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dc.contributor.authorKeane, Kevin
dc.contributor.authorCruzat, V.
dc.contributor.authorCalton, E.
dc.contributor.authorHart, P.
dc.contributor.authorSoares, M.
dc.contributor.authorNewsholme, P.
dc.contributor.authorYovich, J.
dc.identifier.citationKeane, K. and Cruzat, V. and Calton, E. and Hart, P. and Soares, M. and Newsholme, P. and Yovich, J. 2017. Molecular actions of Vitamin D in reproductive cell biology. Reproduction. 153 (1): pp. R29-R42.

Vitamin D (VitD) is an important secosteroid and has attracted attention in several areas of research due to common VitD deficiency in the population, and its potential to regulate molecular pathways related to chronic and inflammatory diseases. VitD metabolites and the VitD receptor (VDR) influence many tissues including those of the reproductive system. VDR expression has been demonstrated in various cell types of the male reproductive tract, including spermatozoa and germ cells, and in female reproductive tissues including the ovaries, placenta and endometrium. However, the molecular role of VitD signalling and metabolism in reproductive function have not been fully established. Consequently, the aim of this work is to review current metabolic and molecular aspects of the VitD-VDR axis in reproductive medicine and to propose the direction of future research. Specifically, the influence of VitD on sperm motility, calcium handling, capacitation, acrosin reaction and lipid metabolism is examined. In addition, we will also discuss the effect of VitD on sex hormone secretion and receptor expression in primary granulosa cells, along with the impact on cytokine production in trophoblast cells. The review concludes with a discussion of the recent developments in VitD-VDR signalling specifically related to altered cellular bioenergetics, which is an emerging concept in the field of reproductive medicine.

dc.publisherBioScientifica Ltd.
dc.titleMolecular actions of Vitamin D in reproductive cell biology
dc.typeJournal Article
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusOpen access via publisher

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