Sentences with phrase «in osteoclast»

The role of calcium release activated calcium channels in osteoclast differentiation.

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.»

I think when there's absolute Growth hormone deficiency you may have an increase in osteoclast activity.

TRANCE is necessary and sufficient for osteoblast - mediated activation of bone resorption in osteoclasts.

Tobias Heckel (Hoflack, TUD)-- «Revealing Src tyrosine kinase - dependent signaling pathways in osteoclasts: Implications on actin organization and cell polarity» (2008)

The Cdc42 guanine nucleotide exchange factor FGD6 coordinates cell polarity and endosomal membrane recycling in osteoclasts.

Not exact matches

In the bone, macrophages take the form of osteoclasts — the cells responsible for the resorptive processes associated with continuous bone remodeling.

«After six weeks, we saw reversals in inflammation, both clinically and by looking at cellular and molecular measures of osteoclast formation and inflammatory cytokines.»

Not only can IL - 17 encourage inflammation, but it can also encourage the development of osteoclasts, cells that break down bone, in this case teeth.

In a study exploring the molecules controlling osteoclast differentiation in the cancer setting, Ell et al. have identified miRNAs (microRNAs are small noncoding RNAs that regulate gene expression) whose levels were consistently down - or up - regulated in differentiating osteoclastIn a study exploring the molecules controlling osteoclast differentiation in the cancer setting, Ell et al. have identified miRNAs (microRNAs are small noncoding RNAs that regulate gene expression) whose levels were consistently down - or up - regulated in differentiating osteoclastin the cancer setting, Ell et al. have identified miRNAs (microRNAs are small noncoding RNAs that regulate gene expression) whose levels were consistently down - or up - regulated in differentiating osteoclastin differentiating osteoclasts.

They found evidence of Del - 1 in the same areas as osteoclast activity, then followed up by generating human and mouse osteoclasts in vitro and found Del - 1 mRNA and protein expressed at high levels.

With this new understanding of how Del - 1 can inhibit periodontal bone loss — both by reducing inflammation and by restraining the activity of osteoclasts that resorb bone tissue — the researchers tested it, in a preclinical model of periodontitis observing that Del - 1 significantly reduced inflammation and tissue damage and that there was significantly less bone loss.

Further experimentation in vitro with human osteoclasts and in vivo in mice identified a portion of the Del - 1 protein that was particularly important for containing osteoclast activity, though additional parts of the molecule were needed to have the most potent inhibition of inflammation and bone loss.

A messenger protein called IL - 6 produced in bone marrow helps to encourage the growth of osteoclasts.

High levels of bone destruction and reduced bone density caused by excessive osteoclasts are characteristic of osteoporosis, a common bone disease in which bones become fragile and susceptible to fracture.

«Clarifying the interplay between bone cells in bone remodeling: Spatiotemporal intercellular interactions between mature osteoblasts and mature osteoclasts in bone homeostasis in vivo demonstrated.»

Therefore, it is important to understand the spatial - temporal relationship and interaction between osteoblasts and terminally differentiated osteocytes (bone cells) and osteoclasts in vivo.

But if osteoclasts aren't working properly, «in the end, what you get is disorganized bone,» Malchodi says.

«MCP - 1 is a chemokine, which induces cells to move along a gradient recruiting white cells and osteoclasts in tissues,» says Dr. Partridge.

In the present study, the researchers focused on the role of MCP - 1 in PTH - induced osteoclast formatioIn the present study, the researchers focused on the role of MCP - 1 in PTH - induced osteoclast formatioin PTH - induced osteoclast formation.

They had been suspected of being involved in the regulation of bone resorption through the osteoclasts.

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.

So Steven Teitelbaum, a bone cell biologist at Washington University School of Medicine in St. Louis, Missouri, decided to focus instead on the bone dismantlers, the osteoclasts.

As might be expected, it reduces the number of bone - dissolving cells, or osteoclasts, in mice with a condition resembling osteoporosis.

Initially, fluoxetine protects bone by inhibiting the cells in the skeleton (osteoclasts) that constantly break down and resorb bone.

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.

This indicates that microgravity's effect on bone density likely involves changes in mechanical force that lowers overall physical activity and therefore causes osteoclast activation

Genetic analysis also revealed significant increase in activity in two genes that may be involved in mitochondria function, suggesting that osteoclast activation might be linked to the reaction of mitochondria to microgravity.

Martin Sztacho (Hoflack, TUD)-- «F - BAR proteins PSTPIP1 and PSTPIP2 regulate sealing zones in bone resorbing osteoclasts» (2014)

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).

He showed evidence of decreased bone volume in SMA mouse models of various severity, as well as increased fractures and osteoclast formation.

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.

(K) Quantification of TRAP + osteoclasts in (J).

Moreover, we found that treatment with a selective allosteric inhibitor of the ABL kinases or simultaneous depletion of both ABL kinases in breast cancer cells impaired breast cancer bone metastases and decreased osteoclast activation in vitro and osteolysis in vivo.

Inhibition of interleukin - 6 receptor directly blocks osteoclast formation in vitro and in vivo

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 impairs tumor - induced osteoclast activation in part by decreasing IL - 6 secretion.

To directly examine whether ABL kinases regulate tumor - induced osteoclast activation, we used an in vitro osteoclastogenesis assay (Fig. 5A).

His Ph.D. thesis topic was the implication of prostanoids and phospholipases A2 in the biology of osteoclasts.

To investigate the underlying mechanisms, we undertook (1) bioinformatic, functional genomic annotation and human osteoblast expression studies; (2) gene - function prediction; (3) skeletal phenotyping of 120 knockout mice with deletions of genes adjacent to lead independent SNPs; and (4) analysis of gene expression in mouse osteoblasts, osteocytes and osteoclasts.

In breast cancer cells, the ABL kinases activated the transcriptional coactivator TAZ and the transcription factor STAT5, which triggered the transcription of genes encoding factors that activate osteoclasts (cells that break down bone) and those that enhance the survival of breast cancer cells in the bone microenvironmenIn breast cancer cells, the ABL kinases activated the transcriptional coactivator TAZ and the transcription factor STAT5, which triggered the transcription of genes encoding factors that activate osteoclasts (cells that break down bone) and those that enhance the survival of breast cancer cells in the bone microenvironmenin the bone microenvironment.

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.

It stimulates the production of calcitonin, the hormone responsible for inhibiting cells (osteoclasts) that breaks bone down and activates alkaline phosphatase, an enzyme that forms new calcium crystals in 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.

To get slightly more scientific in terms of bone health, an acidic environment has been shown to encourage the activity of osteoclast cells.

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.»

In addition, during puberty and into the third decade, oestrogen has an anabolic effect on the osteoblast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and appendicular bonIn addition, during puberty and into the third decade, oestrogen has an anabolic effect on the osteoblast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and appendicular bonin axial and appendicular bone.