PMID- 31980722
OWN - NLM
STAT- MEDLINE
DCOM- 20201120
LR  - 20210123
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 10
IP  - 1
DP  - 2020 Jan 24
TI  - Matrix metallopeptidase expression and modulation by transforming growth 
      factor-beta1 in equine endometrosis.
PG  - 1119
LID - 10.1038/s41598-020-58109-0 [doi]
LID - 1119
AB  - Equine endometrial fibrosis (endometrosis) is described as a degenerative chronic 
      condition in the uterus. Its characteristic feature is excessive deposition of 
      extracellular matrix (ECM) components around the endometrial glands and stroma. 
      Although matrix metallopeptidases (MMPs) that mediate ECM turnover are important 
      factors in the process of fibrosis, knowledge of their expression and regulation 
      in endometrosis is limited. In other species, one of the important regulators of 
      MMPs and tissue inhibitors of MMPs (TIMPs) is transforming growth factor 
      (TGF)-beta1. The goal of this study was to determine (i) endometrial expression of 
      MMPs and TIMPs during endometrosis and (ii) the effect of TGF-beta1 on expression of 
      MMPs and TIMPs in equine endometrial fibroblasts and epithelial cells. In the 
      follicular phase of the estrous cycle, MMP-1, -2, -9, and TIMP concentrations 
      were higher during endometrosis than in healthy endometrium (P < 0.05). In the 
      midluteal phase, MMP-3 concentration was lower in severe endometrosis compared to 
      healthy endometrium (P < 0.05). In fibroblasts, TGF-beta1 upregulated MMP-1, -9, 
      -13, and TIMP1, but downregulated MMP-3 secretion (P < 0.05). In epithelial 
      cells, TGF-beta1 upregulated MMP-1, -9, -13, and TIMP secretion (P < 0.05). 
      Endometrial expression of MMPs and TIMPs is altered during endometrosis. TGF-beta1 
      is a regulator of endometrial ECM remodeling via its effect on MMPs and TIMPs in 
      equine endometrial fibroblasts and epithelial cells.
FAU - Szostek-Mioduchowska, Anna
AU  - Szostek-Mioduchowska A
AD  - Department of Reproductive Immunology and Pathology, Institute of Animal 
      Reproduction and Food Research, Polish Academy of Sciences, 10-748, Olsztyn, 
      Poland. a.szostek-mioduchowska@pan.olsztyn.pl.
FAU - Slowinska, Mariola
AU  - Slowinska M
AUID- ORCID: 0000-0002-4366-9535
AD  - Department of Gamete and Embryo Biology,Institute of Animal Reproduction and Food 
      Research, Polish Academy of Sciences, 10-748, Olsztyn, Poland.
FAU - Pacewicz, Joanna
AU  - Pacewicz J
AD  - Department of Reproductive Immunology and Pathology, Institute of Animal 
      Reproduction and Food Research, Polish Academy of Sciences, 10-748, Olsztyn, 
      Poland.
FAU - Skarzynski, Dariusz J
AU  - Skarzynski DJ
AD  - Department of Reproductive Immunology and Pathology, Institute of Animal 
      Reproduction and Food Research, Polish Academy of Sciences, 10-748, Olsztyn, 
      Poland.
FAU - Okuda, Kiyoshi
AU  - Okuda K
AD  - Laboratory of Reproductive Physiology Graduate School of Natural Science and 
      Technology, Okayama University, 700-8530, Okayama, Japan.
AD  - Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200124
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (RNA, Messenger)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Tissue Inhibitor of Metalloproteinases)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Endometriosis/enzymology/physiopathology/*veterinary
MH  - Endometrium/metabolism/pathology
MH  - Epithelial Cells/drug effects/metabolism
MH  - Estrous Cycle
MH  - Female
MH  - Fibroblasts/drug effects/metabolism
MH  - Fibrosis
MH  - *Gene Expression Regulation, Enzymologic/drug effects
MH  - Horse Diseases/enzymology/*physiopathology
MH  - Horses
MH  - Matrix Metalloproteinases/*biosynthesis/genetics
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Tissue Inhibitor of Metalloproteinases/biosynthesis/genetics
MH  - Transforming Growth Factor beta1/pharmacology/*physiology
PMC - PMC6981191
COIS- The authors declare no competing interests.
EDAT- 2020/01/26 06:00
MHDA- 2020/11/21 06:00
PMCR- 2020/01/24
CRDT- 2020/01/26 06:00
PHST- 2019/05/30 00:00 [received]
PHST- 2020/01/07 00:00 [accepted]
PHST- 2020/01/26 06:00 [entrez]
PHST- 2020/01/26 06:00 [pubmed]
PHST- 2020/11/21 06:00 [medline]
PHST- 2020/01/24 00:00 [pmc-release]
AID - 10.1038/s41598-020-58109-0 [pii]
AID - 58109 [pii]
AID - 10.1038/s41598-020-58109-0 [doi]
PST - epublish
SO  - Sci Rep. 2020 Jan 24;10(1):1119. doi: 10.1038/s41598-020-58109-0.