PC‐PLC is involved in osteoclastogenesis induced by TNF‐α through upregulating IP3R1 expression

Xia, Lin; Zhang, Dongyan; Wang, Chune; Fang, Wei; Hu, Yingwei

doi:10.1016/j.febslet.2012.07.015

Cited by 10 publications

(9 citation statements)

References 36 publications

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“…In addition to direct actions on osteoclasts and their precursors, TNF-α may indirectly promote osteoclast activity through induction of expression of both RANKL and M-CSF in osteoblasts and marrow stromal cells [21,36,41] . Last but not least, TNF-α increases the expression of IP3R1, an important calcium channel responsible for evoking intracellular calcium oscillation, which promotes RANKL-induced osteoclastogenesis of mouse BMMs [42] . This scenario may explain why the increase in proinflammatory cytokines induced by prosthetic wear particles strongly enhances osteoclast formation and bone resorption in vivo.…”

Section: Discussionmentioning

confidence: 99%

Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Zhu

et al. 2013

Acta Pharmacol Sin

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Section: Discussionmentioning

confidence: 99%

Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Zhu

et al. 2013

Acta Pharmacol Sin

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“…Besides acting on PC-PLC, this molecule was also reported to affect PLD activity and to inhibit sphingomyelin synthase in some cell types [156]. However, strong evidence for a specific inhibitory effect of D609 on PC-PLC was provided in our previous studies [62,65,68,69,157], as well as by other groups [158][159][160]. Mellert et al [161] studied the effect of this drug on HIV-1 infection, showing that a D609/undecanoic acid combination inhibited HIV-1 replication in infected lymphoma cells, likely interfering with virus assembly.…”

Section: Plcs In Hiv-1 Infectionmentioning

confidence: 89%

Phospholipases: at the crossroads of the immune system and the pathogenesis of HIV-1 infection

Cecchetti

Spadaro

Gessani

et al. 2016

Journal of Leukocyte Biology

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Multiple host factors and their interactions with viral proteins contribute to the complexity of HIV-1 pathogenesis and disease progression. The virus exploits the cell-signaling networks to prepare the ground for viral replication, to affect functions of either infected or uninfected bystander cells, and to evade the immune response. These events are hallmarks of HIV-1 pathogenesis that lead toward AIDS. Phospholipases are essential mediators of intracellular and intercellular signaling. They function as phospholipid-hydrolyzing enzymes, generating many bioactive lipid mediators or second messengers, which control multiple cellular functions, thus regulating a variety of physiologic and pathophysiologic processes. These enzymes also represent important components of the cell-signaling networks exploited by HIV-1 and its proteins to favor viral replication and persistence, as well as immune response dysfunction. Although some individual phospholipases were studied in the context of HIV-1 infection, the mechanisms whereby they regulate diverse infection-associated processes, as well as the interaction among different phospholipases have yet to be fully elucidated. In this review, we discuss the principal aspects of the complex interaction between phospholipases, HIV-1, and the immune system. A thorough understanding of the signaling networks that involve phospholipases in both HIV-1-infected cells and individuals is essential to determine whether therapeutic targeting of these enzymes may represent a novel approach to control viral replication, as well as the associated inflammation and comorbidities.

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“…It was found that TNF-α promoted RANKL-induced osteoclastogenesis, at least partially, through the PC-PLC/inositol-1,4,5-trisphosphate (IP 3 ) receptors/NFAT1 pathway [333]. …”

Section: Non-specific Phospholipase Cmentioning

confidence: 99%

Phospholipases of Mineralization Competent Cells and Matrix Vesicles: Roles in Physiological and Pathological Mineralizations

Mébarek

Abousalham

Magne

et al. 2013

IJMS

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The present review aims to systematically and critically analyze the current knowledge on phospholipases and their role in physiological and pathological mineralization undertaken by mineralization competent cells. Cellular lipid metabolism plays an important role in biological mineralization. The physiological mechanisms of mineralization are likely to take place in tissues other than in bones and teeth under specific pathological conditions. For instance, vascular calcification in arteries of patients with renal failure, diabetes mellitus or atherosclerosis recapitulates the mechanisms of bone formation. Osteoporosis—a bone resorbing disease—and rheumatoid arthritis originating from the inflammation in the synovium are also affected by cellular lipid metabolism. The focus is on the lipid metabolism due to the effects of dietary lipids on bone health. These and other phenomena indicate that phospholipases may participate in bone remodelling as evidenced by their expression in smooth muscle cells, in bone forming osteoblasts, chondrocytes and in bone resorbing osteoclasts. Among various enzymes involved, phospholipases A1 or A2, phospholipase C, phospholipase D, autotaxin and sphingomyelinase are engaged in membrane lipid remodelling during early stages of mineralization and cell maturation in mineralization-competent cells. Numerous experimental evidences suggested that phospholipases exert their action at various stages of mineralization by affecting intracellular signaling and cell differentiation. The lipid metabolites—such as arachidonic acid, lysophospholipids, and sphingosine-1-phosphate are involved in cell signaling and inflammation reactions. Phospholipases are also important members of the cellular machinery engaged in matrix vesicle (MV) biogenesis and exocytosis. They may favour mineral formation inside MVs, may catalyse MV membrane breakdown necessary for the release of mineral deposits into extracellular matrix (ECM), or participate in hydrolysis of ECM. The biological functions of phospholipases are discussed from the perspective of animal and cellular knockout models, as well as disease implications, development of potent inhibitors and therapeutic interventions.

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PC‐PLC is involved in osteoclastogenesis induced by TNF‐α through upregulating IP3R1 expression

Cited by 10 publications

References 36 publications

Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Calcineurin/NFAT pathway mediates wear particle-induced TNF-α release and osteoclastogenesis from mice bone marrow macrophages in vitro

Phospholipases: at the crossroads of the immune system and the pathogenesis of HIV-1 infection

Phospholipases of Mineralization Competent Cells and Matrix Vesicles: Roles in Physiological and Pathological Mineralizations

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