Role of 17β-estradiol and testosterone in apoptosis

Vasconsuelo, Andrea Anahi; Pronsato, Lucía; Ronda, Ana Carolina; Boland, Ricardo; Milanesi, Lorena Magdalena

doi:10.1016/j.steroids.2011.08.001

Cited by 77 publications

(59 citation statements)

References 128 publications

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“…Cells exposed to the crude extract, to the hexane or to the chloroform sub-extracts shown typical apoptotic morphology (nuclear condensation / fragmentation, mitochondrial picnosis and clustering of the organelle near the nucleus) similar to H2O2 treatment. Opposing to ours previous works in which we observed that 17β-estradiol protects the skeletal muscle cells inhibiting the H2O2-induced apoptosis [52], here we found that the crude extract and sub-extracts of hexane and chloroform from N. glauca induced apoptosis in C2C12 cells. Indeed, in accordance with the results from Tunel assays, we found an important activation of caspases when cells were treated with the lipid hexane and chloroform sub-extracts, being the hexane sub-extract the most potent.…”

Section: Discussioncontrasting

confidence: 97%

EXTRACTS FROM <em>Nicotiana glauca</em> INDUCE APOPTOSIS THROUGH CASPASES IN SKELETAL MUSCLE CELLS

Lincor

Musso

Vasconsuelo

et al. 2017

Proceedings of the 21st International Electronic Conference on Synthetic Organic Chemistry

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Phytoestrogens are plant compounds which have generated considerable interests. A litany of health benefits including a lowered risk of osteoporosis, breast cancer, and menopausal symptoms, are frequently attributed to phytoestrogens but without the knowledge of their side effects. We investigate the effects of lipid extracts from the Solanaceae Nicotiana glauca on skeletal muscle cells, in relation to apoptosis. Opposite to the effects of 17β-estradiol, the crude extract from N. glauca and its sub-extracts induced apoptosis in C2C12 cells. This apoptotic action involved caspase 3/7 activation. These data suggest that the traditional use of this medicinal plant could affect the skeletal muscle homeostasis.

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Section: Discussioncontrasting

confidence: 97%

EXTRACTS FROM <em>Nicotiana glauca</em> INDUCE APOPTOSIS THROUGH CASPASES IN SKELETAL MUSCLE CELLS

Lincor

Musso

Vasconsuelo

et al. 2017

Proceedings of the 21st International Electronic Conference on Synthetic Organic Chemistry

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“…Although the classical target of estrogens is the nucleus, it has been demonstrated in the last years that E 2 can act at different cellular sites including mitochondria (reviewed in Vasconsuelo et al (2011)). In previous studies, we showed that E 2 abrogates H 2 O 2 -induced apoptosis in skeletal muscle cells involving both ERa and ERb, PI3K/Akt/Bad, HSP27, and MAPKs (Vasconsuelo et al 2008, Ronda et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…One of the reasons for this opening out in the non-conventional estrogen actions was the finding of ER in non-classical tissues and with non-classical intracellular localizations. For example, the presence of ERs in mitochondria of C2C12 skeletal myoblasts has previously been shown (reviewed in Vasconsuelo et al (2011)). Although the localization of mitochondrial ERs is well established, allowing one to envision an influence of E 2 upon mitochondrial functions, the physiological role of the steroid at this cellular level remains unclear.…”

Section: Introductionmentioning

confidence: 95%

“…The actions of E 2 have been typically linked to reproductive functions. However, during the last decade it has been shown that practically every animal cell/tissue/organ system responds to the hormone to some extent (reviewed in Vasconsuelo et al (2011)). One of the reasons for this opening out in the non-conventional estrogen actions was the finding of ER in non-classical tissues and with non-classical intracellular localizations.…”

Section: Introductionmentioning

confidence: 99%

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Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Colla¹,

Vasconsuelo²,

Boland³

2012

Journal of Endocrinology

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Abstract17b-Estradiol (E 2 ) protects several non-reproductive tissues from apoptosis, including skeletal muscle. We have shown that E 2 at physiological concentrations prevented apoptosis induced by H 2 O 2 in C2C12 skeletal myoblasts. As we also demonstrated the presence of estrogen receptors in mitochondria, the present work was focused on the effects of E 2 on this organelle. Specifically, we evaluated the actions of E 2 on the mitochondrial permeability transition pore (MPTP) by the calcein-acetoxymethylester/cobalt method using fluorescence microscopy and flow cytometry. Pretreatment with E 2 prevented MPTP opening induced by H 2 O 2 , which preceded loss of mitochondrial membrane potential. In addition, it was observed that H 2 O 2 induced translocation of Bax to mitochondria; however, in the presence of the steroid this effect was abrogated suggesting that members of the Bcl-2 family may be regulated by E 2 to exert an antiapoptotic effect. Moreover, E 2 increased mitochondrial manganese superoxide dismutase protein expression and activity, as part of a mechanism activated by E 2 that improved mitochondrial performance. Our results suggest a role of E 2 in the regulation of apoptosis with a clear action at the mitochondrial level in C2C12 skeletal myoblast cells. Key Words" 17b-estradiol " C2C12 skeletal myoblasts

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“…27 The role of GPER in mediating the growth-regulating effects of estrogen in the vasculature remains unclear. In other tissues, both pro-and antiapoptotic effects of estrogens have been reported 28 as have pro-and antiproliferative effects. 29 Studies from our laboratory have highlighted the opposing effects on apoptosis of GPER versus ERα in vascular cells.…”

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confidence: 99%

Extent of Vascular Remodeling Is Dependent on the Balance Between Estrogen Receptor α and G-Protein–Coupled Estrogen Receptor

et al. 2016

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Abstract-Estrogens are important regulators of cardiovascular function. Some of estrogen's cardiovascular effects are mediated by a G-protein-coupled receptor mechanism, namely, G-protein-coupled estrogen receptor (GPER). Estradiol-mediated regulation of vascular cell programmed cell death reflects the balance of the opposing actions of GPER versus estrogen receptor α (ERα). However, the significance of these opposing actions on the regulation of vascular smooth muscle cell proliferation or migration in vitro is unclear, and the significance in vivo is unknown.To determine the effects of GPER activation in vitro, we studied rat aortic vascular smooth muscle cells maintained in primary culture. GPER was reintroduced using adenoviral gene transfer. Both estradiol and G1, a GPER agonist, inhibited both proliferation and cell migration effects that were blocked by the GPER antagonist, G15. To determine the importance of the GPER-ERα balance in regulating vascular remodeling in a rat model of carotid ligation, we studied the effects of upregulation of GPER expression versus downregulation of ERα. Reintroduction of GPER significantly attenuated the extent of medial hypertrophy and attenuated the extent of CD45 labeling. Downregulation of ERα expression comparably attenuated the extent of medial hypertrophy and inflammation after carotid ligation. These studies demonstrate that the balance between GPER and ERα regulates vascular remodeling. Receptor-specific modulation of estrogen's effects may be an important new approach in modifying vascular remodeling in both acute settings like vascular injury and perhaps in longer term regulation like in hypertension. Our initial focus on ERα (versus ER β , which is also expressed in rat aortic vascular smooth muscle cells [VSMCs]) was based on our demonstration that in isolated rat VSMCs, estradiol's (E2) antiapoptotic effects were mediated via ERα. 30 In contrast, E2 acting via GPER was proapoptotic. However, the in vivo implications of these receptor-specific opposing effects of estradiol on growth regulation have yet to be established.In these studies, we examined the process of vascular remodeling to understand how E2 regulates vascular growth via GPER versus ERα. Remodeling occurs subsequent to several vascular stressors including hypertension, 31 atherosclerosis, 32 and vascular injury 33 and can be associated with both adaptive responses (as in vascular injury) and maladaptive responses (as in hypertension and in vascular restenosis). The VSMC hypertrophy and hyperplasia that occurs in remodeling processes has been linked to a shift in the balance between proliferative and apoptotic mechanisms and a dedifferentiation of VSMCs from a contractile phenotype, as seen under normal conditions in situ, to a so-called synthetic phenotype, 34 as seen after vascular injury. This latter phenotype is characterized as having higher proliferative rates and greater migratory behavior. This synthetic phenotype is more similar to the phenotype of VSMCs maintained in primary culture, 35 th...

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Role of 17β-estradiol and testosterone in apoptosis

Cited by 77 publications

References 128 publications

EXTRACTS FROM <em>Nicotiana glauca</em> INDUCE APOPTOSIS THROUGH CASPASES IN SKELETAL MUSCLE CELLS

EXTRACTS FROM <em>Nicotiana glauca</em> INDUCE APOPTOSIS THROUGH CASPASES IN SKELETAL MUSCLE CELLS

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Extent of Vascular Remodeling Is Dependent on the Balance Between Estrogen Receptor α and G-Protein–Coupled Estrogen Receptor

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