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Introduction
The actions of relaxin in certain target tissues
appear to require exposure to estrogen, and in
certain cell types relaxin action is potentiated
by estrogen priming. The precise role of estrogen and the mechanisms utilized by estrogen in
the cellular response to relaxin have not been
well defined in any relaxin target tissue. One
possible mechanism by which estrogen may enhance the response to relaxin is by upregulating
expression of the relaxin receptor.
We have previously used an in vitro model of
human term pregnancy cervix, human lower
uterine segment fibroblasts, as a system for
studying of the effects of relaxin upon human
cervical function.1,2 We therefore used this system to test the hypothesis that estrogen amplification of the relaxin response in target tissues is
due to regulation of receptor expression. We determined whether LGR7 mRNA is expressed
and if it is regulated by estrogen in our in vitro
model of human lower uterine segment fibroblasts.
Human lower uterine segment fibroblasts
at passages 1012 were plated in T75 tissue
Relaxin and Related Peptides: Fifth International Conference: Ann. N.Y. Acad. Sci. 1160: 9192 (2009).
C 2009 New York Academy of Sciences.
doi: 10.1111/j.1749-6632.2009.04048.x
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