About: ER-alpha agonist induces conversion of fibroblasts into myofibroblasts, while ER-beta agonist increases ECM production and wound tensile strength of healing skin wounds in ovariectomised rats     Goto   Sponge   NotDistinct   Permalink

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  • Oestrogen deprivation is one of the major factors responsible for many age-related processes, including poor wound healing in women. Previously, it has been shown that oestrogens have a modulatory effect in different wound-healing models. Therefore, in this study, the effect of selective oestrogen receptor (ER) agonists (PPT - ER-alpha agonist, DPN - ER-beta agonist) on excisional and incisional wound-healing models was compared in ovariectomised rats in vivo as well as on human dermal fibroblasts (HDF) and human umbilical endothelial cells (HUVEC) in vitro. In the in vivo study, 4 months after either ovariectomy or sham ovariectomy, Sprague-Dawley rats were randomly divided into four groups and subjected to two incisional and excisional wounds: (i) control sham operated, vehicle-treated; (ii) ovariectomised, vehicle-treated; (iii) ovariectomised, PPT treated; (iv) ovariectomised, DPN treated. In the in vitro study, HDFs and HUVECs were used. After treatment with ER agonists, cells were processed for immunocytochemistry and gelatin zymography. Our study shows that stimulation of ER-alpha leads to the differentiation of fibroblasts into myofibroblasts both in vivo and in vitro. On the other hand, the formation of extracellular matrix was more prominent, and wound tensile strength (TS) was increased when ER-beta was stimulated. In contrast, stimulation of ER-alpha led to a more prominent increase in the expression of MMP-2 and decrease in wound T'S. New information is presented in this investigation concerning oestrogen replacement therapy (ERT) in different wound-healing models. This study demonstrates that the ERT should be both wound and receptor-type specific.
  • Oestrogen deprivation is one of the major factors responsible for many age-related processes, including poor wound healing in women. Previously, it has been shown that oestrogens have a modulatory effect in different wound-healing models. Therefore, in this study, the effect of selective oestrogen receptor (ER) agonists (PPT - ER-alpha agonist, DPN - ER-beta agonist) on excisional and incisional wound-healing models was compared in ovariectomised rats in vivo as well as on human dermal fibroblasts (HDF) and human umbilical endothelial cells (HUVEC) in vitro. In the in vivo study, 4 months after either ovariectomy or sham ovariectomy, Sprague-Dawley rats were randomly divided into four groups and subjected to two incisional and excisional wounds: (i) control sham operated, vehicle-treated; (ii) ovariectomised, vehicle-treated; (iii) ovariectomised, PPT treated; (iv) ovariectomised, DPN treated. In the in vitro study, HDFs and HUVECs were used. After treatment with ER agonists, cells were processed for immunocytochemistry and gelatin zymography. Our study shows that stimulation of ER-alpha leads to the differentiation of fibroblasts into myofibroblasts both in vivo and in vitro. On the other hand, the formation of extracellular matrix was more prominent, and wound tensile strength (TS) was increased when ER-beta was stimulated. In contrast, stimulation of ER-alpha led to a more prominent increase in the expression of MMP-2 and decrease in wound T'S. New information is presented in this investigation concerning oestrogen replacement therapy (ERT) in different wound-healing models. This study demonstrates that the ERT should be both wound and receptor-type specific. (en)
Title
  • ER-alpha agonist induces conversion of fibroblasts into myofibroblasts, while ER-beta agonist increases ECM production and wound tensile strength of healing skin wounds in ovariectomised rats
  • ER-alpha agonist induces conversion of fibroblasts into myofibroblasts, while ER-beta agonist increases ECM production and wound tensile strength of healing skin wounds in ovariectomised rats (en)
skos:prefLabel
  • ER-alpha agonist induces conversion of fibroblasts into myofibroblasts, while ER-beta agonist increases ECM production and wound tensile strength of healing skin wounds in ovariectomised rats
  • ER-alpha agonist induces conversion of fibroblasts into myofibroblasts, while ER-beta agonist increases ECM production and wound tensile strength of healing skin wounds in ovariectomised rats (en)
skos:notation
  • RIV/00216208:11130/11:7099!RIV12-MSM-11130___
http://linked.open...avai/predkladatel
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • I, Z(MSM0021620806)
http://linked.open...iv/cisloPeriodika
  • 9
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
http://linked.open.../riv/druhVysledku
http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
http://linked.open...dnocenehoVysledku
  • 197878
http://linked.open...ai/riv/idVysledku
  • RIV/00216208:11130/11:7099
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • cell differentiation; hormone replacement therapy; myofibroblast; oestrogen receptor; regeneration; tissue repair; estrogen-receptor-beta; matrix-metalloproteinase activity; hormone replacement therapy; activated protein-kinase; breast-cancer cells; endothelial-cells; in-vivo; expression; repair; 17-beta-estradiol (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • DK - Dánské království
http://linked.open...ontrolniKodProRIV
  • [876E7041656E]
http://linked.open...i/riv/nazevZdroje
  • Experimental Dermatology
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 20
http://linked.open...iv/tvurceVysledku
  • Dvořánková, Barbora
  • Novotný, M.
  • Smetana, Karel
  • Bobrov, N.
  • Gal, P.
  • Matthews, BJO
  • Mojzis, J.
  • Sabol, F.
  • Sarissky, M.
  • Szabo, Pavol
  • Toporcerova, S.
  • Varinska, L.
  • Vasilenko, T.
http://linked.open...ain/vavai/riv/wos
  • 000294594000002
http://linked.open...n/vavai/riv/zamer
issn
  • 0906-6705
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  • 11130
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