Nonylphenol affects myocardial contractility and L-type Ca2+ channel currents in a non-monotonic manner via G protein-coupled receptor 30

Gao, Qinghua; Liu, Shuyuan; Guo, Feng; Liu, Shuice; Yu, Xiao-Chun; Hu, Huiyuan; Sun, Xiaohong; Liang, Hao; Zhu, Tong

doi:10.1016/j.tox.2015.06.004

Cited by 23 publications

(12 citation statements)

References 31 publications

(35 reference statements)

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“…This effect could be related to the different Ca 2+ channels that are activated by either of these compounds in different cell types [31,32,33,75,76]. Interestingly, the ADAM17 activation induced by NP was higher than that induced by BPA in Ca 2+ -containing medium, but in a Ca 2+ -free medium BPA- and NP-induced ADAM17 sheddase activity was similar, demonstrating that both compounds have a similar basal effect.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17

Urriola-Muñoz

Lagos-Cabré

Patiño-García

et al. 2018

IJMS

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Endocrine-disruptor chemicals (EDCs), such as bisphenol A (BPA) and nonylphenol (NP), have been widely studied due to their negative effects on human and wildlife reproduction. Exposure to BPA or NP is related to cell death, hormonal deregulation, and cancer onset. Our previous studies showed that both compounds induce A Disintegrin And Metalloprotease 17 (ADAM17) activation. Here, we show that BPA and NP induce apoptosis in prostate and ovary cancer cell lines, in a process dependent on ADAM17 activation. ADAM17 knockdown completely prevented apoptosis as well as the shedding of ADAM17 substrates. Both compounds were found to induce an increase in intracellular calcium (Ca2+) only in Ca2+-containing medium, with the NP-treated cells response being more robust than those treated with BPA. Additionally, using a phosphorylated protein microarray, we found that both compounds stimulate common intracellular pathways related to cell growth, differentiation, survival, and apoptosis. These results suggest that BPA and NP could induce apoptosis through ADAM17 by activating different intracellular signaling pathways that may converge in different cellular responses, one of which is apoptosis. These results confirm the capacity of these compounds to induce cell apoptosis in cancer cell lines and uncover ADAM17 as a key regulator of this process in response to EDCs.

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Section: Discussionmentioning

confidence: 99%

Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17

Urriola-Muñoz

Lagos-Cabré

Patiño-García

et al. 2018

IJMS

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“…Nonylphenol is an extensively used compound in both commercial and household products that also binds GPER and induces adenylyl cyclase activity (129). In the heart, nonylphenol has non-monotonic effects on myocardial contractility, and a GPER antagonist prevents low but not high dose effects (143). BPA also induces negative effects on the cardiac extracellular matrix and the baroreflex (144), but whether these effects occur via GPER is yet to be determined.…”

Section: Environmental Healthmentioning

confidence: 99%

GPER–novel membrane oestrogen receptor

et al. 2016

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The recent discovery of the G protein-coupled estrogen receptor (GPER) presents new challenges and opportunities for understanding the physiology, pathophysiology, and pharmacology of many diseases. This review will focus on the expression and function of GPER in hypertension, kidney disease, atherosclerosis, vascular remodeling, heart failure, reproduction, metabolic disorders, cancer, environmental health, and menopause. Furthermore, this review will highlight the potential of GPER as a therapeutic target.

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“…105 Whether rapid signaling from GPER by E2 modulates cardiomyocyte E-C coupling needs further confirmation.…”

Section: Estrogen and Ers In Cardiac Electrophysiology And Contractionmentioning

confidence: 99%

The Role of Estrogen and Estrogen Receptors on Cardiomyocytes: An Overview

Luo

Kim

2016

Canadian Journal of Cardiology

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Sex differences in the onset and manifestation of cardiovascular diseases are well known, yet the mechanism behind this discrepancy remains obscure. Estrogen and its corresponding receptors have been studied for their positive salutary effects in females for decades. Estrogen protects the heart from various forms of stress, including cytotoxic, ischemic and hypertrophic stimuli. The postulated underlying mechanism is complex, and involves the actions of the hormone on the endothelium and myocardium. While the effects of estrogen on the coronary endothelium are well-described, delineation of the hormone’s action on cardiomyocytes is still evolving. The focus of this article is to review the accumulated literature and latest data on the role of estrogen and its receptors on cardiomyocytes, the contractile cellular units of the myocardium.

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Nonylphenol affects myocardial contractility and L-type Ca2+ channel currents in a non-monotonic manner via G protein-coupled receptor 30

Cited by 23 publications

References 31 publications

Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17

Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17

GPER–novel membrane oestrogen receptor

The Role of Estrogen and Estrogen Receptors on Cardiomyocytes: An Overview

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