The role of osteopontin in the pathogenesis of placenta percreta

Özer, Alev; Yaylali, Aslı; Koçarslan, Sezen

doi:10.5603/gp.a2018.0075

Cited by 4 publications

(3 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One of the most robustly downregulated genes in IL15Δ/Δ rat implantation sites was Spp1 , the gene encoding OPN. OPN is a prime candidate as a potential regulator of placental development, due in part to its known role as a regulator of cell invasion ( Qi et al, 2014 ; Wu et al, 2015 ) and its altered expression patterns in pregnancy complications ( Xia et al, 2009 ; Özer et al, 2018 ; Long et al, 2019 ). OPN was robustly detected within the decidua basalis and adjacent to the ectoplacental cone, areas in which PRF staining was evident.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-15 deficient rats have reduced osteopontin at the maternal-fetal interface

Baines

Klausner

Patterson

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Introduction: Uterine Natural Killer (NK) cells are the predominant immune cells within the decidua during early pregnancy. These cells are thought to regulate aspects of decidualization and placental development, but their functions remain poorly characterized, especially in species with deeply invading trophoblasts such as humans and rats. Interleukin-15 (IL-15) is a cytokine required for NK cell development and survival. IL-15 mutant (IL15Δ/Δ) rats lack NK cells and exhibit altered placental development with precocious trophoblast invasion. In this study, we profiled gene expression differences between wild-type and IL15Δ/Δ implantation sites to reveal candidate factors produced by uterine NK cells that may regulate placentation and trophoblast invasion.Methods: Clariom S gene expression profiling was performed using implantation sites collected from pregnant wild-type and IL15Δ/Δ rats on gestational day 9.5. Levels and localization of perforin and osteopontin in implantation sites from wild-type and IL15Δ/Δ rats were further analyzed. The effect of osteopontin on the invasive capacity of rat trophoblasts was evaluated using Matrigel-based Transwell assays.Results: There were 257 genes differentially expressed between wild-type and IL15Δ/Δ implantation sites on gestational day 9.5, including decreased expression of various NK cell markers in IL15Δ/Δ rats, as well as Spp1, which encodes osteopontin. In wild-type rats, osteopontin was present within the decidua basalis and adjacent to the primitive placenta, and osteopontin colocalized with the NK cell marker perforin. Osteopontin was also detectable in uterine glands. Conversely, in IL15Δ/Δ rats, osteopontin and perforin were not readily detectable in the decidua despite robust osteopontin levels in uterine glands. Neutralization of osteopontin in media conditioned by cells isolated from the decidua decreased invasion of rat trophoblasts, suggesting that reduced levels of osteopontin are unlikely to account for the precocious trophoblast invasion in IL15Δ/Δ rats.Conclusion: Osteopontin is expressed by NK cells at the maternal-fetal interface in rats and may contribute to modulation of trophoblast invasion.

show abstract

Section: Discussionmentioning

confidence: 99%

Interleukin-15 deficient rats have reduced osteopontin at the maternal-fetal interface

Baines

Klausner

Patterson

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…EVTs are also expanded in previa, even though placental overinvasion is not characteristic of this disease 17 . The misexpression of several molecules within trophoblasts have been shown to correlate with disease, including lower levels of β-catenin in previa and accreta 18 , higher levels of HMG1 and VEGF in previa 19 , higher levels of DOCK4 in accreta trophoblasts 20 , and absence of osteopontin staining in percreta 21 . An in-depth examination of the involvement of trophoblasts, even years after uterine damage, is thus intriguing and critical for understanding disease etiology.…”

Section: Introductionmentioning

confidence: 99%

PRG2 and AQPEP are misexpressed in fetal membranes in placenta previa and percreta

Zhang

Hannibal

Rivera

et al. 2020

Preprint

View full text Add to dashboard Cite

The obstetrical conditions placenta accreta spectrum (PAS) and placenta previa are a significant source of pregnancy-associated morbidity and mortality, yet the specific molecular and cellular underpinnings of these conditions are not known. In this study, we identified misregulated gene expression patterns in tissues from placenta previa and percreta (the most extreme form of PAS) compared with control cases. By comparing this gene set with existing placental single-cell and bulk RNA-Seq datasets, we show that the upregulated genes predominantly mark extravillous trophoblasts. We performed immunofluorescence on several candidate molecules and found that PRG2 and AQPEP protein levels are upregulated in both the fetal membranes and the placental disk in both conditions. While this increased AQPEP expression remains restricted to trophoblasts, PRG2 is mislocalized and is found throughout the fetal membranes. Using a larger patient cohort with a diverse set of gestationally aged-matched controls, we validated PRG2 as a marker for both previa and PAS and AQPEP as a marker for only previa in the fetal membranes membranes. Our findings suggest that the extraembryonic tissues surrounding the conceptus, including both the fetal membranes membranes and the placental disk, harbor a signature of previa and PAS that reflects increased trophoblast invasiveness.

show abstract

“…Özer ve ark. 'ları perkreata olgularında osteopontin ekspresyonunun azaldığını rapor etmişlerdir (38). Böylelikle PA ya ait trofoblastik hücrelerin reseptör düzeyinde farklılıklar gösterdiği ileri sürülmüştür (31)(32)(33)(34)(35)(36).…”

Section: Introductionunclassified

Plasenta Akreata; Geçmi̇şten Bugüne Öyküsü

Koçarslan

2020

Kahramanmaraş Sütçü İmam Üniversitesi Tıp Fakültesi Dergisi

Self Cite

View full text Add to dashboard Cite

Placenta accreta (PA) develops when the placental villi invade the myometrium extraordinarily. It is divided into three grades based on histopathology: placenta accreta where the placental villi are in connection with the myometrium, placenta increta where the placental villi invade the myometrium, and placenta percreta where the placental villi penetrate the uterine serosa. Major risk factor for placenta accreta is a previous cesarean delivery particularly when accompanied with a coexisting placenta previa. Insufficient decidualization and trophoblastic changes of the placental bed in placenta accreta are secondary to the uterine scar. Antenatal diagnosis seems to be a key factor in managing maternal outcome. Diagnosis can be achieved by ultrasound in the majority of cases. PA management has need to the presence of a multidisciplinary surgical team. Cesarean hysterectomy is probably the preferable treatment. In carefully selected cases, conservative management may be considered for fertility.

show abstract

The role of osteopontin in the pathogenesis of placenta percreta

Cited by 4 publications

References 17 publications

Interleukin-15 deficient rats have reduced osteopontin at the maternal-fetal interface

Interleukin-15 deficient rats have reduced osteopontin at the maternal-fetal interface

PRG2 and AQPEP are misexpressed in fetal membranes in placenta previa and percreta

Plasenta Akreata; Geçmi̇şten Bugüne Öyküsü

Contact Info

Product

Resources

About