Abstract
Endometriosis is a common gynecological disease that is characterized by the presence of functional endometrial-like lesions in the abdominal cavity. Aside from epithelial cells, these lesions consist of stromal cells that have the capacity to migrate, adhere, proliferate, and induce neuro- and lymphangiogenesis, which allows them to survive at ectopic locations. However, the exact underlying mechanisms that regulate these changes are yet to be elucidated. The common ground of these processes, however, is the second messenger, calcium. In this regard, members of the superfamily of transient receptor potential (TRP) ion channels, which are known to be calcium-permeable and expressed in the endometrium, have emerged as key regulators. Here, we assessed the molecular and functional expression of TRP channels in stromal cells isolated from the eutopic endometrium of endometriosis patients and controls. Using RT-qPCR, high mRNA levels of TRPV2, TRPV4, TRPM4, TRPM7, TRPC1, TRPC3, TRPC4, and TRPC6 were observed in the whole endometrium throughout the menstrual cycle. Additionally, and in line with previous reports of control patients, TRPV2, TRPV4, TRPC1/4, and TRPC6 were present in human endometrial stromal cells (hESC) from endometriosis patients both at the molecular and functional level. Moreover, proliferation and migration assays illustrated that these parameters were not affected in stromal cells from endometriosis patients. Furthermore, comparison between eutopic and ectopic endometrial samples revealed that the RNA expression pattern of TRP channels did not differ significantly. Collectively, although a functional expression of specific ion channels in hESCs was found, their expression did not correlate with endometriosis.
Highlights
Endometriosis is a gynecological disease, characterized by the presence of functional, endometrial-like lesions located outside the uterine cavity
In line with previous reports of control patients, TRPV2, TRPV4, TRPC1/4, and TRPC6 were present in human endometrial stromal cells from endometriosis patients both at the molecular and functional level
These results are in line with the expression pattern of the transient receptor potential (TRP) genes in whole endometrial biopsies of endometriosis patients during the luteal phase (Figure 1B–D). These results showed no difference in the level of TRP channel expression between control and endometriosis patients in endometrial biopsies and in primary cultures of stromal cells of the eutopic endometrium
Summary
Endometriosis is a gynecological disease, characterized by the presence of functional, endometrial-like lesions located outside the uterine cavity. The most commonly accepted theory is the retrograde menstruation of Sampson, i.e., that lesions occur due to the shedding of the eutopic endometrial lining via the fallopian tubes into the abdominal cavity (Figure 1A) [3] As this is a natural process which occurs in 90% of reproductive women [4], endometriosis lesions are assumed to acquire additional capacities, such as migration, adhesion, proliferation, and neuroangiogenesis, in order for them to establish and flourish in the abdominal cavity [5]. The characterization of TRP channel expression between (i) the eutopic tissue of endometriosis and controls, and (ii) the eutopic and ectopic endometrium of endometriosis patients would be an interesting feature towards the understanding of the pathogenesis of endometriosis To this end, mRNA expression studies, and functional Ca2+-microfluorimetry and proliferation/migration assays were performed on human biopsies and the primary cell cultures of both endometriosis patients and controls, to investigate the contribution of TRP channels in stromal cells towards the development of endometriosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
