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Tartrate-resistant acid phosphatase

About: Tartrate-resistant acid phosphatase is a research topic. Over the lifetime, 1115 publications have been published within this topic receiving 45937 citations. The topic is also known as: HPAP & SPENCDI.


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Journal ArticleDOI
TL;DR: Intermittent administration of PTHrP (1-34) exhibited an inhibitory effect on alveolar bone resorption and the gingival inflammation in periodontal tissues of diabetic rats.

8 citations

Journal ArticleDOI
TL;DR: DFCsRUNX2+/m disturbs bone remodelling activity during tooth eruption through RANK/RANKL/OPG signalling pathway and may thus be responsible for impaired permanent tooth eruption in CCD patients.
Abstract: Objectives To explore the role of dental follicle cells (DFCs) with a novel cleidocranial dysplasia (CCD) causative gene RUNX2 mutation (DFCsRUNX2+/m ) in delayed permanent tooth eruption. Materials and methods A CCD patient with typical clinical features was involved in this study. DFCsRUNX2+/m were cultured and DNA was extracted for RUNX2 mutation screening. Measurements of cell proliferation, alkaline phosphatase (ALP) activity, alizarin red staining and osteoblast-specific genes expression were performed to assess osteogenesis of DFCsRUNX2+/m . Co-culture of DFCs and peripheral blood mononuclear cells (PBMCs), followed tartrate-resistant acid phosphatase (TRAP) staining, real-time PCR and western blot were performed to evaluate osteoclast-inductive capacity of DFCsRUNX2+/m . Results A missense RUNX2 mutation (c. 557G>C) was found in DFCsRUNX2+/m from the CCD patient. Compared with normal controls, this mutation did not affect the proliferation of DFCsRUNX2+/m , but down-regulated the expression of osteogenesis-related genes, leading to a decrease in ALP activity and mineralisation. Co-culture results showed that DFCsRUNX2+/m reduced the formation of TRAP+ multinucleated cells and the expression of osteoclastogenesis-associated genes. Furthermore, the mutation reduced the ratio of RANKL/OPG in DFCsRUNX2+/m . Conclusions DFCsRUNX2+/m disturbs bone remodelling activity during tooth eruption through RANK/RANKL/OPG signalling pathway and may thus be responsible for impaired permanent tooth eruption in CCD patients.

8 citations

Journal ArticleDOI
TL;DR: TRAP is a novel human adipokine produced by macrophages and secreted from the subcutaneous adipose tissue in vivo and in vitro, suggesting that TRAP is involved in fat accumulation and adipose inflammation.
Abstract: OBJECTIVE: Tartrate-resistant acid phosphatase (TRAP) expressed by adipose tissue macrophages (ATMs) induces mice obesity and human adipocyte differentiation in vitro. This study aimed to investigate whether TRAP was secreted differently from human obese versus lean adipose tissues and to identify the cellular source of adipose tissue TRAP. DESIGN: Subcutaneous adipose tissues obtained from healthy subjects. Enzyme-linked immunosorbent assays (ELISAs) for total (5a+5b) and cleaved TRAP (5b) were used. TRAP secretion was determined in adipose tissue biopsies, and mRNA expression was studied in cell types isolated from the same. SUBJECTS: Results of 24 lean and 24 obese women (in vitro) and 8 subjects (in vivo) were compared. The main outcome measurements were TRAP expression and secretion in vitro and in vivo. RESULTS: In-house total TRAP ELISA showed high sensitivity and a coefficient of variance of 11%. Adipose secretion of total TRAP was linear in vitro with time and was evident in vivo. Total TRAP secretion in vitro was similar in lean and obese women expressed per unit weight of the adipose tissue but correlated positively with the number/size of adipocytes (P ≤ 0.01) and with adipose secretion of tumor necrosis factor-α and interleukin-6 (P<0.01). TRAP 5b was not secreted from the adipose tissue. ATMs displayed highest cellular expression of TRAP mRNA in adipose tissue cells derived from lean or obese women. CONCLUSIONS: TRAP is a novel human adipokine produced by macrophages and secreted from the subcutaneous adipose tissue in vivo and in vitro. Secretion is linked to the size and number of adipocytes, as well as to concomitant secretion of inflammatory mediators, suggesting that TRAP is involved in fat accumulation and adipose inflammation.

8 citations

Journal Article
TL;DR: Rheumatoid arthritis represents an excellent model for gaining insights into the effects of local as well as systemic consequences of inflammatory processes on skeletal tissue remodeling, and several groups have demonstrated that cells cultured from synovial tissues from RA patients or animal models of inflammatory arthritis can be induced to form osteoclasts.
Abstract: 287 The rheumatic diseases include a diverse group of disorders that share in common their propensity to affect joint and periarticular structures. Inflammatory joint diseases, of which rheumatoid arthritis is the prototype, may produce marked alterations in remodeling of the joint components leading to loss of joint function and destruction of structural integrity. Although the disease mechanisms vary, in many instances the disorders are initiated by disturbances in immune regulation that involve complex interactions between unique host genetic susceptibility and specific environmental factor(s). In these disorders, skeletal tissues may be involved not only at juxtaarticular and subchondral sites, but in addition there is evidence that many of these conditions may produce generalized effects on bone remodeling that affect the entire skeleton. Rheumatoid arthritis (RA) represents an excellent model for gaining insights into the effects of local as well as systemic consequences of inflammatory processes on skeletal tissue remodeling. Three principal forms of bone disease have been described in RA. The first is characterized by a focal process that affects the bone at the joint margins adjacent to the inflammatory synovial lesion. In RA, the synovial lining of diarthrodial joints is the target of an intense immunologic and inflammatory process that is associated with the proliferation of the synovial lining cells and infiltration of the tissue by inflammatory cells, including lymphocytes, plasma cells and activated macrophages. The proliferative synovial tissue (pannus) attaches to the immediately adjacent bone at the joint margins and induces a progressive focal osteolytic process that gives rise to the characteristic cystic bone "erosions" that can be detected radiographically 1,2 . Recent studies employing magnetic resonance imaging have shown that these erosions occur very early in the course of the disease and progress throughout the illness unless therapeutic interventions are employed 3,4 . Examination of the interface between the pannus and bone at the sites of erosions reveals the presence of resorption lacunae populated by multinucleated cells expressing the full repertoire of authentic osteoclasts, including the expression of tartrate resistant acid phosphatase, cathepsin K, and the calcitonin receptor 5-11 . Several groups have demonstrated that cells cultured from synovial tissues from RA patients or animal models of inflammatory arthritis can be induced to form osteoclasts, suggesting that the osteoclast-like cells at the bone-pannus interface are derived from precursors present within the inflamed synovial tissues 9-14 . Further evidence implicating osteoclasts in the pathogenesis of focal joint erosions is provided by two recent studies in which inflammatory arthritis was induced in animals lacking the ability to form osteoclasts. In the studies by Pettit et al. 15 receptor activator of NF-kB ligand knockout mice were employed and in the studies by Redlich et al., animals lacking the c-fos gene were utilized 16 . In both mod

8 citations

01 Jan 1999
TL;DR: Tartrate resistant acid phosphatase (TRAP) is a secreted product of osteoclasts and a lysosomal hydrolase of some tissue macrophages as discussed by the authors.
Abstract: Tartrate‐resistant acid phosphatase (TRAP) is a secreted product of osteoclasts and a lysosomal hydrolase of some tissue macrophages. To determine whether TRAP expression is rate‐limiting in bone resorption, we overexpressed TRAP in transgenic mice by introducing additional copies of the TRAP gene that contained the SV40 enhancer. In multiple independent mouse lines, the transgene gave a copy number–dependent increase in TRAP mRNA levels and TRAP activity in osteoclasts, macrophages, serum, and other sites of normal low‐level expression (notably, liver parenchymal cells, kidney mesangial cells, and pancreatic secretory acinar cells). Transgenic mice had decreased trabecular bone consistent with mild osteoporosis. Measurements of the bone formation rate suggest that the animals compensate for the increased resorption by increasing bone synthesis, which partly ameliorates the phenotype. These mice provide evidence that inclusion of an irrelevant enhancer does not necessarily override a tissue‐specific promoter.

8 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20239
202238
202126
202025
201913
201821