Examples of using Osteoclasts in English and their translations into Hebrew
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Another type(osteoclasts) dissolves(resorbs) particles of bone.
Metchnikoff said that if there were no osteoclasts, we would live forever.
Another type(osteoclasts) resorbs(dissolves) particles of bone.
Bisphosphonates are drugs that inhibit the activity of osteoclasts.
Then one can ask why God allowed the osteoclasts to grow alongside the bones?
TRAP-positive cells with two or more nuclei were counted as osteoclasts.
These osteoclasts, too, are part of creation, and we have them within us by the millions.
In turn,insulin also acts directly on osteoblasts and indirectly on osteoclasts.
If He had not allowed the osteoclasts to grow, we would not be slowly devoured throughout life.
Bone resorption is a process by which bone is broken down by osteoclasts in response to different stimuli.
As the results indicate,using RANKL is not the equivalent of using TNF-α to generate osteoclasts.
Specialized cells called osteoclasts eat out way all the damaged bone other cells- osteoblasts rebuild it with newer, stronger material.
While at 100, 1,000 ng anti-c-fms antibody,there was a significant decrease in the number of osteoclasts compared to control.
These results provide information about the robust nature of RANKL in producing osteoclasts while a concentration of 50 ng/mL of RANKL was used, and a concentration of 100 ng/mL of TNF-α was needed to obtain the same number of osteoclasts.
At 1 ng/mL anti-c-fms antibody,there was no significant decrease in the number of osteoclasts compared to control(0 ng/mL).
M-CSF is a key factor for osteoclast formation as the op/op mice which lack Csf1 the gene coding for M-CSF show an osteopetrotic phenotype due to complete lack of osteoclasts16.
As we showed, the concentration of anti-c-fms antibody which was needed to inhibit osteoclast formation is not equal among the methods by which osteoclasts were obtained(RANKL or TNF-α), thus any results obtained with regard to the concentration of anti-c-fms have to be carefully examined in future experiments.
This protocol demonstrates the isolation of murine bone marrow cells from long bones, and the steps to generate bone marrow macrophages(BMM) which are regarded as osteoclast precursors and to induce the differentiation of BMM into multinuclear osteoclasts by two methods; either RANKL or TNF-α.
It is driven by various types of cells, most notably osteoblasts,which secrete new bone, and osteoclasts, which break it down.
The osteoclast formation in M-CSF+RANKL culture with anti-c-fms antibody is shown in Figure 1.
GPR55 promotes osteoclast cell function, which facilitates bone reabsorption.
Figure 2: Effect of anti-c-fms antibody on TNF-α-induced osteoclast formation.
Both M-CSF and RANKL are important for osteoclast differentiation2.
The osteoclast formation in M-CSF+TNF-α culture with anti-c-fms antibody is shown in Figure 2.
We have also provided a way to testanti-c-fms antibody suitable concentration for inhibiting osteoclast formation under different culture conditions.
The purpose of this protocol is to evaluate the effect of anti-c-fms antibody on osteoclast formation in the presence of RANKL or TNF-α, and to determine the effect of M-CSF on osteoclast precursors proliferation.
Both of these methods are suitable for osteoclast generation but the decision of which is superior depends on the downstream application in the context of the reagents to be used later.
The process by which bone marrow is extracted and subsequently used to generate osteoclast precursors is reliable in producing large quantities of pure osteoclast cultures which can be used in multiple downstream applications such as drug testing.
In this protocol, we used anti-c-fms antibody to inhibit osteoclastogenesis, and by looking at the results, we find that a concentration of 100 ng/mL of anti-c-fms antibodywas needed to produce significant decrease in osteoclast number in RANKL wells.
These results taken side by side suggest that anti-c-fms antibody may work as a therapeutic to arrest osteoclastogenesis in TNF-α induced osteolytic diseases at low concentration,at the same time this concentration will spare osteoclast formation induced by RANKL and M-CSF which will allow for bone remodeling to occur.