Endometriosis, a common gynecological disorder that causes
infertility and
pelvic pain, is defined as the presence of endometrial glands and stroma within extra-uterine sites. However, despite extensive studies its etiology and pathogenesis are not completely understood. Differentially expressed genes were investigated in epithelial and stromal cells from deep
endometriosis and matched eutopic endometrium using
cDNA microarrays and
laser capture microdissection. Validation of results of several up- and down-regulated genes was performed by quantitative real-time RT-PCR. Our data showed that
platelet-derived growth factor receptor alpha (PDGFRA),
protein kinase C beta1 (PKC beta1) and
janus kinase 1 (JAK1) were upregulated, and Sprouty2 and
mitogen-activated protein kinase kinase 7 (MKK7) were downregulated in
endometriosis stromal cells, suggesting the involvement of the RAS/RAF/MAPK signaling pathway through PDGFRA in
endometriosis pathophysiology. In addition, two potential negative regulators of
aromatase expression, chicken
ovalbumin upstream promoter
transcription factor 2 (COUP-TF2) and
prostaglandin E2 receptor subtype EP3 (PGE2EP3), were downregulated in
endometriosis epithelial cells, which might result in increased local production of
estrogen in
endometriosis epithelial cells. Furthermore, three potential candidate genes that might be involved in
endometriosis related
pain were identified:
tyrosine kinase receptor B (TRkB) in
endometriosis epithelial cells, and
serotonin transporter (5HTT) and
mu opioid receptor (MOR) in
endometriosis stromal cells were all upregulated. One of the candidate genes, MOR, may be involved in a defective immune system in
endometriosis. This study has provided new insights into
endometriosis pathophysiology.