Related Experiment Video

Updated: Jul 10, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader
07:13

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

C-reactive protein increases plasminogen activator inhibitor-1 expression in human endothelial cells

Changyi Chen1, Bicheng Nan, Peter Lin

  • 1The Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, United States. jchen@bcm.tmc.edu

Thrombosis Research
|October 24, 2007
PubMed

Insights

C-reactive protein (CRP) increases plasminogen activator inhibitor-1 (PAI-1) in endothelial cells. This effect involves oxidative stress and the p38 signaling pathway, suggesting mechanisms for cardiovascular disease development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Signaling

Background:

  • C-reactive protein (CRP) is a key inflammatory marker linked to cardiovascular disease (CVD).
  • The direct impact of CRP on endothelial cell function and gene expression, particularly PAI-1, remains incompletely understood.
  • Plasminogen activator inhibitor-1 (PAI-1) plays a crucial role in fibrinolysis and is implicated in thrombotic events.

Purpose of the Study:

  • To investigate the effects of C-reactive protein (CRP) on plasminogen activator inhibitor-1 (PAI-1) expression in human endothelial cells.
  • To elucidate the molecular mechanisms underlying CRP-induced PAI-1 expression, including receptor involvement and signaling pathways.
  • To determine if CRP influences PAI-1 expression across various human endothelial cell types.

Main Methods:

  • Human coronary artery endothelial cells (HCAEC) and other endothelial cell types were treated with varying concentrations and durations of CRP.
  • PAI-1 mRNA, protein levels, and enzyme activity were quantified.
  • CD32 receptor expression, MAPK p38 phosphorylation, and the effects of antioxidant curcumin were assessed.

Main Results:

  • CRP significantly upregulated PAI-1 mRNA, protein, and enzyme activity in HCAEC in a dose- and time-dependent manner.
  • CRP treatment increased CD32 receptor expression and enhanced MAPK p38 phosphorylation.
  • The CRP-induced PAI-1 expression was confirmed in multiple endothelial cell types and was inhibited by anti-CD32 antibody and curcumin.

Conclusions:

  • C-reactive protein (CRP) significantly elevates PAI-1 expression in human endothelial cells, including HCAEC.
  • CRP-induced PAI-1 expression is potentially mediated through oxidative stress and the p38 signaling pathway, possibly involving the CD32 receptor.
  • These findings provide insights into the molecular mechanisms linking inflammation and endothelial dysfunction in cardiovascular disease.

More Related Videos

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment10:59

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment

Published on: November 23, 2017

A Cell Culture Model of Resistance Arteries10:54

A Cell Culture Model of Resistance Arteries

Published on: September 8, 2017

Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...