Abstract

INTRODUCTION: To determine the interaction between hormones and the expression of vaginal structural proteins and inflammatory marker expression in the vagina. METHODS: Real time PCR was used to analyze hormone receptor, inflammatory marker, and tight cell junction expression in immortalized human tissue cell lines of the vaginal mucosa (VK2) and ectocervix (ECT1) following treatment with low (0.1 nM), moderate (100 nM), and high (1 μM) doses of estrogen, progesterone, and testosterone. RESULTS: ECT1 cells treated with estrogen and testosterone had increased expression of tight junction proteins (ZO3, occludin, claudin1, and ICAM) and inflammatory markers (IL1-beta, ILB, 1F127, VegF, NFKB1) with the greatest increase at 0.1 nM estrogen and 1 μM testosterone. Estrogen receptor alpha and beta (ER) were not increased above the control (GAPDH) with estrogen or testosterone treatment in ECT1. VK2 cells treated with estrogen had elevated expression in occludin at 0.1 nM and VegF at 1 μM but expression of additional markers had no increase above GAPDH. VK2 had elevated expression of tight cell junction proteins (ZO1, ZO3, occludin, claudin1 and 2) and inflammatory marker (IL1-beta). ER-alpha expression was increased in VK2 treated with 1 μM progesterone but was not otherwise elevated above GAPDH. CONCLUSION: In this limited study, the vaginal mucosa was noted to be far less responsive to hormone treatment compared to the ectocervix. These results indicate there are likely additional factors involved with the cellular signaling which governs the structural integrity and health of the vaginal mucosa.

Full Text
Paper version not known

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 call

Disclaimer: 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.