ArticleJournal of inflammation (London, England)2009
Upregulation of prolylcarboxypeptidase (PRCP) in lipopolysaccharide (LPS) treated endothelium promotes inflammation.
Article in Journal of inflammation (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 39 citations in OpenAlex.
- Specimen Inactivation Methods for Proteomics─Comparisons of Irradiation, Chemical, and Heat Treatments on Downstream Serum Analyses.Journal of proteome research · 2025Article
- Bradykinin B1 receptor signaling triggers complement activation on endothelial cells.Frontiers in immunology · 2025Article
- Increased Prolylcarboxypeptidase Expression Can Serve as a Biomarker of Senescence in Culture.Molecules (Basel, Switzerland) · 2024Article
- Increased Expression of NOTCH-1 and T Helper Cell Transcription Factors in Patients with Acquired Aplastic Anemia.Iranian biomedical journal · 2023Article
- Prolyl Carboxypeptidase Activity Is Present in Human Adipose Tissue and Is Elevated in Serum of Obese Men with Type 2 Diabetes.International journal of molecular sciences · 2022Article
- Prolyl Carboxypeptidase Mediates the C-Terminal Cleavage of (Pyr)-Apelin-13 in Human Umbilical Vein and Aortic Endothelial Cells.International journal of molecular sciences · 2021Article
- A comprehensive review of COVID-19 characteristics.Biological procedures online · 2020Review
- Pro-opiomelanocortin and its Processing Enzymes Associate with Plaque Stability in Human Atherosclerosis - Tampere Vascular Study.Scientific reports · 2018Article
- Prolyl carboxypeptidase activity in the circulation and its correlation with body weight and adipose tissue in lean and obese subjects.PloS one · 2018Article
- Prolyl carboxypeptidase activity decline correlates with severity and short-term outcome in acute ischemic stroke.Neurochemical research · 2015Article
- Genetic determinants in the development of sensitization to environmental allergens in early childhood.Immunity, inflammation and disease · 2014Article
- Article
- Prolyl carboxypeptidase and its inhibitors in metabolism.Trends in endocrinology and metabolism: TEM · 2013Article
- Angiotensin II type 2 receptor-stimulated activation of plasma prekallikrein and bradykinin release: role of SHP-1.American journal of physiology. Heart and circulatory physiology · 2012Article
- Enzymatic processing of angiotensin peptides by human glomerular endothelial cells.American journal of physiology. Renal physiology · 2012Article
- PF-04886847 (an inhibitor of plasma kallikrein) attenuates inflammatory mediators and activation of blood coagulation in rat model of lipopolysaccharide (LPS)-induced sepsis.Cardiovascular & hematological agents in medicinal chemistry · 2012Article
- Influence of a novel inhibitor (UM8190) of prolylcarboxypeptidase (PRCP) on appetite and thrombosis.Current medicinal chemistry · 2012Article
- High molecular weight kininogen activates B2 receptor signaling pathway in human vascular endothelial cells.The Journal of biological chemistry · 2011Article
- The kallikrein-kinin system as a regulator of cardiovascular and renal function.Comprehensive Physiology · 2011Review
- Highly selective hydrolysis of kinins by recombinant prolylcarboxypeptidase.Biochemical and biophysical research communications · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProlylcarboxypeptidase (Prcp) gene, along with altered PRCP and kallikrein levels, have been implicated in inflammation pathogenesis. PRCP regulates angiotensin 1-7 (Ang 1-7) - and bradykinin (BK) - stimulated nitric oxide production in endothelial cells. The mechanism through which kallikrein expression is altered during infection is not fully understood. Investigations were performed to determine the association between PRCP and kallikrein levels as a function of the upregulation of PRCP expression and the link between PRCP and inflammation risk in lipopolysaccharide (LPS)-induced endothelium activation.
methodsThe Prcp transcript expression in LPS-induced human umbilical vein endothelial cells (HUVEC) activation was determined by RT-PCR for mRNA. PRCP-dependent kallikrein pathway was determined either by Enzyme Linked ImmunoSorbent Assay (ELISA) or by biochemical assay.
resultsWe report that PRCP is critical to the maintenance of the endothelial cells, and its upregulation contributes to the risk of developing inflammation. Significant elevation in kallikrein was seen on LPS-treated HUVECs. The conversion of PK to kallikrein was blocked by the inhibitor of PRCP, suggesting that PRCP might be a risk factor for inflammation.
conclusionThe increased PRCP lead to a sustained production of bradykinin in endothelium following LPS treatment. This amplification may be an additional mechanism whereby PRCP promotes a sustained inflammatory response. A better appreciation of the role of PRCP in endothelium may contribute to a better understanding of inflammatory vascular disorders and to the development of a novel treatment.
Identifiers
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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.