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Presensce of gp96, both forms of Hsp70 and their receptors CD91 and TLR4 at maternal-fetal interface of blighted ovum and missed abortion

INTRODUCTION: Heat shock proteins (hsps) are ubiquitous and phylogenetically conserved intracellular molecules with cytoprotective functions acting as molecular chaperone. Various cell types that occurred during tissue remodelling at maternal-fetal interface could release hsps in extracellular space where hsps by themselves as in the complex with peptides become forceful immunogens. They bind to surface receptors on antigen presenting cells and elicit innate and adaptive proinflammatory immune responses, which are possibly harmful for pregnancy. Blighted ovum and missed abortion belong to the clinical group of non-continuing pregnancy and can be explained in the context of lower progesterone levels and specific cytokine network at maternal-fetal interface. From a clinical point of view, missed abortion represents early fetal death while blighted ovum denotes a pathological pregnancy in which genetic defects prevent the development of the fertilisation products. The aim of our study was to evaluate the expression and distribution of gp96, both forms of Hsp70 and its receptors CD91 and TLR4 in early pathological pregnancy (blighted ovum and missed abortion). MATERIAL AND METHODS: Single labelling using immunohistology and double labelling with immunofluorescence were applied to detect presence and localization gp96, both forms of Hsp70, CD91 and TLR4 in paraffin embedded decidual tissue of blighted ovum and missed abortion. Site of implantation was visualized by cytokeratin labelling. RESULTS: In missed abortion, gp96 was diffusively intensively stained, when compared to blighted ovum. Hsc70 is widely distributed and more intensively labelled in both pathological pregnancies compared to Hsp70. The intensity of CD91 and TLR4 was higher in the blighted ovum, when compared to missed abortion. CONCLUSION: The presence of gp96, both forms of Hsp70, CD91 and TLR4 at the implantation site of blighted ovum and missed abortion provides a molecular basis for their interaction and may have an important implication on the pathological processes.

Hsp70; CD91; fetaloplacental unit; glycoprotein 96; TLR4; missed abortion; blighted ovum

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