ABSTRACT: Transcriptional profiles of MET transformed osteoblast clones (MET-HOB) and mesenchymal stem cells (MSC) where osteoblast differentiation was induced
Project description:The osteogenic differentiation process consists in a well-coordinated multi-step sequence of events, in which each stage is characterized by the expression of distinct protein markers, as well as by individual morphological features. In order to precisely identify the step at which cells are permissive to MET-driven transformation, we used expression profiling. We compared the transcriptional profiles of MET-HOB and MSC cells where osteoblast differentiation was induced. Using microarrays, we evaluated the expression profiles of MET-HOB and MSC cells where osteoblast differentiation was induced, by culturing cells in the presence of ascorbic acid, α-glycerophosphate and dexamethasone for 7, 14 and 21 days
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and parental HOBs were compared.
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and osteosarcoma cell lines were compared.
Project description:The osteogenic differentiation process consists in a well-coordinated multi-step sequence of events, in which each stage is characterized by the expression of distinct protein markers, as well as by individual morphological features. In order to precisely identify the step at which cells are permissive to MET-driven transformation, we used expression profiling. We compared the transcriptional profiles of MET-HOB and MSC cells where osteoblast differentiation was induced.
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and osteosarcoma cell lines were compared. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and parental HOBs were compared. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays
Project description:We describe here a novel role for CHD1 in regulating the osteoblast cell fate by studying the effect of CHD1 depletion on the epigenetic landscape and on mRNA expression in mesenchymal stem cells (MSC) (Simonsen et al. 2012) and fetal Osteoblast (hFOB 1.19) (Harris et al. 1995) during osteoblast differentiation.
Project description:Osteoporosis, a prevalent age-related bone disorder, stems from imbalanced osteoclast/osteoblast activity and skewed mesenchymal stem cell (MSC) lineage commitment. Although lactate is linked to osteoporosis pathogenesis, the role of protein lactylation in MSC osteogenic differentiation remains unelucidated. This experiment explored protein lactylation during early MSC osteogenic differentiation, focusing on histone variant MacroH2A1. Proteomics identified 375–318 lactylated proteins across undifferentiated, osteogenic differentiation Day 3 (OB3), and adipogenic differentiation Day 3 (AD3) MSCs; MacroH2A1 lactylation at lysine 134 (K134) was downregulated in OB3. MacroH2A1(K134Ala) mutation (disrupting lactylation) enhanced MSC osteogenesis. In ovariectomized mice, AAV-MacroH2A1(K134Ala) increased femoral trabecular bone mass and reduced marrow adipose tissue. This experiment demonstrates that MacroH2A1 K134 lactylation regulates MSC osteogenic commitment via epigenetic and transcriptional modulation, offering mechanistic insights and a potential therapeutic target for osteoporosis.
