Evaluation of tissue metalloproteinase inhibitor TIMP-1 and Survivin levels during third trimester pregnancy — a preliminary report

Abstract

Objectives: A proper implantation of trophoblastic cells and an appropriate metalloproteinases activity is required to cause disintegration of basal membranes of cells. The activity of tissue matrix metaloproteinases can be inhibited by their matrix inhibitors -TIMP-s. Survivin is a member of inhibitor of apoptosis proteins family (IAP), that suppresses caspase activation, influences VEGF expression and promotes proliferative action of endothelial cells. Material and methods:The aim of the study was to assess concentrations of two independent anti-apoptotic factors. TIMP-1 and survivin in serum of women in their third trimester of pregnancy and in umbilical cord blood of neonates -drawn separately from veins and arteries. The study group consisted of 29 pregnant women in physiological pregnancy and with correct fetal development, in gestational age between 37 to 40 weeks of gestation. Blood used in the study was collected from maternal cubital fossa veins and from neonatal umbilical cords (from veins and from arteries separately). The research was conducted using TIMP-1 and Survivin ELISA kits from R & D Systems according to manufacturers' recommendations and protocols. Results:The concentrations of TIMP-1 were similar and independent of the source of blood samples. Arterial values of TIMP-1 in umbilical cord compared to maternal and fetal veins were slightly lower, but no statistical difference was found. The mean concentrations of Survivin were comparable but we found that in some cases the results in cord blood serum in both vessels-vein and arteries were almost negative. Arterial values of Survivin in umbilical cord compared to maternal blood were higher, but no statistical difference was found. Conclusions:In III-rd trimester of pregnancy parameters of Timp-1 and Survivin -anti-apoptotic substances concentration were similar in maternal and cord blood in both artery and vein. We found no increased activity of selected antiapoptotic factors.

Sexual dimorphism in placental development and function: Comparative physiology with an emphasis on the pig

“…Apoptosis is well characterized in the human placenta and has been demonstrated to be essential for trophoblast invasion, differentiation and survival (Heazell & Crocker, 2008; Huppertz et al, 2006; Huppertz & Kaufmann, 1999; Kang & Rosenwaks, 2018; Levy et al, 2000; Marzusch et al, 1995; Mayhew et al, 1999; Straszewski‐Chavez et al, 2005). Dysregulated apoptosis has been linked to pregnancy complications including gestational trophoblast disease (Chiu et al, 2001; Halperin et al, 2000), pre‐eclampsia (Allaire et al, 2000; Cali et al, 2013; Can et al, 2014; Leung et al, 2001; Levy, 2005), and aintrauterine growth restriction (IUGR) (Börzsönyi et al, 2013; Cali et al, 2013; Heazell et al, 2011; Ishihara et al, 2002; Jeschke et al, 2006; Karowicz‐Bilińska et al, 2007; Longtine et al, 2012; Smith et al, 1997) highlighting the importance of appropriately regulated cell death for conceptus development.…”

Changes in activity of metalloproteinases 2 and 9 in rat liver in experimental model of cholestasis taking into account its duration and assessment of selected features

“…Zaburzenia aktywności MMPs i TIMPs wykazano w marskości wątroby zarówno alkoholowej, jak i pozapalnej, a także w hemochromatozie. Nadmierne włóknienie wątroby w przebiegu marskości spowodowane jest prawdopodobnie niedostateczną degradacją kolagenu, wynikającą ze spadku aktywności MMPs i wzrostu aktywności TIMPs [15,24,25]. Badanie metaloproteinaz w płynach ustrojowych i wyciągach tkankowych polega na oznaczaniu ich aktywności i stężenia.…”

The placental cell-derived exosomes as a promising predictive biomarker of preeclampsia in symptomatic pregnancies

“…tissue matrix metalloproteinase inhibitor and survivin (a member of apoptosis proteins family inhibitors), which are actively transferred by exosomes, in physiological pregnancy. These anti-apoptotic molecules suppress caspases, influence on expression of vascular endothelial growth factor(s) and promote proliferative capability of endothelial cells and their precursors depending on gestation age [10], while their role in preeclampsia are still uncertain. Consequently, the results received recently [2] maintain the hypothesis that impaired immune phenotype of PCDE may be a personal biomarker of preeclampsia as life-threatening vascular complication in pregnancy.…”