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Cited by 13Estrogen and related hormone effectsMitochondrial Function and PathologyIon Channels and Receptors

Estradiol effects on intracellular Ca2+ homeostasis in bovine brain-derived endothelial cells

Suman, Matteo, Giacomello, Marta, Corain, Livio, Ballarin, Cristina, Montelli, Stefano, Cozzi, Bruno, Peruffo, Antonella·2012·Cell and Tissue Research
DOI 10.1007/s00441-012-1460-2
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Abstract

Estrogens diversely affect various physiological processes by genomic or non-genomic mechanisms, in both excitable and non-excitable cells. Additional to the trophic effects of estrogens promoting cell growth and differentiation, recent experimental evidence highlights their involvement in the regulation of intracellular Ca(2+) homeostasis. The effects of estrogens on excitable cells are well documented. However, these steroids also influence numerous physiological events in non-excitable cells, such as fibroblasts or vascular endothelial cells. We have focused our attention on an immortalized endothelial-like cell line derived from fetal bovine cerebellum. Estradiol (E(2)) effects on intracellular Ca(2+) homeostasis were tested by varying the exposure time to the hormone (8, 24, 48 h). Calcium measurements were performed with genetically encoded Ca(2+) probes (Cameleons) targeted to the main subcellular compartments involved in intracellular Ca(2+) homeostasis (cytosol, endoplasmic reticulum, mitochondria). Mitochondrial Ca(2+) uptake significantly decreased after 48-h exposure to E(2), whereas cytosolic and endoplasmic reticulum responses were unaffected. The effect of E(2) on mitochondrial Ca(2+) handling was blocked by ICI 182,780, a pure estrogen receptor antagonist, suggesting that the effect was estrogen-receptor-mediated. To evaluate whether the decrease of Ca(2+) uptake affected mitochondrial membrane potential (ΔΨm), cells were monitored in the presence of tetra-methyl-rhodamine-methylester; no significant changes were seen between cells treated with E(2) and controls. To investigate a mechanism of action, we assessed the possibile involvement of the permeability transition pore (PTP), an inner mitochondrial membrane channel influencing energy metabolism and cell viability. We treated cells with CyclosporinA (CsA), which binds to the matrix chaperone cyclophilin-D and regulates PTP opening. CsA reversed the effects of a 48-h treatment with E(2), suggesting a possible transcriptional modulation of proteins involved in the mitochondrial permeability transition process.

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  • 17β-estradiol regulates multiple other aspects of mitochondrial function through ERs, including ROS generation, antioxidant defense, and Ca2+ handling.

    “Moreover, 17β-estradiol also appears to regulate multiple other aspects of mitochondrial function through ERs, including ROS generation, antioxidant defense, and Ca2+ handling (126–131).”

    From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [130]

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Authors
Suman, M., Giacomello, M., Corain, L., Ballarin, C., Montelli, S., Cozzi, B., & Peruffo, A.
Affiliations
University of Padua (IT)
Corresponding author
Peruffo, Antonella
ORCID
Venue
Cell and Tissue Research
Publisher
Springer Science and Business Media LLC
Published
2012-07-20
Volume
350
Issue
1
Pages
109-118
ISSN
  • 0302-766X (ISSN-L)
  • 1432-0878
DOI
10.1007/s00441-012-1460-2
OpenAlex
W1971420033
Cited by
13
References
49
Citations by year
2025: 1 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 1 · 2017: 1 · 2016: 2 · 2014: 2
FWCI
0.38
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Cell and Tissue Research (publishedVersion)
  • PubMed (publishedVersion)
  • Padua Research Archive (University of Padova) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
estradiol, intracellular calcium homeostasis, mitochondrial calcium uptake, endothelial cells, estrogen receptor, mitochondrial permeability transition pore, cyclosporine, cyclophilin D, mitochondrial membrane potential, non-genomic estrogen signaling, fulvestrant
MeSH terms
Animals, Brain, Calcium, Cattle, Cell Line, Cytosol, Estradiol, Homeostasis, Immunohistochemistry, Kinetics, Male, Microscopy, Fluorescence, Mitochondria, Receptors, Estrogen, Transfection, DNA, Complementary, Intracellular Space, Endothelial Cells

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