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Updated: Jun 19, 2026
11:35
Decellularization and Recellularization Methodology for Human Saphenous Veins
Published on: July 27, 2018
Bone marrow-derived progenitor cells prevent thrombin-induced increase in lung vascular permeability
Yidan D Zhao1, Hiroshi Ohkawara, Stephen M Vogel
1Department of Pharmacology, Center for Lung and Vascular Biology, University of Illinois College of Medicine, 835 S. Wolcott Ave., Rm. E403-MSB, Chicago, IL 60612, USA. yyzhao@uic.edu
Summary
Bone marrow-derived progenitor cells (BMPCs) protect endothelial barrier function against thrombin. BMPCs prevent increased endothelial permeability by enhancing adherens junction integrity and activating Cdc42 signaling.
Area of Science:
- Vascular Biology
- Cellular Biology
- Regenerative Medicine
Background:
- Endothelial cells (ECs) form a barrier regulating vascular permeability.
- Thrombin increases endothelial permeability via adherens junction (AJ) disassembly and myosin light chain (MLC) phosphorylation.
- Bone marrow-derived progenitor cells (BMPCs) may influence endothelial barrier function.
Purpose of the Study:
- To investigate the effect of BMPCs on thrombin-induced endothelial hyperpermeability.
- To elucidate the molecular mechanisms underlying BMPC-mediated endothelial barrier protection.
Main Methods:
- Endothelial monolayers and mouse pulmonary microvessels were used to assess barrier function.
- Transendothelial electrical resistance (TEER) and microvessel filtration coefficient were measured.
- Vascular endothelial cadherin expression, Cdc42 activity, and MLC phosphorylation were analyzed.
- Small interfering RNA (siRNA) was used to deplete Cdc42 in ECs.
Main Results:
- BMPCs prevented the thrombin-induced decrease in TEER and increase in microvessel filtration coefficient.
- BMPC treatment increased vascular endothelial cadherin expression and Cdc42 activity in ECs.
- Cdc42 depletion abrogated the BMPC-induced endothelial barrier protection.
- BMPCs inhibited thrombin-induced MLC phosphorylation in ECs.
Conclusions:
- BMPCs protect endothelial barrier integrity against thrombin-induced hyperpermeability.
- This protection involves adherens junction annealing, Cdc42 activation, and inhibition of MLC phosphorylation.
- BMPCs represent a potential therapeutic strategy for vascular barrier dysfunction.
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