Journal article
Follistatin is essential for normal postnatal development and function of mouse oviduct and uterus
SJ Holdsworth-Carson, RG Craythorn, WR Winnall, K Dhaliwal, R Genovese, CJ Nowell, PAW Rogers, DM De Kretser, MP Hedger, JE Girling
Reproduction Fertility and Development | CSIRO PUBLISHING | Published : 2015
DOI: 10.1071/RD13372
Abstract
Female mice lacking the follistatin gene but expressing a human follistatin-315 transgene (tghFST315) have reproductive abnormalities (reduced follicles, no corpora lutea and ovarian-uterine inflammation). We hypothesised that the absence of follistatin-288 causes the abnormal reproductive tract via both developmental abnormalities and abnormal ovarian activity. We characterised the morphology of oviducts and uteri in wild type (WT), tghFST315 and follistatin-knockout mice expressing human follistatin-288 (tghFST288). The oviducts and uteri were examined in postnatal Day-0 and adult mice (WT and tghFST315 only) using histology and immunohistochemistry. Adult WT and tghFST315 mice were ovarie..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
The authors wish to thank the staff of the Monash Medical Centre Animal House and Sarah Badelow, Matthew Chapman (Victorian Cancer Biobank, Royal Melbourne Hospital), Sue Haywood, Fiona Lederman, Michelle Lockhart, Carl Sprung, Yuqing Yang and Marina Zaitseva for their technical help and assistance. The research was supported by a National Health and Medical Research Council Project Grant (No. 606545) to J. E. G., M. P. H., D. M. deK. and P. A. W. R., the Victorian Government's Operational Infrastructure Support Program and a Monash Postgraduate Scholarship to R. G. C.