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| Status |
Public on Nov 30, 2021 |
| Title |
VE-cadherin is essential for trophoblast migration and endovascular invasion |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Vascular endothelial (VE-)cadherin is a homotypic adhesion protein that is expressed selectively by ECs in which it enables formation of tight vessels and regulation of vascular permeability. Since VE-cadherin is also strongly expressed in placental trophoblasts, it is a prime candidate for a molecular mechanism of vascular mimicry by those cells. Here, we show that the VE-cadherin is required for trophoblast migration and endovascular invasion into the maternal decidua. VE-cadherin deficiency results in loss of spiral artery remodeling due to a lack of invasive trophoblasts, leading to decreased flow of maternal blood into the placenta, fetal growth retardation and death. Loss of trophoblast invasion prevents decidualization, extracellular matrix remodeling, and immune cell clearance. These studies identify VE-cadherin as essential for trophoblast migration and coordination of decidual changes during endovascular invasion. They further suggest endothelial proteins such as VE-cadherin that are expressed by trophoblasts may play functionally distinct roles that do not simply mimic those in ECs.
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| Overall design |
Examination of E12.5 deciduas from control and trophoblast-specific VE-cadherin knockout placentas
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| Contributor(s) |
Derek C S, Mark L K, Apoorva B |
| Citation(s) |
35486098 |
| |
| Submission date |
Nov 23, 2021 |
| Last update date |
May 25, 2022 |
| Contact name |
Apoorva Babu |
| Organization name |
University of Pennsylvania
|
| Department |
Cardiovascular Institute
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| Street address |
SCTR, 3400 Civic Center Blvd
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| City |
Philadelphia |
| State/province |
PA |
| ZIP/Postal code |
19104 |
| Country |
USA |
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| Platforms (1) |
| GPL17021 |
Illumina HiSeq 2500 (Mus musculus) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA782961 |
| SRA |
SRP347431 |