Premium
Estradiol Enhances Hyaluronic Acid Secretion from Vaginal Epithelial Cells
Author(s) -
Kitchel Alyssa,
Teat Stephanie,
WoodardGrice Alencia
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb712
Subject(s) - hyaluronic acid , secretion , estrogen , hyaluronan synthase , extracellular matrix , stimulation , glycosaminoglycan , chemistry , extracellular , endocrinology , medicine , biology , biochemistry , anatomy
Hyaluronic acid (HA) is a relatively simple structured glycosaminoglycan that is an important hydrating component of the extracellular matrix. Previous literature suggests estradiol (E2) inhibits the secretion of HA in vascular smooth muscle cells (VSMCs) by reducing the levels of hyaluronic acid synthase‐1 (HAS1). However, this relationship has not been investigated in vaginal tissues, which are considerably more hydrated when estrogen is present. We hypothesize that E2 increases the secretion of HA in vaginal epithelial cell cultures. To examine this relationship, vaginal epithelial cells (VK2) were synchronized by serum withdrawal and subsequently stimulated with varying concentrations of E2 for 6 and 24 hours. Following treatment, gene expression of three HAS isoforms was analyzed via qPCR and protein secretion of HA was assessed by ELISA. After 6 and 24 hours, gene expression of HAS1 was decreased with 100 nM E2 (0.309, 0.345 fold respectively) compared to no E2 (p<0.05). Unlike VMSCs, with 100nM of E2 stimulation, HA protein secretion was increased at 6 hours (79.19 pg HA/μg total protein) compared to 0nM and 10nM (p<.007) and 24hrs (228.8 pg HA/μg total protein) compared to all other E2 treatments (p<0.05). These results suggest that estrogen‐dependent regulation of HA in VK2 cells involves a change in HA secretion, not synthesis, in order to maintain a hydrated extracellular matrix.