Related Experiment Video
Updated: Feb 19, 2026
Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
Published on: August 4, 2023
Monocyte-Derived Procoagulant Microvesicles Induced by High Glucose Can Be Attenuated by the Antioxidant
Mingzhen Li1, Xiao Zhang1, Jing Yu1
1Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Department of Diabetes and Gout, Tianjin Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University , Tianjin, China .
Background:
Microvesicles (MVs) are small membrane vesicles that are derived from many different cell types by a process of exocytic budding of the plasma membrane. MVs may be associated with a higher incidence of vascular disease in diabetic patients, but the mechanism of this association is unclear. Diabetic patients also show hypercoagulability and platelet hyperaggregability. In this study, we investigated the generation and activity of high glucose (HG)-induced MVs from monocytes to elucidate the potential mechanism of such MVs in diabetes.
Methods:
HG-induced MV generation from THP-1 monocytes before and after N-acetyl-L-cysteine (NAC) treatment was examined by enzyme-linked immunosorbent assay. MV activity was measured by spectrophotometry. Apoptosis and generation of reactive oxidative species (ROS) from THP-1 cells were detected by flow cytometry. Extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and P38/MAPK pathway components were also analyzed in treated monocytes.
Results:
MVs were generated from THP-1 cells after 20 hr of exposure to HG (4.6-fold higher than untreated control cells), which was concomitant with a 3.3-fold increase in apoptosis (P < 0.01). The procoagulant activity (PCA) of the generated MVs was increased significantly by 4.1-fold (P < 0.01) relative to untreated cells. ROS levels peaked 2 hr after HG exposure. The frequency of MVs was greatly decreased after NAC treatment (P < 0.01). Both the ERK/MAPK and P38/MAPK pathway were activated after HG stimulation, whereas treatment with a P38 inhibitor decreased MV generation by 66% compared to untreated control.
Conclusions:
The generation of monocyte-derived MVs induced by HG was associated with PCA, concomitant with apoptosis and ROS generation. The P38/MAPK pathway was partly involved in this process as evidenced by the reduction in MV generation following treatment with a P38 inhibitor. Our results could provide insights into novel mechanisms of thrombogenicity in an HG state.
Insights
High glucose induces microvesicles (MVs) from monocytes, increasing apoptosis, reactive oxidative species (ROS), and procoagulant activity (PCA). The P38/MAPK pathway partially mediates this, offering insights into diabetes-related thrombogenicity.
Area of Science:
- Cell Biology
- Biochemistry
- Pathophysiology
Background:
- Microvesicles (MVs) are implicated in vascular disease in diabetic patients.
- The precise mechanism linking MVs to diabetes-associated vascular complications remains unclear.
- Diabetic patients exhibit hypercoagulability and platelet hyperaggregability, suggesting a role for MVs.
Purpose of the Study:
- To investigate the generation and activity of high glucose (HG)-induced MVs from monocytes.
- To elucidate the potential role of these MVs in the pathogenesis of diabetes.
- To explore the involvement of specific signaling pathways in HG-induced MV production.
Main Methods:
- THP-1 monocytes were exposed to high glucose (HG) to induce MV generation.
- MV generation and procoagulant activity (PCA) were quantified.
- Apoptosis, reactive oxidative species (ROS) generation, and MAPK pathway activation (ERK/MAPK, P38/MAPK) were analyzed.
- N-acetyl-L-cysteine (NAC) and a P38 inhibitor were used to assess their effects on MV generation.
Main Results:
- HG exposure significantly increased MV generation from THP-1 monocytes.
- HG-induced MVs exhibited increased procoagulant activity (PCA).
- Apoptosis and ROS generation were elevated in HG-treated cells, and the P38/MAPK pathway was activated, with P38 inhibition reducing MV generation.
Conclusions:
- High glucose-induced monocyte-derived MVs are associated with increased PCA, apoptosis, and ROS generation.
- The P38/MAPK pathway plays a partial role in mediating HG-induced MV generation.
- These findings suggest novel mechanisms for thrombogenicity in the hyperglycemic state relevant to diabetes.
More Related Videos
09:35A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
Published on: November 15, 2024
10:59Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment
Published on: November 23, 2017