Possible Association between Cathepsin V and the Development of Placenta Accreta Spectrum Disorders

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. Micro...

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Published inGynecologic and obstetric investigation p. 1
Main Authors Matsukawa, Satoshi, Sumigama, Seiji, Kotani, Tomomi, Wang, Jingwen, Miki, Rika, Moriyama, Yoshinori, Nakano, Tomoko, Mano, Yukio, Tsuda, Hiroyuki, Tamakoshi, Koji, Kikkawa, Fumitaka
Format Journal Article
LanguageEnglish
Published Switzerland 01.01.2019
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Summary: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.
ISSN:1423-002X
DOI:10.1159/000496609