Sentences with word «osteoblasts»

Endogenous sex steroids such as estrogen and testosterone may serve as prodifferentiation agents that inhibit the malignant transformation of osteoblasts (31).

Osteoblasts infiltrate and proliferate on the surface of the material, and bone growth occurs uniformly throughout the defect.

The results showed that the combination of avocado / soybean unsaponifiables (ASU), glucosamine hydrochloride, and chondroitin sulfate is effective in equine cartilage cells (chondrocytes) and bone cells (osteoblasts) at inhibiting expression and decreasing production of mediators involved in joint cartilage breakdown.

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.

The Periosteum also contains immature cells that become Osteoblasts, which are cells involved in bone growth and fracture repair.

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

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).

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.»

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.

Progesterone, on the other hand, boosts the production and activity of cells that build new bone or osteoblasts.

Osteoblasts, the cells that deposit new bone tissue, rely on vitamin K to function properly, and vitamin K helps activate proteins that you need to make healthy bones.

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 density.

Collagen peptides are known to stimulate the growth of «osteoblasts,» which are the cells responsible for bone formation.14 Preliminary studies in rats also indicate that collagen supplementation may also help increase bone mineral density.15

There is evidence of progesterone receptors in osteoblasts (bone building cells) but not for estrogen, indicating a bone - building role for progesterone.10

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

I can not recommend a high - quality organic yogurt enough for your health, so it pays to enjoy yoghurt because lactoferrin's effects were found to be dose - dependent, stimulating an up to a 5-fold increase in osteoblasts at higher doses consumed.

Over time heavy impact work increases the activity of osteoblasts within your body which in turn leads to bigger and stronger bones — now this might not be something you've considered but when you get to middle aged, or elderly, and you fall over you might find yourself thankful for your years of pumping iron as you will likely walk away far less injured then your more sedentary friends.

Boron induces the mineralization activity of what's called your osteoblasts.

Osteoblasts are a type of cell that creates new material to rebuild bones.

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.

Although adiponectin's signaling pathways are generally thought to be distinct from those of insulin, in this case it acts through the same signaling pathway as insulin in both osteoblasts and in the brain.

The reasoning goes as follows: estrogen is a sex hormone that is essential to female bone health because it promotes the activity of osteoblasts, which are cells that produce bone.

High levels of cortisol also decrease the ability of osteoblasts to synthesize new bone and interfere with absorption of Ca2 + from the gastrointestinal tract.

Collagen peptides stimulate osteoblasts, which are the cells responsible for bone formation.

Magnesium is mitogenic (causes cell division) in osteoblasts (the major cellular component of bone) and magnesium depletion inhibits cellular growth.

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

Excess amounts of calcium — especially without other supporting nutrients — potentially slows down your osteoblasts, which build bones.

Zinc regulates secreting the bone - supporting hormone calcitonin, while copper monitors osteoblasts and osteoclasts.

This low bone mass in the MT2 - / - mice was due to an isolated decrease in osteoblasts numbers and bone formation.

Osteoblasts form more bone and the micromotion associated with the fracture is more rapidly eliminated.

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

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).

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

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

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

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).

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

In addition to iPS cells derived from progeria - patients, the researchers successfully applied their method to adult mesenchymal stem cells, which can differentiate into a variety of cell types, including adipocytes, osteoblasts, chondrocytes, cardiomyocytes, and, as described lately, beta - pancreatic islets cells.

Osteoblasts modulate osteoclast activity through secretion of the TNF family member RANKL (receptor activator of nuclear factor κB ligand).

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

Mice lacking molecular - clock components (Per and Cry), or lacking Per genes in osteoblasts, display high bone mass, suggesting that bone remodeling may also be subject to circadian regulation.

Similarity between the osteoblasts and the calicoblastic epithelium cells of scleractinian coral was also shown in the localization of the protein BMP in the tissue of S. pistillata (Zoccola et al., 2009), and for its role in the coral biomineralization (Mass et al., 2016; Zoccola et al., 2009).

The periosteum is a mixed cell population of fibroblasts, osteoblasts, MSCs, and pericytes cells.

Both pathways appear to be responsible for the differentiation and proliferation of cell type similar to bone mass and osteoblasts (Fig. 6).

Comparison of Human alveolar osteoblasts cultured on polymer - ceramic composite scaffolds and tissue culture plates.

Human primary osteoblasts matrices as a model system for bone metastasis research.

Targeted disruption of nuclear factor erythroid - derived 2 - like 1 in osteoblasts reduces bone size and bone formation in mice.

We study cell (endothelial cells, fibroblasts, osteoblasts) guidance cues on biodegradable scaffolds (e.g. polymers).

Preliminary study on the adhesion and proliferation of human osteoblasts on starch - based scaffolds.

Differential osteogenicity of multiple donor - derived human mesenchymal stem cells and osteoblasts in monolayer, scaffold - based 3D culture and in vivo.