Periostin is a collagen associated bone matrix protein regulated by parathyroid hormone

Fortunati, Dario; Reppe, Sjur; Fjeldheim, Åse-Karine; Nielsen, Martin Skovmos; Gautvik, Vigdis T.; Gautvik, Kaare M.

doi:10.1016/j.matbio.2010.07.001

Cited by 36 publications

(35 citation statements)

References 27 publications

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“…These factors may be poorly expressed at periosteal surfaces, in contrast to Postn, which now appears as a major mediator of PTH anabolic effects on the periosteum, as well as osteoblast proliferation and differentiation factors. These observations are in accordance with previous data indicating that knock-down of Postn either by neutralizing antibodies or siRNA induced a defect in the attachment of osteoblastic cells, which affects their differentiation and mineralization processes (23,37).…”

Section: Discussionsupporting

confidence: 93%

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Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin

Bonnet

Conway

Ferrari

2012

Proc. Natl. Acad. Sci. U.S.A.

130

112

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Periostin (Postn) is a matricellular protein preferentially expressed by osteocytes and periosteal osteoblasts in response to mechanical stimulation and parathyroid hormone (PTH). Whether and how periostin expression influences bone anabolism, however, remains unknown. We investigated the skeletal response of adult Postn −/− and Postn +/+ mice to intermittent PTH. Compared with Postn +/+ , Postn −/− mice had a lower bone mass, cortical bone volume, and strength response to PTH. PTH-stimulated bone-forming indices were all significantly lower in Postn −/− mice, particularly at the periosteum. Furthermore, in vivo stimulation of Wnt-β-catenin signaling by PTH, as evaluated in TOPGAL reporter mice, was inhibited in the absence of periostin (TOPGAL;Postn −/− mice). PTH stimulated periostin and inhibited MEF2C and sclerostin (Sost) expression in bone and osteoblasts in vitro. Recombinant periostin also suppressed Sost expression, which was mediated through the integrin αVβ3 receptor, whereas periostin-blocking antibody prevented inhibition of MEF2C and Sost by PTH. In turn, administration of a Sost-blocking antiboby partially restored the PTH-mediated increase in bone mass in Postn −/− mice. In addition, primary osteoblasts from Postn −/− mice showed a lower proliferation, mineralization, and migration, both spontaneously and in response to PTH. Osteoblastic gene expression levels confirmed a defect of Postn −/− osteoblast differentiation with and without PTH, as well as an increased osteoblast apoptosis in the absence of periostin. These data elucidate the complex role of periostin on bone anabolism, through the regulation of Sost, Wnt-β-catenin signaling, and osteoblast differentiation.

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Section: Discussionsupporting

confidence: 93%

“…A relationship between Postn and PTH was first suggested by the observation that Postn is regulated by PTH in mouse and humans osteoblasts (16,23,24). Our study now demonstrates the functional significance of PTH-stimulated Postn expression with regard to bone formation.…”

Section: Discussionsupporting

confidence: 72%

Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin

Bonnet

Conway

Ferrari

2012

Proc. Natl. Acad. Sci. U.S.A.

130

112

View full text Add to dashboard Cite

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“…All these data suggest that PTH may influence osteoblast synthesis and subsequent bone remodeling through periostin via different ways. Finally, periostin knockdown induced a significant reduction of PTHrP mRNA and protein expression by osteoblasts in vitro, suggesting a local regulation loop [45].…”

Section: Periostin Expression Is Regulated By Hormones and Growth Facmentioning

confidence: 86%

“…Gene expression profiles studies on PHPT patients and rodents submitted to continuous infusion of PTH show increased bone turnover associated with higher periostin mRNA levels [43,44]. In vitro, periostin expression may be directly up-regulated by PTH treatment in mouse calvaria osteoblasts [45]. As it has been shown that intermittent PTH promotes periosteal cells differentiation and early progenitors proliferation in vitro and in vivo through ERK-, bone morphogenetic protein (BMP)-, and Wnt-dependent signaling pathways, it is possible that PTH effect on periostin is mediated through one of these pathways [25].…”

Section: Periostin Expression Is Regulated By Hormones and Growth Facmentioning

confidence: 99%

The multiple facets of periostin in bone metabolism

2012

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Periostin is a matricellular glutamate-containing protein expressed during ontogenesis and in adult connective tissues submitted to mechanical strains including bone and, more specifically, the periosteum, periodontal ligaments, tendons, heart valves, or skin. It is also expressed in neoplastic tissues, cardiovascular and fibrotic diseases, and during wound repair. Its biological functions are extensively investigated in fields such as cardiovascular physiology or oncology. Despite its initial identification in bone, investigations of periostin functions in bone-related physiopathology are less abundant. Recently, several studies have analyzed the potential role of periostin in bone biology and suggest that periostin may be an important regulator of bone formation. The aim of this article is to provide an extensive review on the implications of periostin in bone biology and its potential use in benign and metabolic bone diseases.

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“…In particular, among upregulated transcripts, we found signal transduction proteins involved in osteogenic differentiation, such as CAST [62], ID1, and SOCS2 [63]; osteogenic growth factors, such as FGF2, STC1 [64], ADM, and IL18, described as a mitogen to the osteogenic and chondrogenic cells [65], and osteoblastic differentiation markers, such as ADAMTS1 and CLDN11. Among ATP-downregulated genes, we found PBX1, a transcription factor that impaired osteogenic commitment of pluripotent cells and the differentiation of osteoblasts [66] and other transcripts whose expression was inversely related to cell mineralization and terminal differentiation, such as POSTN [67], DPT, ROR2 [68], and SOX4 [69] (Fig. 1C).…”

Section: Gene Expression Profile Of Atp-treated Undifferentiated Bm-hmentioning

confidence: 97%

Extracellular Purines Promote the Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells to the Osteogenic and Adipogenic Lineages

Ciciarello

Zini

Rossi

et al. 2013

Stem Cells and Development

101

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Extracellular nucleotides are potent signaling molecules mediating cell-specific biological functions, mostly within the processes of tissue damage and repair and flogosis. We previously demonstrated that adenosine 5¢-triphosphate (ATP) inhibits the proliferation of human bone marrow-derived mesenchymal stem cells (BMhMSCs), while stimulating, in vitro and in vivo, their migration. Here, we investigated the effects of ATP on BM-hMSC differentiation capacity. Molecular analysis showed that ATP treatment modulated the expression of several genes governing adipogenic and osteoblastic (ie, WNT-pathway-related genes) differentiation of MSCs. Functional studies demonstrated that ATP, under specific culture conditions, stimulated adipogenesis by significantly increasing the lipid accumulation and the expression levels of the adipogenic master gene PPARc (peroxisome proliferator-activated receptor-gamma). In addition, ATP stimulated osteogenic differentiation by promoting mineralization and expression of the osteoblast-related gene RUNX2 (runt-related transcription factor 2). Furthermore, we demonstrated that ATP stimulated adipogenesis via its triphosphate form, while osteogenic differentiation was induced by the nucleoside adenosine, resulting from ATP degradation induced by CD39 and CD73 ectonucleotidases expressed on the MSC membrane. The pharmacological profile of P2 purinergic receptors (P2Rs) suggests that adipogenic differentiation is mainly mediated by the engagement of P2Y1 and P2Y4 receptors, while stimulation of the P1R adenosine-specific subtype A2B is involved in adenosine-induced osteogenic differentiation. Thus, we provide new insights into molecular regulation of MSC differentiation.

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Periostin is a collagen associated bone matrix protein regulated by parathyroid hormone

Cited by 36 publications

References 27 publications

Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin

Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin

The multiple facets of periostin in bone metabolism

Extracellular Purines Promote the Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells to the Osteogenic and Adipogenic Lineages

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