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dc.contributor.authorMarshall, SA
dc.contributor.authorNg, L
dc.contributor.authorUnemori, EN
dc.contributor.authorGirling, JE
dc.contributor.authorParry, LJ
dc.date.accessioned2021-02-03T23:47:47Z
dc.date.available2021-02-03T23:47:47Z
dc.date.issued2016-03-22
dc.identifierpii: 10.1186/s12958-016-0148-y
dc.identifier.citationMarshall, S. A., Ng, L., Unemori, E. N., Girling, J. E. & Parry, L. J. (2016). Relaxin deficiency results in increased expression of angiogenesis- and remodelling-related genes in the uterus of early pregnant mice but does not affect endometrial angiogenesis prior to implantation. REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY, 14 (1), https://doi.org/10.1186/s12958-016-0148-y.
dc.identifier.issn1477-7827
dc.identifier.urihttp://hdl.handle.net/11343/258969
dc.description.abstractBACKGROUND: Extensive uterine adaptations, including angiogenesis, occur prior to implantation in early pregnancy and are potentially regulated by the peptide hormone relaxin. This was investigated in two studies. First, we took a microarray approach using human endometrial stromal (HES) cells treated with relaxin in vitro to screen for target genes. Then we aimed to investigate whether or not relaxin deficiency in mice affected uterine expression of representative genes associated with angiogenesis and uterine remodeling, and also blood vessel proliferation in the pre-implantation mouse endometrium. METHODS: Normal HES cells were isolated and treated with recombinant human relaxin (10 ng/ml) for 24 h before microarray analysis. Reverse transcriptase PCR was used to analyze gene expression of relaxin and its receptor (Rxfp1) in ovaries and uteri; quantitative PCR was used to analyze steroid receptor, angiogenesis and extracellular matrix remodeling genes in the uteri of wild type (Rln+/+) and Rln-/- mice on days 1-4 of pregnancy. Immunohistochemistry localized endometrial endothelial cell proliferation and mass spectrometry measured steroid hormones in the plasma. RESULTS: Microarray analysis identified 63 well-characterized genes that were differentially regulated in HES cells after relaxin treatment. Expression of some of these genes was increased in the uterus of Rln+/+ mice by day 4 of pregnancy. There was significantly higher vascular endothelial growth factor A (VegfA), estrogen receptor 1 (Esr1), progesterone receptor (Pgr), Rxfp1, egl-9 family hypoxia-inducible factor 1 (Egln1), hypoxia inducible factor 1 alpha (Hif1α), matrix metalloproteinase 14 (Mmp14) and ankryn repeat domain 37 (Ankrd37) in Rln-/- compared to Rln+/+ mice on day 1. Progesterone receptor expression and plasma progesterone levels were higher in Rln-/- mice compared to Rln+/+ mice. However, endometrial angiogenesis was not advanced as pre-implantation endothelial cell proliferation did not differ between genotypes. CONCLUSIONS: Relaxin treatment modulates expression of a variety of angiogenesis-related genes in HES cells. However, despite accelerated uterine gene expression of steroid receptor, progesterone and angiogenesis and extracellular matrix remodeling genes in Rln-/- mice, there was no impact on angiogenesis. We conclude that although relaxin deficiency results in phenotypic changes in the pre-implantation uterus, endogenous relaxin does not play a major role in pre-implantation angiogenesis in the mouse uterus.
dc.languageEnglish
dc.publisherBIOMED CENTRAL LTD
dc.titleRelaxin deficiency results in increased expression of angiogenesis- and remodelling-related genes in the uterus of early pregnant mice but does not affect endometrial angiogenesis prior to implantation
dc.typeJournal Article
dc.identifier.doi10.1186/s12958-016-0148-y
melbourne.affiliation.departmentUniversity General
melbourne.affiliation.departmentObstetrics and Gynaecology
melbourne.affiliation.departmentFlorey Department of Neuroscience and Mental Health
melbourne.affiliation.departmentSchool of BioSciences
melbourne.affiliation.facultyUniversity Services
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.affiliation.facultyScience
melbourne.source.titleReproductive Biology and Endocrinology
melbourne.source.volume14
melbourne.source.issue1
melbourne.identifier.nhmrc1064845
dc.rights.licenseCC BY
melbourne.elementsid1048453
melbourne.contributor.authorParry, Laura
melbourne.contributor.authorMarshall, Sarah
melbourne.contributor.authorGirling, Jane
melbourne.contributor.authorNG, LEELEE
dc.identifier.eissn1477-7827
melbourne.identifier.fundernameidNHMRC, 1064845
melbourne.accessrightsOpen Access


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