dc.contributor.author |
Boss, Anna L |
|
dc.contributor.author |
Chamley, Lawrence W |
|
dc.contributor.author |
Brooks, Anna ES |
|
dc.contributor.author |
James, Joanna L |
|
dc.coverage.spatial |
England |
|
dc.date.accessioned |
2024-02-07T03:09:01Z |
|
dc.date.available |
2024-02-07T03:09:01Z |
|
dc.date.issued |
2023-11 |
|
dc.identifier.citation |
(2023). Molecular Human Reproduction, 29(12), gaad041-. |
|
dc.identifier.issn |
1360-9947 |
|
dc.identifier.uri |
https://hdl.handle.net/2292/67395 |
|
dc.description.abstract |
Growth-restricted placentae have a reduced vascular network, impairing exchange of nutrients and oxygen. However, little is known about the differentiation events and cell types that underpin normal/abnormal placental vascular formation and function. Here, we used 23-colour flow cytometry to characterize placental vascular/perivascular populations between first trimester and term, and in foetal growth restriction (FGR). First-trimester endothelial cells had an immature phenotype (CD144+/lowCD36-CD146low), while term endothelial cells expressed mature endothelial markers (CD36+CD146+). At term, a distinct population of CD31low endothelial cells co-expressed mesenchymal markers (CD90, CD26), indicating a capacity for endothelial to mesenchymal transition (EndMT). In FGR, compared with normal pregnancies, endothelial cells constituted 3-fold fewer villous core cells (P < 0.05), contributing to an increased perivascular: endothelial cell ratio (2.6-fold, P < 0.05). This suggests that abnormal EndMT may play a role in FGR. First-trimester endothelial cells underwent EndMT in culture, losing endothelial (CD31, CD34, CD144) and gaining mesenchymal (CD90, CD26) marker expression. Together this highlights how differences in villous core cell heterogeneity and phenotype may contribute to FGR pathophysiology across gestation. |
|
dc.format.medium |
Print |
|
dc.language |
eng |
|
dc.publisher |
Oxford University Press (OUP) |
|
dc.relation.ispartofseries |
Molecular human reproduction |
|
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. |
|
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
|
dc.rights.uri |
https://creativecommons.org/ licenses/by-nc/4.0/ |
|
dc.subject |
Endothelial Cells |
|
dc.subject |
Placenta |
|
dc.subject |
Humans |
|
dc.subject |
Fetal Growth Retardation |
|
dc.subject |
Pregnancy |
|
dc.subject |
Pregnancy Trimester, First |
|
dc.subject |
Female |
|
dc.subject |
Dipeptidyl Peptidase 4 |
|
dc.subject |
cell heterogeneity |
|
dc.subject |
endothelial to mesenchymal transition |
|
dc.subject |
foetal growth restriction |
|
dc.subject |
high-dimensional flow cytometry |
|
dc.subject |
vascular development |
|
dc.subject |
3215 Reproductive Medicine |
|
dc.subject |
32 Biomedical and Clinical Sciences |
|
dc.subject |
Pediatric Research Initiative |
|
dc.subject |
Clinical Research |
|
dc.subject |
2.1 Biological and endogenous factors |
|
dc.subject |
1.1 Normal biological development and functioning |
|
dc.subject |
2 Aetiology |
|
dc.subject |
1 Underpinning research |
|
dc.subject |
Reproductive health and childbirth |
|
dc.subject |
Science & Technology |
|
dc.subject |
Life Sciences & Biomedicine |
|
dc.subject |
Developmental Biology |
|
dc.subject |
Obstetrics & Gynecology |
|
dc.subject |
Reproductive Biology |
|
dc.subject |
MESENCHYMAL TRANSITION |
|
dc.subject |
ANGIOGENESIS |
|
dc.subject |
DIFFERENTIATION |
|
dc.subject |
VASCULOGENESIS |
|
dc.subject |
STILLBIRTH |
|
dc.subject |
EXPRESSION |
|
dc.subject |
GESTATION |
|
dc.subject |
ORIGINS |
|
dc.subject |
DISEASE |
|
dc.subject |
ARTERY |
|
dc.subject |
0606 Physiology |
|
dc.subject |
1103 Clinical Sciences |
|
dc.subject |
1114 Paediatrics and Reproductive Medicine |
|
dc.subject |
3101 Biochemistry and cell biology |
|
dc.title |
Human placental vascular and perivascular cell heterogeneity differs between first trimester and term, and in pregnancies affected by foetal growth restriction |
|
dc.type |
Journal Article |
|
dc.identifier.doi |
10.1093/molehr/gaad041 |
|
pubs.issue |
12 |
|
pubs.begin-page |
gaad041 |
|
pubs.volume |
29 |
|
dc.date.updated |
2024-01-25T01:35:42Z |
|
dc.rights.holder |
Copyright: The authors |
en |
dc.identifier.pmid |
38059603 (pubmed) |
|
pubs.author-url |
https://academic.oup.com/molehr/article/29/12/gaad041/7459907 |
|
pubs.publication-status |
Published |
|
dc.rights.accessrights |
http://purl.org/eprint/accessRights/OpenAccess |
en |
pubs.subtype |
research-article |
|
pubs.subtype |
Journal Article |
|
pubs.elements-id |
1002862 |
|
pubs.org-id |
Medical and Health Sciences |
|
pubs.org-id |
School of Medicine |
|
pubs.org-id |
Obstetrics and Gynaecology |
|
dc.identifier.eissn |
1460-2407 |
|
dc.identifier.pii |
7459907 |
|
pubs.number |
ARTN gaad041 |
|
pubs.record-created-at-source-date |
2024-01-25 |
|
pubs.online-publication-date |
2023-12-06 |
|