Advances in the osteoblast lineage

1998 ◽  
Vol 76 (6) ◽  
pp. 899-910 ◽  
Author(s):  
Jane E Aubin
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Osteoblast Differentiation ◽  
Skeletal Development ◽  
Proliferation And Differentiation ◽  
Gene Expression Heterogeneity ◽  
Adult Organism ◽  
Differential Gene ◽  
Osteoblast Markers ◽  
Osteoblast Lineage

Osteoblasts are the skeletal cells responsible for synthesis, deposition and mineralization of the extracellular matrix of bone. By mechanisms that are only beginning to be understood, stem and primitive osteoprogenitors and related mesenchymal precursors arise in the embryo and at least some appear to persist in the adult organism, where they contribute to replacement of osteoblasts in bone turnover and in fracture healing. In this review, we describe the morphological, molecular, and biochemical criteria by which osteoblasts are defined and cell culture approaches that have helped to clarify transitional stages in osteoblast differentiation. Current understanding of differential expression of osteoblast-associated genes during osteoprogenitor proliferation and differentiation to mature matrix synthesizing osteoblasts is summarized. Evidence is provided to support the hypothesis that the mature osteoblast phenotype is heterogeneous with subpopulations of osteoblasts expressing only subsets of the known osteoblast markers. Throughout this paper, outstanding uncertainties and areas for future investigation are also identified.Key words: skeletal development, differential gene expression, heterogeneity.

Effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 osteoblast-like cells

2016 ◽  
Vol 27 (6) ◽  
Author(s):  
Maryam Torshabi ◽  
Zeinab Rezaei Esfahrood ◽  
Parisan Gholamin ◽  
Elahe Karami
Keyword(s):  
Gene Expression ◽  
Vitamin E ◽  
Bone Loss ◽  
Marker Genes ◽  
Proliferation And Differentiation ◽  
Osteogenic Gene Expression ◽  
Polymerase Chain ◽  
Presence And Absence ◽  
Osteoblast Markers ◽  
Osteogenic Gene

AbstractBackground:Evidence shows that oxidative stress induced by nicotine plays an important role in bone loss. Vitamin E with its antioxidative properties may be able to reverse the effects of nicotine on bone. This study aimed to assess the effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 (osteosarcoma) human osteoblast-like cells.Methods:We treated the cells with 5 mM nicotine. The viability and morphology of cells were evaluated respectively using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) and crystal violet assays. The effect of nicotine on osteogenic gene expression in MG-63 cells was assessed by real-time reverse-transcription polymerase chain reaction of osteoblast markers, namely, alkaline phosphatase, osteocalcin and bone sialoprotein.Results:The results revealed that survival and proliferation of MG-63 cells were suppressed following exposure to nicotine, and cytoplasm vacuolization occurred in the cells. Nicotine significantly down-regulated the expression of osteogenic marker genes. Such adverse effects on morphology, viability and osteogenic gene expression of MG-63 cells were reversed by vitamin E therapy.Conclusions:In conclusion, vitamin E supplementation may play a role in proliferation and differentiation of osteoblasts, and vitamin E can be considered as an anabolic agent to treat nicotine-induced bone loss.

scholarly journals 307 CYTOKININ-RESPONSIVE GENES IN Phaseolus vulgaris.

HortScience ◽  
1994 ◽  
Vol 29 (5) ◽  
pp. 474c-474
Author(s):  
Kerrie McDaniel ◽  
David Lightfoot
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Phaseolus Vulgaris ◽  
Leaf Tissue ◽  
Suspension Cell Culture ◽  
Suspension Cells ◽  
Gene Response ◽  
Cytokinin Treatment ◽  
Differential Gene ◽  
L 22

Physiological differences between cttokinins are well documented. An explanation for these differences is that cytokinins differentially regulate genes. Gene response has been analyzed in cell culture and organized tissue of Phaseolus vulgaris L. cv. Great Northern. Two novel cDNAs, L-221 and L-22, have been identified that are cytokinin responsive. In leaf tissue L-221 was repressed by zeatin, benzyladenine and thidiazuron at 50 μM. In suspension cell culture mRNA abundance of L-221 remained constant regardless of cytokinin treatment. By contrast, the abundance of L-22 mRNA was increased differentially by treatment with each of the 3 cytokinins in leaf tissue. Suspension cells analyzed for expression of L-22 after cytokinin treatment also showed differential gene expression. S-1 Nuclease Protection Assays revealed that gene expression is a transient phenomenon dependent upon the time of cytokinin application and cytokinin concentration. Callus bioassays showed that dihydrozeatin and O-glucosylzeatin gave greater responses than the co-application of zeatin and dihydrozeatin or zeatin and O-glucosylzeatin. The conjugate and the reduction derivative also gave greater responses than zeatin alone. Effects of dihydrozeatin and O-glucosylzeatin on gene expression will be reported.

scholarly journals Select Gene Expression Across Variable PrPSc Permissive Ovine Microglia

2019 ◽  
Author(s):  
Valerie McElliott ◽  
Kelcey Dinkel ◽  
Zachary Nesbit ◽  
James B. Stanton
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Prion Protein ◽  
Differential Gene Expression ◽  
Cellular Prion Protein ◽  
Transmissible Spongiform Encephalopathies ◽  
Specific Cell ◽  
Culture Models ◽  
Differential Gene ◽  
Cell Culture Models

Abstract Abstract Abstract Background: Transmissible spongiform encephalopathies (TSEs) are a group of fatal, neurodegenerative diseases that affect multiple species, including sheep, cattle, and humans. A misfolded, pathogenic isoform (PrPD) of the normal, host-encoded, cellular prion protein (PrPC) is the causative agent for TSEs. While there have been advances in understanding TSEs, antemortem diagnostic tests are limited in many species, and there are no effective treatment protocols. Filling these reagent gaps will require knowledge of the molecular pathophysiology of PrPD accumulation. Previous work has suggested that the extracellular matrix (i.e., fibronectin 1) and physiological functions (i.e., cell division) maybe key factors for cellular prion permissibility, at least in specific cell culture models. Using a natural scrapie isolate, six immortalized, ovine microglial clones, of varying permissiveness to classical scrapie were evaluated for differential gene expression in seven genes based on previous RNASeq studies (fibronectin 1 [FN1], follistatin-like 1 [FSTL1], osteonectin [SPARC], survivin [BIRC5], syndecan 4 [SDC4], AXL receptor tyrosine kinase [AXL], and prion protein [PRNP]), and to determine correlations with prion permissibility. Results: Significant differential gene expression was frequently observed for survivin, follistatin-like 1 and osteonectin between clones, and when evaluated relative to PRNP expression. However, only fibronectin 1 and survivin were significantly correlated with prion permissibility, and only when evaluated relative to PRNP expression. Inoculation had a significant effect on follistatin-like 1, syndecan 4, and osteonectin. Conclusions: Similar to previous studies in other systems, fibronectin and mitotic rate show promise as potential determinants of prion permissibility in ovine microglia. As determinants of prion permissibility, the expression of fibronectin 1 and survivin coupled with PRNP could be utilized as biomarkers for detection of prion permissibility phenotype in ovine microglia, and perhaps other cell culture models of prion disease.

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