Transforming growth factor-α, like epidermal growth factor, stimulates cell proliferation and inhibits prolactin secretion in the human decidual cells in vitro

Michiyoshi Taga, Masahiko Saji, Kumiko Suyama, H. Minaguchi
In: Journal of Endocrinological Investigation · 1996 · vol. 19(10) , pp. 659–662 · doi:10.1007/bf03349035 · PMID:9007696 · W2053687058
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Transforming growth factor-alpha stimulated DNA synthesis and inhibited prolactin secretion in cultured human decidual cells, similar to epidermal growth factor.

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The paper examined how transforming growth factor-α (TGF-α) affects cultured human decidual cells, focusing on cell proliferation via DNA synthesis and on prolactin (PRL) secretion. In vitro, TGF-α increased DNA synthesis, indicating stimulation of cell proliferation, while simultaneously inhibiting PRL secretion. The authors interpret these effects as supporting a regulatory role for TGF-α in decidual function, analogous to epidermal growth factor (EGF). The study is limited to in vitro observations in cultured decidual cells rather than in vivo confirmation. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match for uterine/decidual biology related to hormonally driven pelvic conditions.

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Abstract

In order to clarify the biological action of transforming growth factor alpha (TGF-α) in the human decidua, we investigated the effects of TGF-α on cell proliferation and prolactin (PRL) secretion in cultured decidual cells in vitro. TGF-α had a stimulatory effect on DNA synthesis in decidual cells and an inhibitory effect on PRL secretion from these cells. These results suggest that TGF-α, like epidermal growth factor (EGF), may be one of the substances which regulate decidual function. Similar content being viewed by others

References

Taga M., Sakakibara H., Saji M., Minaguchi H. Regulation of human decidual function by epidermal growth factor. Hormone Res. 44(suppl 2): 23, 1995. Saji M., Taga M., Minaguchi H. Epidermal growth factor stimulates cell proliferation and inhibits prolactin secretion of the human decidual cells in culture. Endocrinol. Jpn. 37: 171, 1990. Sakakibara H., Taga M., Saji M., Kida H., Minaguchi H. Gene expression of epidermal growth factor in human endometrium during decidualization. J. Clin. Endocrinol. Metab. 79: 223, 1994. Tomita K., Macoshen J.A., Friesen H.G., Tyson J.E. Quantitative comparison between biological and immunological activities of prolactin from human fetal and maternal source. J. Clin. Endocrinol. Metab. 55: 269, 1982. Golander A., Barrett J., Herley T., Barry S., Handswerger S. Failure of bromocriptine, dopamine and thyrotropinreleasing hormone to affect prolactin secretion by human decidual tissue in vitro. J. Clin. Endocrinol. Metab. 49: 787, 1979. Nelson K.G., Takahashi T., Lee D.C., Luetteke N.C., Bossert N.L., Ross K., Eitzman B.E., McLachlan J.A. Transforming growth factor-α is a potential mediator of estrogen action in the mouse uterus. Endocrinology 131: 1657, 1992. Chengi N., Leder P. Epidermal growth factor binding to human amnion, chorion, decidua, and placenta from mid and term pregnancy: quantitative light microscopic autoradiographic studies. J. Clin. Endocrinol. Metab. 61: 529, 1985. Adanson E.D., Meek J. The ontogeny of epidermal growth factor receptors during mouse development. Dev. Biol. 103: 62, 1984. Machida T., Taga M., Minaguchi H. The effect of epidermal growth factor and transforming growth factor-α on the mouse trophoblast outgrowth in vitro. Eur. J. Endocrinol. 133: 741, 1995. Schreiber A.B., Winker M.E., Derynck R. Transforming growth factor-α: a potent angiogenic mediator than epidermal growth factor. Science 232: 1250, 1986. Author information Authors and Affiliations Rights and permissions About this article Cite this article Taga, M., Saji, M., Suyama, K. et al. Transforming growth factor-α, like epidermal growth factor, stimulates cell proliferation and inhibits prolactin secretion in the human decidual cells in vitro . J Endocrinol Invest 19, 659–662 (1996). https://doi.org/10.1007/BF03349035 Accepted: Published: Issue date: DOI: https://doi.org/10.1007/BF03349035

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