cGMP produced in response to ANP and CNP regulates proliferation and differentiation of osteoblastic cells

Hagiwara, Hiromi; Inoue, Atsuto; Yamaguchi, Akira; Yokose, Satoshi; Furuya, Masako; Tanaka, Sayoko; Hirose, Shigehisa

doi:10.1152/ajpcell.1996.270.5.c1311

Cited by 115 publications

(81 citation statements)

References 27 publications

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“…[21][22][23][24][25][26][27] In the OE, CNP is expressed in the distal processes and footpads of the sustentacular cells, positioning it to act on a variety of neuronal precursors. 16 Its receptor, guanylyl cyclase B (GC-B), is expressed within the basal layer of the OE and in more mature OSNs.…”

Section: Introductionmentioning

confidence: 99%

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Simpson

Moon²,

Kleman

et al. 2007

Cell Cycle

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ACKnowlEdGEMEntSWe thank Amy Palmer for helpful discussions and reading of the manuscript, and Susan McTeer for manuscript preparation. This work was supported by grants NIDCD RO3 DC005704 to P.J.S., NIDCD RO1 DC02979 and NINDS RO1 NS39657 to G.V.R. AbStRACtNeuronal stem cell expansion and differentiation is a process involving stages of proliferation and maturation governed by the sequential and combinatorial exposure of cells to extrinsic factors. The olfactory epithelium is an excellent model to investigate regulation of this process, as it undergoes neuronal replacement post-natally. We have shown that the neurotrophins NGF and BDNF sequentially promote proliferation of developing olfactory sensory neuronal precursors, although their kinetics of proliferation and cell fate outcomes differ. Interestingly, CNP inhibits this neurotrophin-induced proliferation and promotes the maturation of these precursors to their next developmental stage. Here, we investigate the mechanisms behind these actions. Both NGF and BDNF increase the expression of cyclin D1 and cyclin-dependent kinase 4 (cdk4), with temporal expression patterns that parallel the proliferation kinetics of their cellular targets. The timing of cyclin D1 expression reflects differences in the need for transcription and translation in early and late stage precursors. CNP inhibits neurotrophin-induced cyclin D1 expression, and induces the expression of different profiles of inhibitory cell cycle proteins, which are neurotrophin-specific and correlate with the attainment of different maturational cell fates. Inhibition of protein degradation reverses the effects of neurotrophins and CNP on cyclin D1 and inhibitor expression levels, respectively. These results suggest a model for cell cycle regulation that involves the simultaneous expression of progressive and inhibitory cell cycle regulatory proteins in response to both proliferation and differentiation agents, followed by selective degradation of these proteins, providing a mechanism for rapid and exquisite control of the cell cycle.

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Section: Introductionmentioning

confidence: 99%

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Simpson

Moon²,

Kleman

et al. 2007

Cell Cycle

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“…Over and above actions in chondrocytes, in vitro studies in rodents show that CNP transcripts are present in cells of osteoblast lineage (Suda et al 1996(Suda et al , 1999 and that CNP production from these cell lines can be augmented by TGFb (Suda et al 1996). Further the addition of CNP to murine preosteoblasts, acting via NPR-B and cGMP, inhibits cell proliferation while enhancing differentiation and markers of osteoblast maturation (ALP and osteocalcin; Hagiwara et al 1996). CNP also increases the formation of mineralised nodules.…”

Section: Discussionmentioning

confidence: 99%

Effect of sex steroids on plasma C-type natriuretic peptide forms: stimulation by oestradiol in lambs and adult sheep

Prickett¹,

Barrell²,

Wellby³

et al. 2008

Journal of Endocrinology

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Although C-type natriuretic peptide (CNP) is crucial to postnatal endochondral growth, roles for the hormone in pubertal bone growth and the physiological effects of sex steroid substitution on CNP synthesis are not known. Using a plasma marker of CNP tissue synthesis (amino-terminal proCNP, NTproCNP), we have studied the effect of exogenous oestrogen (E 2 ) or testosterone (T) on plasma CNP forms and bone alkaline phosphatase (bALP) in pre-pubertal lambs.Responses to E 2 in non-cycling adult ewes were also studied. In 15-week-old intact ewe lambs, E 2 promptly increased plasma NTproCNP and CNP (P!0 . 001) to peak on day 2, and bALP (P!0 . 001 peaking on day 7), whereas no significant stimulation in response to T was observed in male lambs. Linear bone growth and live weight were unaffected. In adult anoestrous ewes, basal concentrations of CNP forms and bALP were lower than in ewe lambs, in keeping with skeletal maturity, but adults responded similarly to E 2 . Prompt and sustained increases in NTproCNP and CNP, and a later threefold rise in bALP (all P!0 . 001), were induced by E 2 . Possible contributions to these increases in plasma CNP forms by reproductive tissues (a known site of E 2 -induced CNP expression) were excluded by showing similar E 2 -induced CNP responses in adult ewes after surgical removal of reproductive tissues. These results are the first to show that E 2 stimulates plasma CNP forms and bALP in lambs and adult sheep and raise the possibility that CNP also participates in bone formation in the mature skeleton.

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“…1,2) CNP stimulates the differentiation of osteoblastic lineage cells through its specific receptor, B-type natriuretic peptide receptor (NPR-B). [3][4][5] The targeted disruption of the genes coding for CNP 6) and NPR-B 7) causes dwarfism due to an impaired longitudinal growth of long bone, while the transgenic overexpression of CNP causes skeletal overgrowth, 8) suggesting that the CNP/NPR-B signaling pathway has an essential role in the regulation of bone metabolism. Recently, we have shown that the activation of CNP/NPR-B signaling causes the enhancement of bone for- * To whom correspondence should be addressed: Faculty of Pharmaceutical Sciences, Toho University, 2-2-1 Miyama, Funabashi, Chiba 274-8510, Japan.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 Enhances B-Type Natriuretic Peptide Receptor Expression in Calvarial Osteoblasts through EP1 Subtype of Prostaglandin E2 Receptor

Kaneki

Kurokawa-Nagai

Sugano

et al. 2009

JOURNAL OF HEALTH SCIENCE

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The B-type natriuretic peptide receptor (NPR-B) is a specific receptor for the C-type natriuretic peptide (CNP) and the binding of the peptide to NPR-B stimulates the bone formation by osteoblasts. However, the mechanism behind the regulation of NPR-B expression in osteoblasts remains unknown. In this study, we examined the role of prostaglandin E 2 (PGE 2 ) through the PGE 2 receptor subtypes, EP1, EP2, EP3 and EP4, in the regulation of NPR-B expression using calvarial osteoblasts from rats of various ages. Reverse Transcription-PCR (RT-PCR) and Western blotting analyses revealed that PGE 2 or 17-phenyl-ω-trinor PGE 2 , an EP1 agonist, increased the expression of NPR-B of calvarial osteoblasts from 25-week-old rats in a time-and dose-dependent manner. The PGE 2 -and EP1 agonist-induced increase in NPR-B expression was blocked by treating with SC19220, an EP1 antagonist. By contrast, agonists for EP2, EP3, and EP4 failed to affect the NPR-B expression. The basal mRNA level of NPR-B and EP1 continuously decreased with the age of cell donors between 10 to 60 weeks and remained constant over 60 weeks. The degree of EP1 agonist-induced increase in NPR-B mRNA level gradually decreased with age of cell donors between 10 to 60 weeks, and no significant effect of EP1 agonist on the NPR-B mRNA level was observed over 60 weeks. From these results, we concluded that PGE 2 acts as a regulator of NPR-B expression through the EP1 receptor in osteoblasts and age-related decrease in EP1 expression causes a decrease in NPR-B expression.

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cGMP produced in response to ANP and CNP regulates proliferation and differentiation of osteoblastic cells

Cited by 115 publications

References 27 publications

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Effect of sex steroids on plasma C-type natriuretic peptide forms: stimulation by oestradiol in lambs and adult sheep

Prostaglandin E2 Enhances B-Type Natriuretic Peptide Receptor Expression in Calvarial Osteoblasts through EP1 Subtype of Prostaglandin E2 Receptor

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