Inositol Polyphosphate 4-Phosphatase B as a Regulator of Bone Mass in Mice and Humans

Ferron, Mathieu; Boudiffa, Maya; Arsenault, Michel; Rached, Mohamed; Pata, Monica; Giroux, Sylvie; Elfassihi, Latifa; Kisseleva, Marina V.; Majerus, Philip W.; Rousseau, François; Vacher, Jean

doi:10.1016/j.cmet.2011.08.013

Cited by 51 publications

(66 citation statements)

References 38 publications

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“…This set includes TYROBP (5 DAP12), INPP4B, and OSTM1, which are important regulators of OC genesis in mouse and human hematopoiesis. [37][38][39] As other examples, we found that the transcription factors SPI1 (5 PU.1), GATA2, and LIMD1 were upregulated, in agreement with their proven role in mouse OC development. [40][41][42] Gfi-1, which contributes to DC development, 43 was downregulated.…”

Section: Discussionsupporting

confidence: 62%

Macrophages and osteoclasts stem from a bipotent progenitor downstream of a macrophage/osteoclast/dendritic cell progenitor

Xiao¹,

Palomero²,

Grabowska³

et al. 2017

Blood Advances

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Key Points• Under homeostatic conditions, MFs, OCs, and DCs develop from a tripotent progenitor, the MODP.• (CDP) has been described as committed to plasmacytoid and conventional DC development.However, the human CDP proved identical to the MODP population, whereas the mouse CDP largely overlapped with the MODP population and was accordingly oligopotent for MF, OC, and DC development. The CX 3 CR1 1 MF/DC progenitor (MDP) population described in the mouse generated MFs and OCs but not DCs. Thus, monocytes/MFs, OCs, and DCs share a common progenitor that gives rise to a bipotent MF/OC progenitor, but a dedicated DC progenitor is currently undefined. The definition of these progenitor populations may serve diagnostics and interventions in diseases with pathogenic activity of MFs, OCs, or DCs.

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Section: Discussionsupporting

confidence: 62%

Macrophages and osteoclasts stem from a bipotent progenitor downstream of a macrophage/osteoclast/dendritic cell progenitor

Xiao¹,

Palomero²,

Grabowska³

et al. 2017

Blood Advances

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“…A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 9 Interestingly, based on mouse models, INPP4 deficiency alone (potentially impacting PI(3,4)P2 accumulation), similar to SHIP deficiency (potentially impacting PIP3 accumulation), does not result in spontaneous tumor formation [38,49,50], while PTEN deficiency alone (potentially impacting accumulation of both lipids) has long been known to cause high incidence of cancer [51]. This raises the possibility that malignant transformation through PI3K dysregulation may require uncontrolled production of both PIP3 and PI(3,4)P2.…”

Section: Inpp4b In Cancermentioning

confidence: 96%

“…In vivo insights into the function of INPP4B were available using INPP4B deficient mice [38] with similar mutation to the weeble INPP4A deficient mice [29]. INPP4B deficiency did not lead A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT 8 to major defects in development or life span but was associated with defects in bone homeostasis.…”

Section: Inpp4b Is a Modulator Of Osteoclast Differentiationmentioning

confidence: 98%

Phosphatidylinositol (3,4) bisphosphate-specific phosphatases and effector proteins: A distinct branch of PI3K signaling

Marshall

2015

Cellular Signalling

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“…Culture medium was replaced every 2 days with fresh RANKL-containing complete medium. Cells were then fixed with formaldehyde (EMD Inc., Mississauga, ON, Canada) and processed for staining of tartrate-resistant acid phosphatase (TRAP), as described previously (27). Alternatively, they were stained with DAPI.…”

Section: Methodsmentioning

confidence: 99%

Macrophage Fusion Is Controlled by the Cytoplasmic Protein Tyrosine Phosphatase PTP-PEST/PTPN12

et al. 2013

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dMacrophages can undergo cell-cell fusion, leading to the formation of multinucleated giant cells and osteoclasts. This process is believed to promote the proteolytic activity of macrophages toward pathogens, foreign bodies, and extracellular matrices. Here, we examined the role of PTP-PEST (PTPN12), a cytoplasmic protein tyrosine phosphatase, in macrophage fusion. Using a macrophage-targeted PTP-PEST-deficient mouse, we determined that PTP-PEST was not needed for macrophage differentiation or cytokine production. However, it was necessary for interleukin-4-induced macrophage fusion into multinucleated giant cells in vitro. It was also needed for macrophage fusion following implantation of a foreign body in vivo. Moreover, in the RAW264.7 macrophage cell line, PTP-PEST was required for receptor activator of nuclear factor kappa-B ligand (RANKL)-triggered macrophage fusion into osteoclasts. PTP-PEST had no impact on expression of fusion mediators such as ␤-integrins, E-cadherin, and CD47, which enable macrophages to become fusion competent. However, it was needed for polarization of macrophages, migration induced by the chemokine CC chemokine ligand 2 (CCL2), and integrin-induced spreading, three key events in the fusion process. PTP-PEST deficiency resulted in specific hyperphosphorylation of the protein tyrosine kinase Pyk2 and the adaptor paxillin. Moreover, a fusion defect was induced upon treatment of normal macrophages with a Pyk2 inhibitor. Together, these data argue that macrophage fusion is critically dependent on PTP-PEST. This function is seemingly due to the ability of PTP-PEST to control phosphorylation of Pyk2 and paxillin, thereby regulating cell polarization, migration, and spreading.

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Inositol Polyphosphate 4-Phosphatase B as a Regulator of Bone Mass in Mice and Humans

Cited by 51 publications

References 38 publications

Macrophages and osteoclasts stem from a bipotent progenitor downstream of a macrophage/osteoclast/dendritic cell progenitor

Macrophages and osteoclasts stem from a bipotent progenitor downstream of a macrophage/osteoclast/dendritic cell progenitor

Phosphatidylinositol (3,4) bisphosphate-specific phosphatases and effector proteins: A distinct branch of PI3K signaling

Macrophage Fusion Is Controlled by the Cytoplasmic Protein Tyrosine Phosphatase PTP-PEST/PTPN12

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