Circulating sensory peptide levels within 24 h of human bone fracture

Onuoha, Gracey N.

doi:10.1016/s0196-9781(01)00434-x

Cited by 36 publications

(26 citation statements)

References 29 publications

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“…Accumulation of cAMP in osteoblasts is proved to be as a result of combined activation of PACAP and VIP and regulates diverse signaling pathways influencing osteoblast differentiation. In line with this, presence of certain neuropeptides was shown to be elevated after bone fracture, indicating their importance in successful regeneration [77]. A recent report demonstrated release of various neuropeptides from periosteal nerve endings resulting in enhancement of intercellular communication and increased metabolic activity of osteoblasts [78].…”

Section: Vip and Pacap In Osteogenic Signaling Cascadesmentioning

confidence: 67%

PACAP and VIP signaling in chondrogenesis and osteogenesis

et al. 2015

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Section: Vip and Pacap In Osteogenic Signaling Cascadesmentioning

confidence: 67%

PACAP and VIP signaling in chondrogenesis and osteogenesis

et al. 2015

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“…Data are the means Ϯ SE of 3 experiments performed with cells from three different donors; **P Ͻ 0.01, *P Ͻ 0.05 vs. conditioned media of untreated cells, Student's t-test. (36). When bone formation must offset bone resorption, as in the case of bone repair with highly activated bone remodeling, CGRP activity may help fulfil the requirements of regeneration processes.…”

Section: Discussionmentioning

confidence: 99%

CGRP inhibits osteoprotegerin production in human osteoblast-like cells via cAMP/PKA-dependent pathway

Villa¹,

Mrak²,

Rubinacci³

et al. 2006

American Journal of Physiology-Cell Physiology

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The osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL)/receptor activator of nuclear factor-κB (RANK) system was evaluated as a potential target of CGRP anabolic activity on bone. Primary cultures of human osteoblast-like cells (hOB) express calcitonin receptor-like receptor (CLR) and receptor activity modifying protein 1, and, because CGRP stimulates cAMP (one of the modulators of OPG production in osteoblasts), it was investigated whether it affects OPG secretion and expression in hOB. CGRP treatment of hOB (10−11 M–10−7 M) dose-dependently inhibited OPG secretion with an EC50 of 1.08 × 10−10 M, and also decreased its expression. This action was blocked by the antagonist CGRP8–37. Forskolin, a stimulator of cAMP production, and dibutyryl cAMP also reduced the production of OPG. CGRP (10−8 M) enhanced protein kinase A (PKA) activity in hOB, and hOB exposure to the PKA inhibitor, H89 (2 × 10−6 M), abolished the inhibitory effect of CGRP on OPG secretion. Conditioned media from CGRP-treated hOB increased the number of multinucleated tartrate-resistant acid phosphatase-positive cells and the secretion of cathepsin K in human peripheral blood mononuclear cells compared with the conditioned media of untreated hOB. These results show that the cAMP/PKA pathway is involved in the CGRP inhibition of OPG mRNA and protein secretion in hOB and that this effect favors osteoclastogenesis. CGRP could thus modulate the balance between osteoblast and osteoclast activity, participating in the fine tuning of all of the bone remodeling phases necessary for the subsequent anabolic effect.

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“…Accumulation of cAMP in osteoblasts is proved to be a result of combined activation of PACAP/VIP and regulates diverse signalling pathways infl uencing osteoblast differentiation. In line with this, presence of certain neuropeptides was shown to be elevated after bone fracture, indicating their importance in successful regeneration [ 88 ]. A recent report demonstrated release of various neuropeptides from periosteal nerve endings resulting in enhancement of intercellular communication and increased metabolic activity of osteoblasts [ 89 ].…”

Section: Bone Formation Under the Control Of Vip And Pacap Signallingmentioning

confidence: 67%

Role of PACAP and VIP Signalling in Regulation of Chondrogenesis and Osteogenesis

Juhász

Tamás

Zákány

et al. 2016

Current Topics in Neurotoxicity

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Pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are multifunctional proteins that can regulate diverse physiological processes. These are also regarded as neurotrophic and antiinfl ammatory substances in the CNS, and PACAP is reported to prevent harmful effects of oxidative stress. In the last decade more and more data accumulated on the similar function of PACAP in various tissues, but its cartilage-and bone-related presence and functions have not been widely investigated yet. In this summary we plan to verify the presence and function of PACAP and VIP signalling tool kit during cartilage differentiation and bone formation. We give evidence about the protective function of PACAP in cartilage regeneration with oxidative or mechanically stress and also with the modulation of PACAP signalling in vitro in osteogenic cells. Our observations imply the therapeutic perspective that PACAP might be applicable as a natural agent exerting protecting effect during joint infl ammation and/or may promote cartilage regeneration during degenerative diseases of articular cartilage.

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Circulating sensory peptide levels within 24 h of human bone fracture

Cited by 36 publications

References 29 publications

PACAP and VIP signaling in chondrogenesis and osteogenesis

PACAP and VIP signaling in chondrogenesis and osteogenesis

CGRP inhibits osteoprotegerin production in human osteoblast-like cells via cAMP/PKA-dependent pathway

Role of PACAP and VIP Signalling in Regulation of Chondrogenesis and Osteogenesis

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