Inhibition of osteoblast differentiation by aluminum trichloride exposure is associated with inhibition of BMP-2/Smad pathway component expression

Yang, Xu; Huo, Hui Jun; Xiu, Chunyu; Song, Miao; Han, Yaling; Li, Yanfei; Zhu, Yanzhu

doi:10.1016/j.fct.2016.09.004

Cited by 22 publications

(14 citation statements)

References 41 publications

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“…Lingqian et al reported that the cotherapy with the parathyroid hormone (PTH) and SDF-1 promoted osteogenic differentiation of human periodontal ligament stem cells by enhancing OCN expression and ALP activity [54], which is in line with the findings of the present study. Osteoblast differentiation is key to bone formation, in which bone morphogenetic protein-2/Smad signaling pathway is involved [55]. As shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

Stromal-Cell-Derived Factor (SDF) 1-Alpha Overexpression Promotes Bone Regeneration by Osteogenesis and Angiogenesis in Osteonecrosis of the Femoral Head

Yang

Xue

Guan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteonecrosis of the femoral head (ONFH) is a devastating orthopedic disease. Previous studies suggested that stromal-cell-derived factor (SDF)-1 was involved in osteogenesis and angiogenesis. However, whether SDF-1 potentiates the angiogenesis and osteogenesis of bone marrow-derived stromal stem cells (BMSCs) in ONFH is not clear. Methods: BMSCs were transfected with green fluorescent protein (GFP) or the fusion gene encoding GFP and SDF-1α, and transgenic efficacy was monitored by immunofluorescence. The expression of SDF-1α, runt-related transcription factor 2 (Runx2, osteocalcin (OCN), and alkaline phosphatase (ALP) at the mRNA level was measured by real-time polymerase chain reactions (RT-PCR). The expression of SDF-1α, Runx2, OCN, and p-Smad1/5 were measured at the protein level by Western blot. Transwell migration assay and tube formation assay were utilized to detect the angiogenesis in vitro, whereas the in vivo angiogenesis was monitored by angiography. Immunohistological staining and micro-CT scanning were conducted to assess the histological changes in morphology. Results: In vitro, SDF-1α overexpression in BMSCs promoted osteogenic differentiation and upregulated the expression of osteogenic-related proteins, such as ALP, Runx2, OCN, and p-Smadl/5. In the methylprednisolone induced ONFH rat model used in our investigation, the overexpression of SDF-1α in BMSCs promoted significantly more bone regeneration and the expression of OCN and Runx2 as compared with the effect of vehicle overexpression. Moreover, the morphology of ONFH was ameliorated after the transplantation of BMSCs with SDF-1α overexpression. Furthermore, SDF-1α overexpression in BMSCs significantly increased osteoblastic angiogenesis as indicated by the increased tube formation ability, CD31 expression, and vessel volume. Conclusion: SDF-1α overexpression in BMSCs promotes bone generation as indicated by osteogenesis and angiogenesis, suggesting SDF-1α may serve as a therapeutic drug target for ONFH treatment.

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Section: Discussionmentioning

confidence: 99%

Stromal-Cell-Derived Factor (SDF) 1-Alpha Overexpression Promotes Bone Regeneration by Osteogenesis and Angiogenesis in Osteonecrosis of the Femoral Head

Yang

Xue

Guan

et al. 2018

Cell Physiol Biochem

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“…Somatic and germinal genetoxicity in mice exposed to Al was associated with chromosomal aberrations and depression of mitosis (D'Souza et al, 2014). Neuronal gene expression is influenced by the binding of Al to DNA (Lukiw et al, 1998) predisposing cells to or causing genotoxicity (Pogue and Lukiw, 2016) and thus Al exposure may lead to reduction of cell proliferation and differentiation (Nam et al, 2014(Nam et al, , 2016Sun et al, 2015;Cao et al, 2016;Li et al, 2016;Yang et al, 2016;Sun et al, , 2017Huang et al, 2017). Neurogenesis was impaired by Al toxicity (Nam et al, 2014(Nam et al, , 2016.…”

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

“…Osteoblastic proliferation and differentiation were inhibited by Al when there was downregulation and inhibition of Wnt/β-catenin signaling pathway (Sun et al, 2015;Cao et al, 2016;Huang et al, 2017;Sun et al, 2017). Osteoblast differentiation was also inhibited by Al through the inhibition of BMP-2 signaling pathway (Yang et al, 2016). In addition, osteoblast mineralization in vitro was inhibited by Al-induced decline in transforming growth factor (TGF)-β1 expression and action, and upregulation of Smad7 expression along with decreased protein expressions of osteopontin, osteocalcin and osteosialoprotein (Song et al, 2017).…”

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

“…Taken together, Al toxicosis may cause muscle damage, inflammation and dysfunction The bone diseases associated with Al exposure are osteoporosis, osteomalcia, rickets, exostosis, osteodystrophy and osteitis fibrosa (Sherrard et al, 1985;Chappard et al, 2016;Rodríguez and Mandalunis, 2018;Klein, 2019). There is increased risk of osteoporosis and low bone mineral density during Al exposure (Cao et al, 2016; because of disruption of bone formation, and inhibition of osteoblast proliferation, differentiation and mineralization (Li et al, 2012(Li et al, , 2016Cao et al, 2016;Yang et al, 2016;Zhu et al, 2016b;Song et al, 2017;Sun et al, 2017;Huang et al, 2017). In individuals with Al overload, undecalcified bone matrix contains Al and bone conditions like exostosis and osteomalacia may occur in circumstances that increase Al uptake and colocalization as observed in celiac disease, hemochromatosis and sickle cell anemia (Chappard et al, 2016).…”

Section: Musculoskeletal Effectsmentioning

confidence: 99%

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Aluminium toxicosis: a review of toxic actions and effects

Igbokwe

Igwenagu

Igbokwe

2019

Interdisciplinary Toxicology

262

149

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Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.

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“…Aluminum exposure impairs bone formation; inhibition of bone formation by aluminum through different signal transduction pathways has been reported [121]. Exposure to Al is associated with low bone mineral density (BMD) and an increased risk of osteoporosis [121][122][123][124]. Fluoride enhances the uptake of aluminum; the simultaneous administration of fluorine and aluminum increased plasma [125], and bone [126] concentrations of aluminum in rats, whereas aluminum suppresses the uptake of fluoride [127].…”

Section: Co-exposure With Other Elementmentioning

confidence: 99%

Progressive Research in the Molecular Mechanisms of Chronic Fluorosis

Shen¹,

Feng²,

Xia³

et al. 2019

Environmental Chemistry and Recent Pollution Control Approaches

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Long-term excessive intake of fluoride (F) leads to chronic fluorosis, resulting in dental fluorosis and skeletal fluorosis. Chronic exposure to high doses of fluoride can also cause damage to soft tissues, especially when it passes through the blood-brain, blood-testis, and blood-placenta barrier, causing damage to the corresponding tissues. Fluorosis has become a public health problem in some countries or regions around the world. Understanding the pathogenesis of fluorosis is very important. Although the exact mechanism of fluorosis has not been fully elucidated, various mechanisms of fluoride-induced toxicity have been proposed. In this chapter, we will introduce the research progress of the mechanism of fluorosis, focusing on dental fluorosis, skeletal fluorosis, nervous and reproductive system toxicity, and influential factors related to fluoride toxicity (i.e., genetic background, co-exposure with other element). In addition, the application of proteomics and metabolomics in the study of the pathogenesis of fluorosis is also introduced. Currently, there is still no specific treatment for fluorosis. However, since fluorosis is caused by excessive intake of fluoride, avoiding excessive fluoride intake is the critical measure to prevent the disease. In endemic regions, health education and supplement diet with vitamins C, D and E, and calcium and antioxidant compounds are important.

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Inhibition of osteoblast differentiation by aluminum trichloride exposure is associated with inhibition of BMP-2/Smad pathway component expression

Cited by 22 publications

References 41 publications

Stromal-Cell-Derived Factor (SDF) 1-Alpha Overexpression Promotes Bone Regeneration by Osteogenesis and Angiogenesis in Osteonecrosis of the Femoral Head

Stromal-Cell-Derived Factor (SDF) 1-Alpha Overexpression Promotes Bone Regeneration by Osteogenesis and Angiogenesis in Osteonecrosis of the Femoral Head

Aluminium toxicosis: a review of toxic actions and effects

Progressive Research in the Molecular Mechanisms of Chronic Fluorosis

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