Osteoporosis is a chronic condition chiefly affecting postmenopausal women, in whom the skeleton loses a significant percentage of its mineralized mass and mechanical resiliency, thereby becoming prone to fracture. Although the effect of the loss of estrogen on bone metabolism has been documented, its mechanism is still poorly understood. In the present proteomic study, we characterized the effect of estrogen deficiency on protein expression in rat bones. Using two-dimensional gel electrophoresis, mass spectrometry and rat protein database, we successfully identified three distinctly changed proteins named thioredoxin peroxidase 1, myosin light polypeptide 2 and ubiquitin-conjugating enzyme E2-17 kD, among which ubiquitin-conjugating enzyme E2-17 kD has been documented to be an estrogen-related protein, but the other two are first reported to be osteoporosis-related proteins in the current study. These results provide valuable experimental evidences for the elucidation of the molecular mechanism of osteoporosis related to the loss of estrogen.
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http://dx.doi.org/10.1016/j.lfs.2004.10.059 | DOI Listing |
Adv Exp Med Biol
January 2025
Molecular Oncology, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
RANK pathway has attracted increasing interest as a promising target in breast cancer, given the availability of denosumab, an anti-RANKL drug. RANK signaling mediates progesterone-driven regulation of mammary gland development and favors breast cancer initiation by controlling mammary cell proliferation and stem cell fate. RANK activation promotes luminal mammary epithelial cell senescence, acting as an initial barrier to tumorigenesis but ultimately facilitating tumor progression and metastasis.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Cancer Research UK Scotland Centre (Edinburgh), Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK.
E-cadherin is a transmembrane protein and central component of adherens junctions (AJs). The extracellular domain of E-cadherin forms homotypic interactions with E-cadherin on adjacent cells, facilitating the formation of cell-cell adhesions, known as AJs, between neighbouring cells. The intracellular domain of E-cadherin interacts with α-, β- and p120-catenins, linking the AJs to the actin cytoskeleton.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Laboratory of Stem Cells and Cancer (LSCC), Université Libre de Bruxelles (ULB), Brussels, Belgium.
This chapter focuses on the mechanisms of regulation of cell fate in breast development, occurring mainly after birth, as well as in breast cancer. First, we will review how the microenvironment of the breast, as well as external cues, plays a crucial role in mammary gland cell specification and will describe how it has been shown to reprogram non-mammary cells into mammary epithelial cells. Then we will focus on the transcription factors and master regulators which have been established to be determinant for basal (BC) and luminal cell (LC) identity, and will describe the experiments of ectopic expression or loss of function of these transcription factors which demonstrated that they were crucial for cell fate.
View Article and Find Full Text PDFJNCI Cancer Spectr
January 2025
Child Health and Development Studies, Public Health Institute, Berkeley, CA, USA.
Background: Adverse events in childhood are linked to cancer risk across the life course, but evidence is lacking regarding parental death during childhood and breast cancer (BrCa) characteristics. We investigated whether parental loss in childhood defines women at higher risk of BrCa incidence and aggressive disease.
Methods: The Child Health and Development Studies (CHDS) comprises over 15,000 families who enrolled during mothers' pregnancies between 1959-1967; family members were followed for cancer incidence and cause-specific mortality.
Am J Physiol Cell Physiol
January 2025
Mechanobiology and Medical Device Research Group (MMDRG), Biomedical Engineering, College of Science and Engineering, University of Galway, Ireland.
Osteoporosis is not merely a disease of bone loss but also involves changes in the mineral composition of the bone that remains. studies have investigated these changes and revealed that estrogen deficiency alters osteoblast mineral deposition, osteocyte mechanosensitivity and osteocyte regulation of osteoclastogenesis. During healthy bone development, vascular cells stimulate bone mineralization via endochondral ossification, but estrogen deficiency impairs vascularization.
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