ned as the presence and growth of functional endometrial tissues
outside the uterine cavity, is a common benign gynecological disease that aff
ects 10-15% of
reproductive aged women. Th
e pathophysiology of endometriosis is not clearly understood.
MicroRNAs (miRNAs) are small (19 to 25 nts) endogenous non-coding RNA molecules that
post-transcriptionally regulate gene expression. In previously study, we found cox2 played a
role in the pathogenesis in the endometriosis. We predicted microRNA-199a is the upregulator
of cox2. Further study of the role of microRNA in the development of endometriosis is
investigated by using eutopic and ectopic endometrial mesenchymal stem cells.
First, we assessed the microRNA-199a expression level by real-time PCR in human
serum of women with (n=58) and without (n=27) endometriosis. Th
e data showed that the
microRNA-199a expression was signifi
cantly higher in endometriosis compare to those without
e microRNA-199a expression in endometrial mesenchymal stem cells (MSCs)
of eutopic and ectopic from the same endometrial donor was investigated.
the biofunction of microRNA on cell migration, invasion and proliferation by wound healing
assay, Matrigel invasion assay, and XTT assay, respectively, in endometrial MSCs. Silencing of
microRNA-199a in ectopic endometrial MSCs led to decreased cell migration, invasion and
In addition to, introducing the microRNA-199a into the eutopic endometrial
MSCs could increase cell motility and growth. Th
ese data indicated that the microRNA-199a
ect on endometriosis progression.
Our study revealed the serum microRNA-199a levels were signifi
cantly higher in the
endometriosis cases. Th
e expression levels of the microRNA-199a were related to cell motility
and growth in eutopic and ectopic endometrial MSCs. Th
ese results suggest the microRNA-
199a could play a role in the development of endometriosis
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