Novel non-transcriptional mechanisms for estrogen receptor signaling in the cardiovascular system

Simoncini, Tommaso; Fornari, Letizia; Mannella, Paolo; Varone, G.L.; Caruso, A.; Liao, James K.; Genazzani, Andrea R.

doi:10.1016/s0039-128x(02)00040-5

Cited by 82 publications

(55 citation statements)

References 46 publications

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“…The immunohistochemical changes in the receptors in the LCs could be a response to the low T biosynthesis rather than a causative factor for the hyperplasia. Prenatal DBP exposure might extend beyond the reproductive organs, to include the systemic physiology, because ERa is expressed in other tissues, for example, the efferent ducts and initial part of the epididymis, the cardiovascular system and bones (Gustafsson 1999;Mueller and Korach 2001;Simoncini et al 2002;Hess 2003;Arias-Loza et al 2006;Ropero et al 2006;Bolego et al 2010). Moreover, there is a need to find out the detailed cellular localization of ERa, ERb, and AR within the testis following prenatal exposure to DBP and their roles in testicular development and normal physiology.…”

Section: Discussionmentioning

confidence: 99%

Effects ofin UteroExposure to Di(n-butyl) Phthalate for Estrogen Receptors α, β, and Androgen Receptor of Leydig Cell on Rats

et al. 2013

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Estrogens and androgens affect male and female reproductive systems. Recently, we reported that prenatal di(n-butyl) phthalate (DBP) exposure induced atypical Leydig cells (LCs) hyperplasia during adulthood. The present study investigated the expression of estrogen receptor a (ERa), estrogen receptor b (ERb), and androgen receptor (AR) in LCs of 5-, 7-, 9-, 14-, and 17-week-old Sprague-Dawley (srl) rats whose dams had been administered DBP intragastrically at 100 mg/kg/day or the vehicle (corn oil) from days 12 to 21 postconception. Immunohistochemical, Western blotting, and reverse transcription polymerase chain reaction analyses revealed that the expressions of ERa, ERb, and AR proteins and mRNAs in the DBP group were similar to those of the vehicle group at 5 and 7 weeks, but significantly higher ERa and lower ERb and AR levels were observed in the DBP group at 9 to 17 weeks. The rats prenatally exposed to DBP had seminiferous tubule degeneration and atypical hyperplasia of LCs during adulthood, which was associated with an increase in expression of ERa and a decrease of ERb and AR in the testis.

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Section: Discussionmentioning

confidence: 99%

Effects ofin UteroExposure to Di(n-butyl) Phthalate for Estrogen Receptors α, β, and Androgen Receptor of Leydig Cell on Rats

et al. 2013

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“…These effects may be mediated by membrane receptors (Thomas et al, 2004;2005) or through interactions between classic steroid receptors and nongenomic intracellular pathways (Kousteni et al, 2001;Boonyaratanakornkit and Edwards, 2004). Several reports have suggested that the actions of steroid hormones on the cardiovascular system are mediated through nongenomic mechanisms (Wehling 1995;Simoncini et al, 2002) but the role of such mechanisms in the control of blood vessels in the primate reproductive system, including the endometrium, is unknown.…”

Section: Discussionmentioning

confidence: 99%

Steroid receptors in blood vessels of the rhesus macaque endometrium: a review

Brenner

Slayden

2004

Archives of Histology and Cytology

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“…This so-called nongenomic ER action (also referred to as membrane-initiated steroid signaling or MISS) (Nemere et al 2003) has been described in many tissues and target organs as the crucial activity for mediating many estrogen responses (Dhandapani & Brann 2002, Ho & Liao 2002, Kousteni et al 2002, Simoncini et al 2002. Recently, a role for nongenomic ER activity in mediating estrogen-induced growth and survival effects has also been described in breast cancer cells, and the existence of membrane ER has now been established by numerous biochemical, immunohistological, and genetic methods (Levin 2002, Pedram et al 2002, Razandi et al 2003b).…”

Section: Er Functions and Crosstalk With Growth Factor Receptor Pathwaysmentioning

confidence: 99%

Resistance to endocrine therapy in breast cancer: exploiting estrogen receptor/growth factor signaling crosstalk

Massarweh¹,

Schiff²

2006

Endocr Relat Cancer

142

129

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Targeting the estrogen receptor (ER) is the oldest form of molecular targeted therapy, and the widespread use of the selective estrogen receptor modulator tamoxifen in breast cancer is responsible for major improvements in cure rates, quality of life, and disease prevention in the last 25 years. Newer forms of endocrine therapy now available for the management of endocrine responsive breast cancer include a new generation of aromatase inhibitors, which lower the estrogen ligand for ER, and pure ER antagonists which destroy the receptor. Despite these recent clinical advances, intrinsic and acquired resistance to these endocrine therapies is still a common feature that limits the success of this therapeutic strategy. Recent research into the molecular biology of ER signaling has revealed a remarkably complex interactive signaling with other growth factor signaling pathways in breast cancer cells, potentially explaining some of the reasons behind endocrine therapy action as well as resistance. This view of a more complex ER signaling system has uncovered new molecular targets which, if present in a cancer cell, might be additionally targeted using various signal transduction inhibitors to overcome or prevent resistance to endocrine therapy. In addition, the dynamic inverse relationship between the expression of ER and growth factor receptors brings more excitement to the potential of restoring ER expression in apparently ER-negative cells by inhibition of growth factor signaling. Ongoing clinical trials of endocrine therapy combined with growth factor pathway inhibitors or their downstream signaling elements promise to further improve the present care for breast cancer patients.

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Novel non-transcriptional mechanisms for estrogen receptor signaling in the cardiovascular system

Cited by 82 publications

References 46 publications

Effects ofin UteroExposure to Di(n-butyl) Phthalate for Estrogen Receptors α, β, and Androgen Receptor of Leydig Cell on Rats

Effects ofin UteroExposure to Di(n-butyl) Phthalate for Estrogen Receptors α, β, and Androgen Receptor of Leydig Cell on Rats

Steroid receptors in blood vessels of the rhesus macaque endometrium: a review

Resistance to endocrine therapy in breast cancer: exploiting estrogen receptor/growth factor signaling crosstalk

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