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Posted On: 05/27/2024 11:54:39 PM
Post# of 148878
Here’s a possible link between plexin-b1 and CCR5 but it takes a minute to get there. Bear with me. It might be a stretch…
I’ll link two papers and provide one quote from each.
First it’s impt to relay that “Osteoblasts and osteoclasts are special cells that help your bones grow and develop. Osteoblasts form new bones and add growth to existing bone tissue. Osteoclasts dissolve old and damaged bone tissue so it can be replaced with new, healthier cells created by osteoblasts.”
This one mostly talks about an optogentic, or light induced, tool to do some stimulating of plexin-b1. But in it’s setup, it links plexin-b1 to osteoclasts and osteoblasts.
https://www.nature.com/articles/ncomms15831
“Abstract
During bone remodelling, osteoclasts induce chemotaxis of osteoblasts and yet maintain spatial segregation. We show that osteoclasts express the repulsive guidance factor Semaphorin 4D and induce contact inhibition of locomotion (CIL) in osteoblasts through its receptor Plexin-B1. To examine causality and elucidate how localized Plexin-B1 stimulation may spatiotemporally coordinate its downstream targets in guiding cell migration, we develop an optogenetic tool for Plexin-B1 designated…” blah, blah, blah.
This one links CCR5 and the regulation of osteoclasts (the destructive half of the osteo things)
https://www.nature.com/articles/s41467-017-02368-5
“Here we show that blockade of CCR5 using specific antibodies impairs human osteoclast function in vitro. Ccr5-deficient (Ccr5 −/−) mice presented with dysfunctional osteoclasts and were resistant to osteoporosis induced by receptor activator of nuclear factor kappa-B ligand (RANKL), which triggers osteoporosis independently of inflammatory and immunomodulatory pathways. Furthermore, Ccr5 deficiency impairs the cellular locomotion and bone-resorption activity of osteoclasts, which is associated with the disarrangement of podosomes and adhesion complex molecules including Pyk2. Overall, the data provides evidence that CCR5 has an essential role in bone-destructive conditions through the functional regulation of osteoclasts.”
My conclusion is possibly meaningless, but confirmed. Plexin-B1 has effect on osteoclasts and osteoblasts. CCR5 also has effect on osteoclasts and osteoblasts.
Now does CCR5 blockade affect the Plexin-B1 / Sema4D axis? Don’t know.
But good question.
I’ll link two papers and provide one quote from each.
First it’s impt to relay that “Osteoblasts and osteoclasts are special cells that help your bones grow and develop. Osteoblasts form new bones and add growth to existing bone tissue. Osteoclasts dissolve old and damaged bone tissue so it can be replaced with new, healthier cells created by osteoblasts.”
This one mostly talks about an optogentic, or light induced, tool to do some stimulating of plexin-b1. But in it’s setup, it links plexin-b1 to osteoclasts and osteoblasts.
https://www.nature.com/articles/ncomms15831
“Abstract
During bone remodelling, osteoclasts induce chemotaxis of osteoblasts and yet maintain spatial segregation. We show that osteoclasts express the repulsive guidance factor Semaphorin 4D and induce contact inhibition of locomotion (CIL) in osteoblasts through its receptor Plexin-B1. To examine causality and elucidate how localized Plexin-B1 stimulation may spatiotemporally coordinate its downstream targets in guiding cell migration, we develop an optogenetic tool for Plexin-B1 designated…” blah, blah, blah.
This one links CCR5 and the regulation of osteoclasts (the destructive half of the osteo things)
https://www.nature.com/articles/s41467-017-02368-5
“Here we show that blockade of CCR5 using specific antibodies impairs human osteoclast function in vitro. Ccr5-deficient (Ccr5 −/−) mice presented with dysfunctional osteoclasts and were resistant to osteoporosis induced by receptor activator of nuclear factor kappa-B ligand (RANKL), which triggers osteoporosis independently of inflammatory and immunomodulatory pathways. Furthermore, Ccr5 deficiency impairs the cellular locomotion and bone-resorption activity of osteoclasts, which is associated with the disarrangement of podosomes and adhesion complex molecules including Pyk2. Overall, the data provides evidence that CCR5 has an essential role in bone-destructive conditions through the functional regulation of osteoclasts.”
My conclusion is possibly meaningless, but confirmed. Plexin-B1 has effect on osteoclasts and osteoblasts. CCR5 also has effect on osteoclasts and osteoblasts.
Now does CCR5 blockade affect the Plexin-B1 / Sema4D axis? Don’t know.
But good question.
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