Mechanically Induced ATP Release from Human Osteoblastic Cells

Romanello, Milena; Pani, B.; Bicego, Massimiliano; D’Andrea, Paola

doi:10.1006/bbrc.2001.6124

Cited by 156 publications

(147 citation statements)

References 34 publications

(48 reference statements)

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“…connexin hemichannels, the P2X7 receptor) but the predominant mechanism appears to be vesicular exocytosis (see review [21]). The extent of cellular ATP release can also be influenced by external stimuli such as hypoxia [22,23], mechanical stress [24,25] and vitamin D [26]. Since ATP hydrolysis is a key source of extracellular pyrophosphate, factors which regulate ATP release may also indirectly affect pyrophosphate levels and thus the local rates of mineralisation.…”

Section: Generation and Regulation Of Extracellular Pyrophosphatementioning

confidence: 99%

“…Since osteocytes are embedded within bone they must be capable of preventing over-mineralisation of their lacunae (which could potentially compromise cell viability and function). ATP, which is released by all bone cells including osteocytes [22,25,[60][61][62][63][64][65], is an important source of pyrophosphate in bone [17,66]. Previous work has shown that endogenous ATP released by osteoblasts acts as an important local brake on mineralisation, an effect mediated by both purinergic signalling and the breakdown to produce pyrophosphate [38, 67,68].…”

Section: Pyrophosphate and Osteocytesmentioning

confidence: 99%

See 1 more Smart Citation

Pyrophosphate: a key inhibitor of mineralisation

Orriss

Arnett

Russell

2016

Current Opinion in Pharmacology

140

105

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Section: Generation and Regulation Of Extracellular Pyrophosphatementioning

confidence: 99%

Section: Pyrophosphate and Osteocytesmentioning

confidence: 99%

Pyrophosphate: a key inhibitor of mineralisation

Orriss

Arnett

Russell

2016

Current Opinion in Pharmacology

140

105

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“…Controlled ATP release has been demonstrated from numerous excitatory and non-excitatory cells. In the bone microenvironment, osteoblasts (Buckley et al, 2003;Genetos et al, 2005;Orriss et al, 2009;Romanello et al, 2001;Rumney et al, 2012), osteoclasts and MLO-Y4 osteocyte-like cells (Genetos et al, 2007;Kringelbach et al, 2014) have all been shown to constitutively release ATP.…”

Section: Extracellular Nucleotides and The Regulation Of Bone Mineralmentioning

confidence: 99%

“…Controlled ATP release from osteoblast-like cells was first described by Romanello et al in 2001(Romanello et al, 2001. Since then several studies have indicated that the primary method of ATP release from osteoblasts is by vesicular exocytosis (Genetos et al, 2005;Orriss et al, 2009;Romanello et al, 2005).…”

Section: Atp Release From Osteoblastsmentioning

confidence: 99%

The role of purinergic signalling in the musculoskeletal system

Orriss

2015

Autonomic Neuroscience

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“…cells to mechanical stimulation, a phenomenon that also has been scientifically documented [3][4][5][6][7]. Renal epithelial cells, especially Madin-Darby canine kidney (MDCK) cells, a well-differentiated cell line derived from distal tubule/collecting duct, was found to respond to nucleotide signaling via P2 receptor activation already 30 years ago [8].…”

mentioning

confidence: 99%

The touching story of purinergic signaling in epithelial and endothelial cells

Öhman

Erlinge

2012

Purinergic Signalling

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Endothelial and epithelial cells have something in commonthey are both the barrier and bridge between different environments. Forming a one-cell layer lining of blood vessels, airways, and urinary tract, they are in constant contact with a wide variety of cells, putting high demands on the communication skills of these cells. The purinergic signaling system offers a dynamic and versatile way for local and rapid intercellular communication and involves three processes: nucleotide release, enzymatic degradation, and activation of purinergic receptors. With an impressive number of molecular members of the system (15 P2 receptor subtypes and in total 16 nucleotide-degrading enzymes), cells have managed to put purines and pyrimidines as well as their derivatives to use in an array of different areas, including regulation of flow, secretion, and vascular tone. Indeed, the purinergic signaling system is an ancient way of intercellular communication that most likely could be found in the first most primitive life form [1]. The scope of this review is to give an overview of exciting features of purinergic signaling and examples of gaps to fill in understanding its role in the cells lining the body-the endothelium and the epithelium. Purinergic signaling-an overviewExtracellular nucleotides exert their paracrine signaling by binding to P2 receptors present at the cell surface. The P2 receptor family is divided into two groups: P2X receptors, which are ligand-activated ion channels, and P2Y receptors, which are G protein-coupled receptors (reviewed in [2]). Each receptor is characterized by its affinity pattern for different nucleotides and different cell types display varying receptor profiles. While P2X receptors respond only to ATP, P2Y receptors can be activated by other nucleotides such as ADP, UTP, and UDP. Extracellular nucleotide concentrations are precisely regulated by ecto-enzymes, which cleave nucleotide tri-/diphosphates. The result of signaling by the extracellular nucleotides ATP/ADP, UTP/UDP and the nucleoside adenosine is both acute, for example the rapid platelet aggregation induced by ADP, and chronic, via changes in gene expression induced by P2 receptor stimulation. Ligand availability for P2 receptors is regulated by a group of enzymes termed ectonucleotidases. NTPDase1 (apyrase; CD39) cleaves ATP to AMP, NTPDase2 (CD39L1) cleaves ATP to ADP, and 5′-ectonucleotidase (CD73) generates adenosine from AMP. Adenosine is the end product of purinergic signaling, acting on adenosine receptors (A1, A2a, A2b, and A3; also termed P1 receptors) or recycling by the cell after reuptake through the equilibrating nucleoside transporters ENT1 and 2. UTP is believed to be released simultaneously with ATP via the same mechanism but at a lower concentration (UTP/ATP, 1:10-100). UTP is degraded in the same way as ATP, but the biological function of uridine is poorly understood and no uridine receptor has been identified. Figure 1 shows an outline of nucleotide metabolism. Purinergic toneAll investigators that have tried t...

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Mechanically Induced ATP Release from Human Osteoblastic Cells

Cited by 156 publications

References 34 publications

Pyrophosphate: a key inhibitor of mineralisation

Pyrophosphate: a key inhibitor of mineralisation

The role of purinergic signalling in the musculoskeletal system

The touching story of purinergic signaling in epithelial and endothelial cells

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