Undifferentiated Cell Markers in the Endometrium

Abstract

The presence of endometrial-like tissue outside the uterus is the hallmark of endometriosis, a benign chronic
illness. Although the precise pathogenic pathways are yet unknown, the aetiology of endometriosis seems to be
polygenic and complex. The pathophysiology of proliferative gynaecological illnesses like endometriosis may be
linked to adult stem cells, which have recently been discovered in a number of human tissues, including the
endometrium. It is very difficult to identify adult stem/progenitor cells (SPCs) in tissues, however undifferentiated
cell markers may be used to make inferences. Using immunohistochemistry (IHC) using a non-biotin polymer
detection technique, this research examined the expression of undifferentiated markers Musashi-1, Oct-4, and c
kit in eutopic endometria of patients with and without endometriosis and endometriotic lesions. Six samples of
eutopic and ectopic endometria from endometriosis patients and four tissue specimens of normal endometrium
were assessed. The Kruskal-Wallis test was used to evaluate immunoreactivity scores (IRS) and the chi-square
test was used to analyse categorical data. Oct-4 staining was mostly nuclear, Musashi-1 protein expression was
cytoplasmic or nuclear, and c-kit protein expression was transmembrane and cytoplasmic. All examined
endometrial compartments (glandular epithelium, stroma, and endothelium) showed positive immunostaining for
the three markers. Patients with endometriosis had a considerably increased proportion of Musashi-1 expressing
cells in their endothelium (p < 0.05). Cell groupings that may represent stem cell clusters were stained by
Musashi-1 and c-kit. All three markers showed strong staining percentages and intensities. Stromal IRS was
considerably greater in eutopic endometrial samples from endometriosis patients (p < 0.05), and c-kit expression
was significantly higher in glandular epithelium than in the stromal compartment (p < 0.05). In summary, putative
endometrial SPCs may contribute to the physiopathology of endometriosis by participating in neoangiogenesis as
well as the development of ectopic implants.