Disruption of biomineralization pathways in spinal tissues of a mouse model of diffuse idiopathic skeletal hyperostosis

Hisataka,; Warraich, Sumeeta; Tenn, Neil A; Quinonez, Diana; Holdsworth, David W.; Hammond, James R.; Dixon, S. Jeffrey; Séguin, Cheryle A.

doi:10.1016/j.bone.2016.05.008

Cited by 18 publications

(42 citation statements)

References 59 publications

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“…A recently developed mouse model might be useful in future studies on DISH. 61 There have been a few case descriptions of familial cases of DISH. 62 63 A single study reported that collagen type I alpha1 and vitamin D receptor polymorphisms do not seem to contribute to DISH aetiology.…”

Section: Pathogenesis Of Dishmentioning

confidence: 99%

Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next

Mader¹,

et al. 2017

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Section: Pathogenesis Of Dishmentioning

confidence: 99%

Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next

Mader¹,

et al. 2017

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“…Previous studies using the Slc29a1 -null mouse showed no obvious gross anatomical abnormalities up to the age of about 4 months. Mice older than 4 months showed spine stiffness and gait disturbances [ 32 , 36 ], likely due to the progressive ectopic mineralization that has been reported in these mice [ 32 , 37 ]. Therefore, the data reported herein are from mice of 3–4 months of age.…”

Section: Methodsmentioning

confidence: 99%

Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice

Best¹,

Bone²,

Vilas³

et al. 2018

PLoS ONE

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Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine if there are similar changes in the microvasculature, and investigate underlying mechanism, we examined aortas isolated from wildtype and Slc29a1-null mice. Aorta macrostructure and gene expression were examined histologically and by qPCR, respectively. Wire myography was used to assess the contractile properties of isolated thoracic aortic rings and their response to adenosine under both normoxic and hypoxic conditions. In vivo haemodynamic parameters were assessed using the tail-cuff method. Slc29a1-null mice had significantly (P<0.05) increased plasma adenosine (2.75-fold) and lower blood pressure (~15% ↓) than wild-type mice. Aortas from Slc29a1-null mice were stiffer with a smaller circumference (11% ↓), and had an enhanced contractile response to KCl and receptor-mediated stimuli. Blockade of ENT1 with nitrobenzylthioinosine significantly enhanced (by ~3.5-fold) the response of aorta from wild-type mice to phenylephrine, but had minimal effect on aortas from Slc29a1-null mice. Adenosine enhanced phenylephrine-mediated constriction in the wild-type tissue under both normoxic (11.7-fold) and hypoxic (3.6-fold) conditions, but had no effect on the Slc29a1-null aortic aorta. In conclusion, aortas from Slc29a1-null mice respond to hypoxic insult in a manner comparable to wild-type tissues that have been pharmacologically preconditioned with adenosine. These data also support a role for ENT1 in the regulation of the protective effects of adenosine on contractile function in elastic conduit arteries such as thoracic aorta.

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“…Knockout mice lacking ENT1 display reduced adenosine uptake and increased circulating levels of adenosine in the plasma [37,38]. Interestingly, these mice show evidence of ectopic bone mineralization with involvement of the spine and sternal fibrocartilaginous tissue, a condition which is similar to lesions seen in diffuse idiopathic skeletal hyperostosis (DISH) [39,40]. Similarly, individuals lacking ENT1 (homozygous for a null mutation in SLC29A1) suffer from ectopic mineralization suggesting the role of ENT1 in bone metabolism in vivo [41].…”

Section: Adenosine Signalingmentioning

confidence: 98%

Regulation of bone and cartilage by adenosine signaling

Strazzulla

Cronstein

2016

Purinergic Signalling

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There is growing recognition that bone serves important endocrine and immunologic functions that are compromised in several disease states. While many factors are known to affect bone metabolism, recent attention has focused on investigating the role of purinergic signaling in bone formation and regulation. Adenosine is a purine nucleoside produced intracellularly and extracellularly in response to stimuli such as hypoxia and inflammation, which then interacts with P1 receptors. Numerous studies have suggested that these receptors play a pivotal role in osteoblast, osteoclast, and chondrocyte differentiation and function. This review discusses the various ways by which adenosine signaling contributes to bone and cartilage homeostasis, while incorporating potential therapeutic applications of these signaling pathways.

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Disruption of biomineralization pathways in spinal tissues of a mouse model of diffuse idiopathic skeletal hyperostosis

Cited by 18 publications

References 59 publications

Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next

Diffuse idiopathic skeletal hyperostosis (DISH): where we are now and where to go next

Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice

Regulation of bone and cartilage by adenosine signaling

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