Interleukin 1 beta suppresses transforming growth factor-induced inorganic pyrophosphate (PPi) production and expression of the PPi-generating enzyme PC-1 in human chondrocytes.

Lotz, Martin; Rosen, Fred; McCabe, G; Quach, Jacqueline; Blanco, F.J.; Dudler, Jean; Solan, Joell L.; Goding, James W.; Seegmiller, J. Edwin; Terkeltaub, Robert

doi:10.1073/pnas.92.22.10364

Cited by 89 publications

(90 citation statements)

References 36 publications

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“…NPP1 is located in the plasma membrane and MVs, while NPP3 is restricted to the pre-Golgi (48) (Figure 4). NPP1 accounts for 50% of the cell-associated NTPPH activity in monolayer cultures of human chondrocytes (52). Western blot analysis of OA articular chondrocytes revealed a major 115-130-kd protein band and a minor 60-kd signal for NPP1 (53), suggesting the presence of a soluble form.…”

Section: Regulation Of Eppi/epi Balance In Articular Cartilage By Ectmentioning

confidence: 93%

“…In cultures of porcine articular chondrocytes, TGF␤1 induces the release of MVs with higher NTPPH activity and CPPD crystal formation (126) as well as the release of CILP/NTPPH proteins, but not NPP1 (128). In contrast, human chondrocytes only release NPP1 after a TGF␤1 treatment, although ePPi is detected under control conditions (52).…”

mentioning

confidence: 99%

“…Ectonucleotidases also contribute to the TGF␤1-induced ePPi production in articular cartilage (126). In human chondrocytes, TGF␤1 increases NTPPH activity (ATP 3 AMP ϩ PPi) and decreases AP activity (PPi 3 2Pi) (52,127), both contributing to the increase in ePPi ( Table 2). NPP1 (52,128) and CILP/NTPPH (116,128) are up-regulated by TGF␤1.…”

mentioning

confidence: 99%

“…In human chondrocytes, TGF␤1 increases NTPPH activity (ATP 3 AMP ϩ PPi) and decreases AP activity (PPi 3 2Pi) (52,127), both contributing to the increase in ePPi ( Table 2). NPP1 (52,128) and CILP/NTPPH (116,128) are up-regulated by TGF␤1. In cultures of porcine articular chondrocytes, TGF␤1 induces the release of MVs with higher NTPPH activity and CPPD crystal formation (126) as well as the release of CILP/NTPPH proteins, but not NPP1 (128).…”

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confidence: 99%

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Extracellular nucleotide metabolism and signaling in the pathophysiology of articular cartilage

Picher¹,

Graff²,

Lee³

2003

Arthritis & Rheumatism

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Section: Regulation Of Eppi/epi Balance In Articular Cartilage By Ectmentioning

confidence: 93%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Extracellular nucleotide metabolism and signaling in the pathophysiology of articular cartilage

Picher¹,

Graff²,

Lee³

2003

Arthritis & Rheumatism

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“…In the absence of the alkaline phosphatase, normally highly expressed as an ectoenzyme by osteoblasts, there is little matrix mineralization and very high serum pyrophosphate accumulation occurs [Whyte et al, 1995]. The pyrophosphate is, to a major extent, produced by a nucleoside pyrophosphatase, PC-1 [Lotz et al, 1995;Hessle et al, 2002]. This gene is also expressed in other organs, where polymorphisms may be related to pathology, but mutations in the bone are not described.…”

Section: Equationmentioning

confidence: 99%

Calcium Signalling and Calcium Transport in Bone Disease

Blair

Schlesinger

Huang

et al.

Subcellular Biochemistry

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Calcium transport and calcium signalling mechanisms in bone cells have, in many cases, been discovered by study of diseases with disordered bone metabolism. Calcium matrix deposition is driven primarily by phosphate production, and disorders in bone deposition include abnormalities in membrane phosphate transport such as in chondrocalcinosis, and defects in phosphate-producing enzymes such as in hypophosphatasia. Matrix removal is driven by acidification, which dissolves the mineral. Disorders in calcium removal from bone matrix by osteoclasts cause osteopetrosis. On the other hand, although bone is central to management of extracellular calcium, bone is not a major calcium sensing organ, although calcium sensing proteins are expressed in both osteoblasts and osteoclasts. Intracellular calcium signals are involved in secondary control including cellular motility and survival, but the relationship of these findings to specific diseases is not clear. Intracellular calcium signals may regulate the balance of cell survival versus proliferation or anabolic functional response as part of signalling cascades that integrate the response to primary signals via cell stretch, estrogen, tyrosine kinase, and tumor necrosis factor receptors Keywords Hypophosphatasia; chondrocalcinosis; osteopetrosis; osteoporosis Although bone is not considered a major calcium sensing organ in humans, the cells of bone tissue control over 99% of the human body's calcium content. The principal calcium sensors that regulate bone calcium uptake and release are in the parathyroid glands. Bone function is also modified by vitamin D and by calcium transport in the kidney and intestine. These indirect mechanisms of controlling bone calcium metabolism are beyond the scope of our considerations here. In spite of processing such massive quantities of the Ca 2+ bone cells use calcium in their homeostatic control processes. The massive movement of calcium is carried out by specialized and regulated transporters. Defects in the transporters cause diseases with affect bone structure or function. Indeed, inborn errors have been very important in defining the calcium transport mechanisms in bone.Additionally, calcium is used by bone forming and bone degrading cells as a secondary mediator of hormone and cytokine action. These actions include roles in intercellular communication within groups of osteoblasts, which are connected by gap junctions [Henriksen et al., 2006]. These osteoblast groups function in a coordinated fashion in bone synthesis and maintenance, and are collectively known as the osteon. Osteoblasts in these groups are connected by gap junctions which are capable of propagating signals in the cell groups, including calcium waves [Xia and Ferrier, 1992]. Calcium is also an important regulator of

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Differential effects of aging on human chondrocyte responses to transforming growth factor-β: Increased pyrophosphate production and decreased cell proliferation

Rosen¹,

McCabe²,

Quach³

et al. 1997

Arthritis & Rheumatism

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Interleukin 1 beta suppresses transforming growth factor-induced inorganic pyrophosphate (PPi) production and expression of the PPi-generating enzyme PC-1 in human chondrocytes.

Abstract: ABSTRACT

Cited by 89 publications

References 36 publications

Extracellular nucleotide metabolism and signaling in the pathophysiology of articular cartilage

Extracellular nucleotide metabolism and signaling in the pathophysiology of articular cartilage

Calcium Signalling and Calcium Transport in Bone Disease

Differential effects of aging on human chondrocyte responses to transforming growth factor-β: Increased pyrophosphate production and decreased cell proliferation

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