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Published on: June 7, 2022
Increased endothelial cell permeability in endoglin-deficient cells.
Mirjana Jerkic1, Michelle Letarte2
1*Molecular Structure and Function Program, The Hospital for Sick Children, Toronto, Ontario, Canada; and Department of Immunology and Keenan Research Centre for Biomedical Science, Anesthesia Research, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada jerkicm@smh.ca.
Endoglin (ENG) deficiency increases vascular permeability by activating RhoA and destabilizing endothelial barriers. This finding is crucial for understanding vascular dysplasia and hemorrhages.
Area of Science:
- Vascular Biology
- Cell Biology
- Biochemistry
Background:
- Endoglin (ENG) is vital for vascular endothelium integrity.
- ENG mutations cause vascular dysplasia and hemorrhages.
- ENG's role in regulating vascular permeability was investigated.
Purpose of the Study:
- To assess the impact of ENG deficiency on endothelial cell (EC) permeability.
- To elucidate the molecular mechanisms underlying ENG-mediated vascular permeability.
Main Methods:
- Comparison of permeability in Eng(-/-), Eng(+/-), and Eng(+/+) mouse embryonic ECs using fluorescent dextran.
- Analysis of protein expression and activity, including RhoA, thrombospondin-1, and VEGF receptor 2.
- Assessment of neutrophil transmigration.
Main Results:
- Eng(-/-) and Eng(+/-) ECs exhibited significantly increased permeability (2.9- and 1.7-fold, respectively).
- Prolonged starvation exacerbated permeability in Eng(-/-) ECs.
- Constitutive RhoA activation and altered expression of barrier-associated proteins were observed in ENG-deficient ECs.
Conclusions:
- ENG deficiency leads to endothelial hyperpermeability.
- Constitutive RhoA activation and endothelial barrier destabilization are key mechanisms.
- Findings highlight ENG's critical role in maintaining vascular integrity.
