Influence of Growth Factors EGF, IGF‐1, and Human Growth Hormone on Human Endometrial Stromal Cells <i>in Vitro</i>

Strowitzki, T.; Wiedemann, R.; Hepp, H

doi:10.1111/j.1749-6632.1991.tb37925.x

Cited by 21 publications

(12 citation statements)

References 8 publications

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“…In the proliferative phase TNF-α might enhance the proliferation of the endometrium by promoting DNA synthesis in endometrial and stromal cells (Hunt et al, 1992). Another mode of action could be the induction of receptors and cytokines with a high proliferative potential, as is seen with epidermal growth factor induction (Tomooka et al, 1986;Strowitzki et al, 1991) by TNF-α as described in glioma cells (Adachi et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor-alpha (TNF-alpha) in human endometrium and uterine secretion: an evaluation by immunohistochemistry, ELISA and semiquantitative RTPCR

Wolff

Claßen-Linke²,

Heid³

et al. 1999

Molecular Human Reproduction

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Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor-alpha (TNF-alpha) in human endometrium and uterine secretion: an evaluation by immunohistochemistry, ELISA and semiquantitative RTPCR

Wolff

Claßen-Linke²,

Heid³

et al. 1999

Molecular Human Reproduction

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“…Local GH actions are also thought to stimulate the development and hatching of mouse pre-implantation embryos (Drakakis et al 1995, Fukaya et al 1998. Paracrine or autocrine actions of GH are similarly thought to be responsible for the growth and differentiation of immune tissues and hematopoietic cells (Auernhammer & Strasburger 1995, Hull & Harvey 1997, and for the growth and differentiation of mammary and uterine tissues (Strowitzki et al 1991, Mol et al 1996), pituitary cells (Gardner et al 1990, fibroblasts (Hauner 1992) and adipocytes (Catalioto et al 1992). The recent demonstration of GH and GHR immunoreactivity in the teeth of perinatal rats is similarly thought to reflect local actions of GH in chondrocyte development (Zhang et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Extra-pituitary growth hormone in peripheral tissues of early chick embryos

Harvey

Johnson²,

Sanders³

2000

Journal of Endocrinology

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Early embryonic growth is independent of pituitary growth hormone (GH), since it occurs prior to the differentiation of pituitary somatotrophs. Embryogenesis is therefore thought to be regulated by local growth factors. As GH is now known to be produced in many extrapituitary sites, in which it acts in an autocrine or paracrine manner, the possibility that extra-pituitary GH may participate in embryogenesis and organogenesis was assessed by determining the immunocytochemical presence and location of GH-and GH-receptor (GHR)-like proteins in the peripheral tissues of chick embryos during their 21-day incubation period.Immunoreactive (IR)-GH, detectable by a monoclonal and two polyclonal antibodies for chicken GH, was specifically and ubiquitously present in tissues of 3-day-old embryos. At embryonic day (ED) 5, IR-GH was widespread in ectodermal, mesodermal and endodermal tissues, but it was not present in every cell of each tissue. IR-GH was particularly abundant in the neural tube, notochord, limb bud, somites, heart, stomach, liver, kidney, Wolffian duct and the amnion. By ED8, IR-GH was still widespread and was now present in limb bud cartilage, although the heart and liver were no longer GH immunoreactive. GH receptor immunoreactivity was also present in most tissues and cells of ED3-ED8 embryos.These results demonstrate that extrapituitary GH is abundantly present during early embryogenesis, prior to the differentiation of pituitary somatotrophs (at ED12). Since GH-and GHR-like proteins are present in most tissues of the chick embryo, it is proposed that extrapituitary GH may act as a local growth factor during embryonic development.

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“…Complement components C3 and C4, mediators of host responses to inflammation, are also increased in the peritoneal fluid of women with endometriosis. These secretory products have been indirectly implicated as adversely affecting fertility and also stimulating the implantation and proliferation of endometrial cells 23‐25…”

Section: Introductionmentioning

confidence: 99%

“…These secretory products have been indirectly implicated as adversely affecting fertility and also stimulating the implantation and proliferation of endometrial cells. [23][24][25] In a small, randomized, controlled trial in which pentoxifylline, a phosphodiesterase inhibitor with anti-inflammatory properties, was tested, pregnancy rates were 31% with treatment and only 18.5% in the placebo group. 26 Although this is only one study and the data are not statistically significant, it supports the hypothesis that inflammation may be a major culprit of endometriosis-associated infertility.…”

Section: Introductionmentioning

confidence: 99%

Endometriosis and Inflammation in Infertility

Halis

Arıcı

2004

Annals of the New York Academy of Sciences

139

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A wealth of publications proposes that endometriosis and inflammation may have an unfavorable influence on fertility. A recent meta-analysis of assisted reproductive technologies demonstrated that, once confounding factors are controlled for, the pregnancy rate in women with endometriosis is approximately 50% of the rate of women with tubal factor infertility. Peritoneal fluid of women with endometriosis contains elevated amounts of macrophages and their secreted products, such as growth factors, cytokines, and angiogenic factors. Because reproductive organs are bathed in and thus will be influenced by peritoneal fluid, these proinflammatory mediators would affect various aspects of reproduction in women with endometriosis. Advanced stages of endometriosis may have easily understandable factors, such as distortion of the anatomy, causing infertility. On the other hand, in minimal or mild endometriosis mechanisms underlying reproductive failure are subtle and remain controversial. Recent reports suggest that inflammatory factors play a role in this endometriosis-associated reproductive failure. This review provides an overview of recent data on the effects of endometriosis-associated inflammation on fertility.

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Influence of Growth Factors EGF, IGF‐1, and Human Growth Hormone on Human Endometrial Stromal Cells in Vitro

Cited by 21 publications

References 8 publications

Tumour necrosis factor-alpha (TNF-alpha) in human endometrium and uterine secretion: an evaluation by immunohistochemistry, ELISA and semiquantitative RTPCR

Tumour necrosis factor-alpha (TNF-alpha) in human endometrium and uterine secretion: an evaluation by immunohistochemistry, ELISA and semiquantitative RTPCR

Extra-pituitary growth hormone in peripheral tissues of early chick embryos

Endometriosis and Inflammation in Infertility

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