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Enzyme
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Gene/Protein
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Target Concepts:
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Query: EC:3.1.3.1 (
alkaline phosphatase
)
47,916
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Nanosystems are able to enhance bone regeneration, a complex process requiring the mutual interplay between immune and skeletal cells. Activated monocytes can communicate pro-osteogenic signals to mesenchymal stem cells and promote osteogenesis. Thus, the activation of monocytes is a promising strategy to improve bone regeneration. Nanomaterials specifically selected to provoke immune-mediated bone formation are still missing. As a proof of concept, we apply here the intrinsic immune-characteristics of graphene oxide (GO) with the well-recognized osteoinductive capacity of calcium phosphate (CaP) in a biocompatible nanomaterial called maGO-CaP (monocytes activator GO complexed with CaP). In the presence of monocytes, the
alkaline phosphatase
activity and the expression of osteogenic markers increased. Studying the mechanisms of action, we detected an up-regulation of Wnt and BMP signaling, two key osteogenic pathways. The role of the immune activation was evidenced by the over-production of
oncostatin M
, a pro-osteogenic factor produced by monocytes. Finally, we tested the pro-osteogenic effects of maGO-CaP in vivo. maGO-CaP injected into the tibia of mice enhanced local bone mass and the bone formation rate. Our study suggests that maGO-CaP can activate monocytes to enhance osteogenesis ex vivo and in vivo.
...
PMID:Stimulation of bone formation by monocyte-activator functionalized graphene oxide in vivo. 3138 39
Vascular calcification is a typical feature of atherosclerosis and is associated with adverse cardiovascular events such as myocardial infarction and stroke. Several studies have suggested that adenosine, an ATP metabolite may function as an endogenous regulator of arterial calcification. However, its effects on vascular smooth muscle cell calcification have not been clarified. In this study, we investigated the inhibitory effects of adenosine on vascular calcification in vitro by utilizing the culture of human aortic smooth muscle cells (HASMCs). Osteoblastic differentiation of HASMCs was induced by the treatment with
oncostatin M
and osteogenic differentiation medium. Adenosine and its metabolically stable analogue, 2-chloroadenosine (CADO) significantly reduced matrix mineralization and
alkaline phosphatase
(
ALP
) activities in HASMCs. The mRNA expression of tissue non-specific
alkaline phosphatase
(TNAP) was down-regulated by adenosine and CADO, but the mRNA expression of other osteoblastic differentiation markers, such as Runt-related transcription factor 2 (RUNX2) and bone sialoprotein (BSP)-II, was not significantly affected by these two reagents. Among the adenosine receptor (AR) subtype-selective agonists used, only IB-MECA (A
3
AR-selective agonist) significantly decreased in vitro mineralization and
ALP
activities in HASMCs, but not with CCPA (A
1
AR-selective agonist), CGS21680 (A
2a
AR-selective agonist), or BAY60-6583 (A
2b
AR-selective agonist). Importantly, IB-MECA also down-regulated expression of TNAP mRNA. Finally, knockdown of A
3
AR, but not A
1
AR, A
2a
AR, or A
2b
AR, significantly reversed the inhibitory actions of adenosine, CADO, or IB-MECA on in vitro calcification and
ALP
activities in HASMCs. These data suggest that adenosine attenuates HASMC calcification through A
3
AR.
...
PMID:Adenosine Attenuates Aortic Smooth Muscle Cell Calcification through A
3
Adenosine Receptor. 3187 81
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