Possible Association between Cathepsin V and the Development of Placenta Accreta Spectrum Disorders.
ADAM Proteins
/ metabolism
Adult
Cathepsins
/ metabolism
Cell Adhesion
/ genetics
Cysteine Endopeptidases
/ metabolism
Female
Humans
Immunohistochemistry
Matrix Metalloproteinases, Secreted
/ metabolism
Myometrium
/ metabolism
Placenta
/ metabolism
Placenta Accreta
/ genetics
Pregnancy
Retrospective Studies
Trophoblasts
/ metabolism
Abnormally invasive placenta
Adherent placenta
Biomarker
Pathogenesis
Placenta creta
Proteinase
Journal
Gynecologic and obstetric investigation
ISSN: 1423-002X
Titre abrégé: Gynecol Obstet Invest
Pays: Switzerland
ID NLM: 7900587
Informations de publication
Date de publication:
2019
2019
Historique:
received:
13
08
2018
accepted:
07
01
2019
pubmed:
14
2
2019
medline:
24
10
2019
entrez:
14
2
2019
Statut:
ppublish
Résumé
The study aimed to evaluate molecular changes related to trophoblast adhesion in placenta accreta spectrum (PAS) disorders. A retrospective analysis of 10 PAS cases in which both the trophoblast adherent site and the non-adherent site were identified was performed in April 2010 and March 2013. Microarray analysis and reverse transcription polymerase chain reaction (RT-PCR) analyses were performed to extract upregulated genes in the adherent site. Gene expression changes were examined by immunohistochemistry. Microarray analysis showed that 157 transcripts were > 3-fold upregulated, including the following: a disintegrin and metalloproteinase-28 (ADAM28), 3.10-fold; cathepsin V (CTSV), 3.73-fold; cathepsin S (CTSS), 3.46-fold; and matrix metalloproteinase-19 (MMP19), 3.41-fold. RT-PCR showed relatively high mRNA expressions. On immunohistochemistry, extravillous trophoblast (EVT) at the non-adherent site showed weak or no CTSV expression, whereas EVT that invaded myometrium at the adherent site showed strong expression (histological score, median [min-max], 115.6 [37.6-153.6] vs. 184.8 [56.4-222.8], p < 0.05). MMP19 showed moderate staining, with no difference between the adherent and non-adherent sites. ADAM28 and CTSS showed weak or no staining. This limited study suggests that CTSV may be involved in the pathogenesis of PAS.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
The study aimed to evaluate molecular changes related to trophoblast adhesion in placenta accreta spectrum (PAS) disorders.
METHODS
METHODS
A retrospective analysis of 10 PAS cases in which both the trophoblast adherent site and the non-adherent site were identified was performed in April 2010 and March 2013. Microarray analysis and reverse transcription polymerase chain reaction (RT-PCR) analyses were performed to extract upregulated genes in the adherent site. Gene expression changes were examined by immunohistochemistry.
RESULTS
RESULTS
Microarray analysis showed that 157 transcripts were > 3-fold upregulated, including the following: a disintegrin and metalloproteinase-28 (ADAM28), 3.10-fold; cathepsin V (CTSV), 3.73-fold; cathepsin S (CTSS), 3.46-fold; and matrix metalloproteinase-19 (MMP19), 3.41-fold. RT-PCR showed relatively high mRNA expressions. On immunohistochemistry, extravillous trophoblast (EVT) at the non-adherent site showed weak or no CTSV expression, whereas EVT that invaded myometrium at the adherent site showed strong expression (histological score, median [min-max], 115.6 [37.6-153.6] vs. 184.8 [56.4-222.8], p < 0.05). MMP19 showed moderate staining, with no difference between the adherent and non-adherent sites. ADAM28 and CTSS showed weak or no staining.
DISCUSSION
CONCLUSIONS
This limited study suggests that CTSV may be involved in the pathogenesis of PAS.
Identifiants
pubmed: 30759440
pii: 000496609
doi: 10.1159/000496609
doi:
Substances chimiques
Cathepsins
EC 3.4.-
Cysteine Endopeptidases
EC 3.4.22.-
CTSV protein, human
EC 3.4.22.43
ADAM Proteins
EC 3.4.24.-
ADAM28 protein, human
EC 3.4.24.-
Matrix Metalloproteinases, Secreted
EC 3.4.24.-
matrix metalloproteinase 19
EC 3.4.24.-
Types de publication
Journal Article
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
396-406Informations de copyright
© 2019 S. Karger AG, Basel.