Sentences with phrase «by osteoblasts»

Osteocalcin, secreted by osteoblasts, is a non-collagenous protein hormone responsible for bone mineralization, ionized calcium homeostasis, insulin sensitivity, and testosterone biosynthesis.

Osteoprotegerin (OPG), a soluble decoy receptor for RANKL, is also produced by osteoblasts and antagonizes the activity of RANKL (31).

Several tumor - derived bone metastasis factors can increase RANKL production or decrease OPG secretion by osteoblasts, thereby promoting osteoclast differentiation and activation (12, 32).

To find out how, he turned to an engineered strain of mice lacking a gene for what was then a mysterious protein called osteocalcin, which is produced by osteoblasts.

To accomplish their functions, bones undergo continuous destruction (resorption) carried out by osteoclasts, and formation by osteoblasts.

Geneticist Gerard Karsenty of Columbia University Medical Center found that osteocalcin — made by osteoblasts — helps regulate blood sugar.

Downstream of the signaling system, Runx2 overexpression led to overexpression of bone - related genes, including genes expressed by osteoblasts, osteoclasts and osteocytes.

Not exact matches

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.

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.

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.

Coban and colleagues gave infected mice alfacalcidol, a derivative of vitamin D that treats osteoporosis by suppressing osteoclasts and stimulating osteoblasts.

Its day job is to keep bone growth in check by telling bone - forming osteoblasts to slow down or stop.

The team led by Li and Chen generated three mouse models by deleting Cbf - beta at various stages of the osteoblast lineage.

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.

«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.

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.

Now, the Laboratory of Malaria Immunology Team at the Immunology Frontier Research Center (IFReC), Osaka University, headed by Professor Cevayir COBAN, have used mouse malaria models to show that robust immune activation and invasion of parasite by - products into the bone marrow during and after malaria infection leads to an adverse balance in bone homeostasis - a process usually tightly controlled - by bone forming osteoblasts and bone resorbing osteoclasts.

These products, including the major malarial by - product hemozoin, malarial proteins and as yet undefined virulence factors, induce MyD88 - dependent inflammatory responses in osteoclast and osteoblast precursors, leading to increased RANKL expression (a key molecule inducing osteoclast differentiation), and over-stimulation of osteoclastogenesis favoring bone resorption.»

«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.

Myocyte enhancer factor 2C, an osteoblast transcription factor identified by dimethyl sulfoxide (DMSO)- enhanced mineralization.

We show that expression of clock genes in osteoblasts is regulated by the sympathetic nervous system and leptin.

Thus, leptin determines the extent of bone formation by modulating, via sympathetic signaling, osteoblast proliferation through two antagonistic pathways, one of which involves the molecular clock.

Through its various targets, MMP1 promotes not only tumor invasion but also breast cancer colonization to bone by mechanisms that include the release of membrane - bound EGF - like growth factors from tumor cells, leading to activation of EGF receptor signaling and suppression of OPG expression in osteoblasts, which in turn promotes the differentiation and activation of osteoclasts required for bone destruction and enhanced tumor growth in the bone microenvironment (32).

These findings suggest that ABL kinases regulate osteoclast maturation indirectly, possibly by modulating osteoblast function.

These findings suggest that ABL kinases promote tumor - induced osteoclast activation in part by increasing OPG abundance in osteoblasts.

IL - 6 can induce osteoclast activation indirectly by altering the expression of RANKL and OPG in osteoblasts (51).

Depletion of ABL kinases in breast cancer cells decreased IL - 6 concentrations and was accompanied by increased OPG expression in osteoblasts.

The first protein is called osteocalcin and is produced in the bone by specialized cells charged with building bone called osteoblasts.

Research has shown that strontium may play a role in the formation of osteoblasts, new bone forming cells, while at the same time slowing the breakdown of old bone by inhibiting osteoclasts.

The Opotowski team, which found that low vitamin A levels had as great an effect lowering BMD as did high vitamin A levels, suggested that vitamin A deficiency may contribute to increased fracture risk by allowing bone matrix to grow faster than it can be mineralized.12 Indeed, although the net effect of vitamin A is to stimulate osteoclasts and slow the growth of osteoblasts, vitamin A also causes osteoblasts to secrete a variety of enzymes and other proteins that are important to bone mineralization, including osteocalcin, which is a protein that plays a direct role in attracting and binding calcium within the bone matrix.6 By slowing the growth of the matrix but increasing the rate at which it is mineralized, adequate vitamin A helps to ensure sufficient bone densitby allowing bone matrix to grow faster than it can be mineralized.12 Indeed, although the net effect of vitamin A is to stimulate osteoclasts and slow the growth of osteoblasts, vitamin A also causes osteoblasts to secrete a variety of enzymes and other proteins that are important to bone mineralization, including osteocalcin, which is a protein that plays a direct role in attracting and binding calcium within the bone matrix.6 By slowing the growth of the matrix but increasing the rate at which it is mineralized, adequate vitamin A helps to ensure sufficient bone densitBy slowing the growth of the matrix but increasing the rate at which it is mineralized, adequate vitamin A helps to ensure sufficient bone density.

Studies showed that curcumin reduced joint swelling by modifying gene expression; inhibited inflammation by regulating NF - κB, a pro-inflammatory protein; and slowed down joint destruction by decreasing activity of osteoblasts, cells involved in bone breakdown.

Here's a quote: «Lactoferrin: Lactoferrin found in foods such as yogurt and kefir will stimulate new bone growth while preventing further breakdown of existing bone tissue, lactoferrin enhances both the growth and the activity of osteoblasts (the cells that build bone), and reduces the rate of bone cell death by 50 to 70 percent and decreases the development of osteoclasts, the cells responsible for breaking down bone.»

Finally, acute changes in blood calcium concentrations do not seem to elicit the secretion of the phosphaturic hormone fibroblast growth factor 23 (FGF - 23), which is produced by bone - forming cells (osteoblasts / osteocytes) in response to increases in phosphorus intake (see the article on Phosphorus)(2).

FGF - 23 is secreted by bone - forming cells (osteoblasts / osteocytes) in response to increases in phosphorus intake.

Additionally, omega 3 intake may improve bone health by helping to regulate calcium balance and osteoblast activity.

Effects on osteoblasts are relevant to cartilage health as changes brought about by mediators on the bone underlying cartilage, known as subchondral bone, can lead to breakdown of cartilage.