role for bradykinin in cerebral malaria pathogenesis?Frontiers in cellular and infection microbiology · 2023Review
- A study on the molecular mechanism of cardiac protection of procarboxylpeptidase in MIRI rats based on the NLRP3 signaling pathway.Science progressArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe examined how prekallikrein (PK) activation on human microvascular endothelial cells (HMVECs) is regulated by the ambient concentration of C1 inhibitor (C1INH) and prolylcarboxypeptidase (PRCP).
objectiveWe sought to examine the specificity of PK activation on HMVECs by PRCP and the role of C1INH to regulate it, high-molecular-weight kininogen (HK) cleavage, and bradykinin (BK) liberation.
methodsInvestigations were performed on cultured HMVECs. Immunofluorescence, enzymatic activity assays, immunoblots, small interfering RNA knockdowns, and cell transfections were used to perform these studies.
resultsCultured HMVECs constitutively coexpressed PK, HK, C1INH, and PRCP. PK activation on HMVECs was modulated by the ambient C1INH concentration. In the absence of C1INH, forming PKa on HMVECs cleaved 120-kDa HK completely to a 65-kDa H-chain and a 46-kDa L-chain in 60 minutes. In the presence of 2 μM C1INH, only 50% of the HK became cleaved. C1INH concentrations (0.0-2.5 μM) decreased but did not abolish BK liberated from HK by activated PK. Factor XII did not activate when incubated with HMVECs alone for 1 hour. However, if incubated in the presence of HK and PK, factor XII became activated. The specificity of PK activation on HMVECs by PRCP was shown by several inhibitors to each enzyme. Furthermore, PRCP small interfering RNA knockdowns magnified C1INH inhibitory activity on PK activation, and PRCP transfections reduced C1INH inhibition at any given concentration.
conclusionsThese combined studies indicated that on HMVECs, PK activation and HK cleavage to liberate BK were modulated by the local concentrations of C1INH and PRCP.
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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.