This study aims to explore the potential pathways and molecular characteristics of fluorine-induced osteoblast apoptosis. In vitro fluorine-induced model was established with an osteogenesis sarcoma cell line Saos-2. Then flow cytometry was used to determine the mitochondrial membrane potential at 24 h after the intervention. 84 apoptosis-related genes in the cells were determined using the functional polymerase chain reaction (PCR) chip and part of the differentially expressed genes was verified with immune blotting. When the stimulated concentration of sodium fluoride were 20 mg/L, 40 mg/L and 80 mg/L, the mitochondrial membrane potential of the osteoblast cells were 27.0%, 28.8% and 38.6%, respectively, significantly higher than that in the blank control group (P<0.05). The PCR chip detection found 13 up-regulating genes and 15 down-regulating genes, among which the expression of Bim, Caspase 9, Caspase 14, B-cell lymphoma-2 (BCL2) and BAX increased with the doses of sodium fluoride, while the expression of Caspase 3 down-regulated in 5 mg/L sodium fluoride but up-regulated at the concentration of sodium fluoride more than 10 mg/L. Caspase 7 expression showed no obvious difference between the different concentration groups. However, Caspase 10 decreased with the increasing doses of sodium fluoride. Fluoride-induced osteoblast apoptosis may be through the mitochondrial pathway (including endoplasmic reticulum stress pathway) and death receptor pathway.
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Sci Rep
January 2025
Department of Molecular Medicine, Biochemistry Unit, University of Pavia, Via Taramelli 3B, 27100, Pavia, Italy.
Perfluorinated compounds (PFAS) are well recognized toxic pollutants for humans, but if their effect is equally harmful for healthy and fragile people is unknown. Addressing this question represents a need for ensuring global health and wellbeing to all individuals in a world facing the progressive increase of aging and aging related diseases. This study aimed to evaluate the impact of perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA) and perfluorohexanoic acid (PFHxA) exposure on development and skeletal phenotype using the osteogenesis imperfecta (OI) zebrafish model Chihuahua (Chi/+), carrying a dominant glycine substitution in the α1 chain of collagen I and their wild-type (WT) littermates.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
Hunan University of Chinese Medicine, Changsha 410208, China.
Objectives: To explore the mechanism by which histone deacetylase 1 (HDAC1) regulates steroid-induced apoptosis of mouse osteocyte-like MLO-Y4 cells.
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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.
View Article and Find Full Text PDFBone Res
January 2025
Department of Internal Medicine 3, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Osteocytes are the main cells in mineralized bone tissue. Elevated osteocyte apoptosis has been observed in lytic bone lesions of patients with multiple myeloma. However, their precise contribution to bone metastasis remains unclear.
View Article and Find Full Text PDFMol Ther Nucleic Acids
March 2025
Department of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an 710061, P.R. China.
Alternative splicing (AS) plays a critical role in gene expression by generating protein diversity from single genes. This review provides an overview of the role of AS in regulating cell fate, focusing on its involvement in processes such as cell proliferation, differentiation, apoptosis, and tumorigenesis. We explore how AS influences the cell cycle, particularly its impact on key stages like G1, S, and G2/M.
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