«Then
osteoblast cells lay down new tissue.»
The WNT7B protein had no effect on the total activity of bone - degrading osteoclasts but substantially increased the number of bone - building
osteoblast cells.
To evaluate whether ABL kinases might regulate the secretion of osteoblast - derived RANKL or OPG leading to osteoclast differentiation, we analyzed RANKL and OPG mRNA abundance in the murine
osteoblast cell line 7F2 in response to conditioned medium from control and ABL1 / ABL2 knockdown breast cancer cells.
The murine
osteoblast cell line 7F2 (ATCC) was cultured in α - MEM with 10 % FBS.
Whereas conditioned medium from ABL1 / ABL2 - depleted breast cancer cells did not affect RANKL abundance in osteoblasts compared with the cells treated with control conditioned medium (Fig. 5E), we found that conditioned medium from breast cancer cells lacking ABL kinases increased OPG abundance in
the osteoblast cell line (Fig. 5F).
Not exact matches
Collagen peptides stimulate
osteoblasts, which are the
cells responsible for bone formation.
Ordinarily, bone is built up by
cells called
osteoblasts and reabsorbed during growth and healing by
cells called osteoclasts.
The process takes place by means of a mechanism — unveiled in this study — that inhibits the activity of the
osteoblasts, the
cells that produce the bone matrix so that bones can grow during childhood and youth, and remain in good condition in adulthood.
A new therapy changes the balance of
osteoblasts (pictured here) and fat
cells in the bone marrow, leading to stronger bones.
Varghese and her team showed that they could control the differentiation of human pluripotent stem
cells into functional
osteoblasts — bone - building
cells — simply by adding the molecule adenosine to their growth medium.
This work stems from a previous study by Varghese's group to understand how calcium phosphate minerals found in bone tissue induce stem
cells to differentiate into
osteoblasts.
Osteoblasts have more cytoskeleton than do adipocytes (fat
cells).
Her team discovered that stem
cells take up calcium phosphate to produce ATP, a metabolic molecule, which then breaks down into adenosine and signals the stem
cells to become
osteoblasts.
The parasites might trigger these problems, the scientists hypothesized, by upsetting the normal balance between
cells known as osteoclasts, which dissolve bone, and
cells called
osteoblasts, which build it back up.
Instead, Sen found that actin was trafficked into the nuclei of the stem
cells, where it had the surprising effect of inducing the
cells to become
osteoblasts.
Cells known as osteoblasts make new bone; other cells, osteoclasts, destroy old
Cells known as
osteoblasts make new bone; other
cells, osteoclasts, destroy old
cells, osteoclasts, destroy old bone.
To find out, Deb and his co-authors genetically tagged cardiac fibroblasts in mice and watched as they transitioned into bone - forming,
osteoblast - like
cells after heart injury.
Bones need a constant new creation of
cells specific to their tissue, including the bone - producing
cells called
osteoblasts.
The progenitor
cells for
osteoblasts are bone marrow mesenchymal stem
cells.
Two types of
cell maintain bone:
osteoblasts, which create new bone tissue, and osteoclasts, which remove old tissue.
«Clarifying the interplay between bone
cells in bone remodeling: Spatiotemporal intercellular interactions between mature
osteoblasts and mature osteoclasts in bone homeostasis in vivo demonstrated.»
The stretched
cells turned into bone - making
cells called
osteoblasts, Chen's team reports in the April issue of Developmental
Cell.
Therefore, it is important to understand the spatial - temporal relationship and interaction between
osteoblasts and terminally differentiated osteocytes (bone
cells) and osteoclasts in vivo.
THE METHODS In 2000, Gerard Karsenty, a molecular geneticist at Columbia University in New York City, discovered that leptin, a hormone made by fat
cells, helps mold and repair the skeleton by acting upon bone - building
cells called
osteoblasts.
This soluble factor was found at higher levels in the blood of animals with lung tumors, could increase the activation of
osteoblasts and contributed to the maturation of neutrophils in cultured
cells.
«Our findings indicate the existence of long - distance interactions between lung tumors and bones: lung tumors remotely activate
osteoblasts, and those bone
cells, in turn, shape immunity by supplying tumors with cancer - promoting neutrophils,» says Pittet, who is an associate professor of Radiology at Harvard Medical School.
Furthermore, since the
cells responsible for synthesising new bone tissue (
osteoblasts) are known to attach close to the tip, it would appear that the electric field distribution signals this point as the centre of damage, becoming a moving beacon for repair efforts as the crack is healed.
Both the number and activity of
osteoblasts —
cells that produce and reshape bone tissue — were increased within the bone marrow of mice with lung tumors compared with cancer - free animals; and reducing the number of
osteoblasts in mice not only limited neutrophil infiltration of tumors but also interrupted tumor progression.
Dissolved metal ions were shown to reach the bone marrow, where they impair mesenchymal stromal
cells (MSCs), the progenitors of
osteoblasts, a type of
cell that is responsible for bone mineralization.
The researchers» investigations revealed that Del - 1 was expressed by at least three
cell types in the bone marrow that support hematopoetic stem
cells: endothelial
cells, CAR
cells and
osteoblasts.
Two nearly identical plots showing
cell counts after exposure to
osteoblasts (bone
cells) lacking a particular protein appear in Figure 6c of the Blood paper.
Proper bone development is maintained through a fine balance of bone - forming (
osteoblast) and bone - resorbing (osteoclast)
cells.
Then bone - making
cells called
osteoblasts and bone - absorbing
cells called osteoclasts grow and sculpt new bone at the site of fracture.
«Our experiments showed that restoring H19 expression hindered by too much p53 restored «protective differentiation» of
osteoblasts to counter events of tumor growth early on in bone cancer,» said co-author, Ihor Lemischka, PhD, Director of The Black Family Stem
Cell Institute within the Icahn School of Medicine.
Too much p53 in bone - making
cells called
osteoblasts dials down a gene, H19, and a related protein, decorin, that would otherwise help stem
cells mature (differentiate) to become normal
osteoblasts.
Leptin acts on human marrow stromal
cells to enhance differentiation to
osteoblasts and to inhibit differentiation to adipocytes
Our bones are in a constant state of flux as the number of bone - making (
osteoblast)
cells fluctuates, while the number of bone - degrading (osteoclast)
cells also adjusts.
Mesenchymal stem
cells express a surface protein called α4β1 integrin as they turn into
osteoblasts.
Osteoblasts, the
cells that rebuild bone, are derived from mesenchymal stem
cells.
Ovine cortical
osteoblasts outperform bone marrow
cells in an ectopic bone assay.
Interactions between human
osteoblasts and prostate cancer
cells in a novel 3D in vitro model.
Perivascular
cells, including pericytes in the smallest blood vessels (e.g., microvessels) and ARCs around larger ones, express mesenchymal stem
cell markers and bear a multi-differentiation fate potential (differentiate into
osteoblasts, chondrocytes, adipocytes, smooth muscle
cells and myocytes) similar to that documented for MSCs in vitro.
Mineralized human primary
osteoblast matrices as a model system to analyse interactions of prostate cancer
cells with the bone microenvironment.
This signaling pathway was found to be important in embryonic bone development (Wan et al., 2013), and in
osteoblasts (bone
cells) regulation (Glass et al., 2005; Harada & Rodan, 2003).
Differential osteogenicity of multiple donor - derived human mesenchymal stem
cells and
osteoblasts in monolayer, scaffold - based 3D culture and in vivo.
Studying the drug - responsiveness of breast cancer
cells cultured within human
osteoblast - derived matrices.
We study
cell (endothelial
cells, fibroblasts,
osteoblasts) guidance cues on biodegradable scaffolds (e.g. polymers).
Both pathways appear to be responsible for the differentiation and proliferation of
cell type similar to bone mass and
osteoblasts (Fig. 6).
Spatial Segregation of BMP / Smad Signaling Affects
Osteoblast Differentiation in C2C12
Cells.
The periosteum is a mixed
cell population of fibroblasts,
osteoblasts, MSCs, and pericytes
cells.