Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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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)

Naringenin, a phytoalexin found in grapefruits and tomatoes, has been reported to exhibit a wide range of pharmacological properties. In this study, we investigated the protective effect of naringenin on hepatic injury induced by dimethylnitrosamine (DMN) in rats. Oral administration of naringenin (20 and 50 mg/kg daily for 4 weeks) remarkably prevented the DMN-induced loss in body and liver weights and inhibited the elevation of serum alanine transaminase, aspartate transaminase, alkaline phosphatase, and bilirubin levels. Naringenin also restored serum albumin and total protein levels, and reduced the hepatic level of malondialdehyde. Furthermore, DMN-induced collagen accumulation, as estimated by histological analysis of liver tissue stained with Sirius red, was reduced in the naringenin-treated rats. A reduction in hepatic stellate cell activation, as assessed by alpha-smooth muscle actin staining, was associated with naringenin treatment. In conclusion, these results demonstrate that naringenin exhibited in vivo hepatoprotective and anti-fibrogenic effects against DMN-induced liver injury. It suggests that naringenin may be useful in preventing the development of hepatic fibrosis.
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PMID:The flavonoid naringenin inhibits dimethylnitrosamine-induced liver damage in rats. 1470 2

Cyclooxygenase (COX)-2, the recently described inducible form ofcyclooxygenase, has been shown to be responsible for the inflammatory and tumorigenic effects of prostaglandins; hence the development and expanding clinical use of COX-2 selective inhibitors termed super aspirins. These pharmacologic agents block COX-2 without abrogating the desired physiologic roles of the constitutively expressed isoform COX-1. Therefore, they are now used in place of nonselective COX inhibitors in patients who require prolonged use of nonsteroidal anti-inflammatory agents. However, there are sporadic reports of COX-2-related nephrotoxicity, and the mechanism of this adverse reaction is not known. Also, the pattern of in situ expression of COX-2 in the human kidney is not known. We therefore studied the immunohistochemical expression of COX-2 in normal kidneys obtained from 53 consecutive total nephrectomy specimens. COX-2 immunohistochemistry was performed using affinity purified polyclonal murine antibody and avidin-biotin detection method with citrate antigen retrieval. Also, to localize COX-2 expression to specific cell types, double immunolabeling was performed using avidin-biotin (for COX-2 detection) and alkaline phosphatase (for detection of alpha-smooth muscle actin or factor VIII related antigen). In the cortex, COX-2 was found to be constitutively expressed in the endothelial cells of arteries, arterioles, and glomeruli in all 53 kidneys. COX-2 expression was also found in the cortical thick ascending limb of the loop of Henle (medullary rays and macula densa) in 50 of 53 cases. In the medulla, COX-2 expression was detected in the endothelial lining of the vasa recta in 52 cases and in the collecting ducts in 5 cases. These data show significant constitutive expression of COX-2 in normal kidney and underscore the need for caution in the use of COX-2 selective inhibitors, especially on a long-term basis.
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PMID:Immunohistochemical expression of cyclooxygenase-2 in normal kidneys. 1516 23

A 72-year-old woman with von Recklinghausen's disease was referred to our hospital because of pain and muscle weakness in her thighs. She had elevated serum values of creatine kinase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and aldolase. Based on these results, a diagnosis of polymyositis was made. Treatment with prednisolone improved muscle strength, and laboratory values returned to normal. Computed tomography, magnetic resonance imaging of the abdomen, and 131I-metaiodobenzyl guanidine MIBG scintigraphy demonstrated a tumor 3 cm in diameter in the region of the left adrenal gland. Endocrinologic investigation disclosed elevation of serum and urine catecholamines. Since the blood pressure was normal, nonfunctioning pheochromocytoma was diagnosed clinically. The nonhypertensive course was attributed to reduced vascular response to noradrenaline. Serum lactate dehydrogenase. alkaline phosphatase. and asparate aminotransferase became elevated, and abdominal computed tomography showed a well-defined mass measuring 13 x 12 x 10 cm in the right lobe of the liver. The patient underwent right trisegmentectomy and left adrenalectomy. Histologically the adrenal tumor was a typical pheochromocytoma. The hepatic tumor was a leiomyosarcoma consisting of elongated spindle-shaped atypical cells arranged in intersecting bundles. Immunohistochemically, the cells of this tumor were reactive for alpha-smooth muscle actin and vimentin. The leiomyosarcoma recurred and metastasized to the liver. Eight months after onset of symptom, the patient developed hepatic coma and died. The mean age at presentation with pheochromocytoma in von Recklinghausen's disease patients age is 42 years. Our patient was considerably older. To the best of our knowledge this is the first report of a patient with von Recklinghausen's disease developing polymyositis. asymptomatic pheochromocytoma, and primary hepatic leiomyosarcoma and illustrates the need to remain aware of the possibility of cancer in von Recklinghausen's disease.
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PMID:[A patient with von Recklinghausen's disease associated with polymyositis, asymptomatic pheochromocytoma, and primary hepatic leiomyosarcoma]. 1523 55

The periodontal ligament (PDL) is a highly specialized tissue connecting the cementum with the tooth socket bone and affects the life span of the tooth. However, little is known about the precise characteristics and regenerative mechanism of PDL cells because of the absence of specific markers and cell lines. Therefore, we aimed to establish three immortalized human PDL fibroblast cell lines by using simian virus40 T-antigen (SV40T-Ag) and human telomerase reverse transcriptase (hTERT) transfection, expecting these cells to have the characteristics of primary cells. The transfected cells were named STPLF. The expression of SV40T-Ag and hTERT in all STPLF lines was verified by using the semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) method, stretch PCR analysis, or Western blotting analysis. All STPLF showed stable proliferation at more than 120 population doublings (PD), whereas primary human PDL fibroblasts (HPLF) stopped at 10-20 PD. Characterization by RT-PCR analysis revealed that all STPLF genes mimicked the expression of their respective original HPLF genes. STPLF expressed runt-related transcription factor-2, osterix, alkaline phosphatase, osteopontin, osteocalcin, periostin, receptor activator of NF-kappa B ligand, osteoprotegerin, epidermal growth factor receptor, alpha-smooth muscle actin, and type XII collagen. STPLF stimulated with 50 micro g/ml ascorbic acid and 2 mM beta-glycerophosphate for 4 weeks produced more calcified deposits than did HPLF cultured with the same reagents. These results suggest that each STPLF line retained the characteristics of the respective original HPLF, that STPLF gained increased calcification activity, and that STPLF are helpful tools for studying the biology and regenerative mechanisms of human PDL.
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PMID:Establishing and characterizing human periodontal ligament fibroblasts immortalized by SV40T-antigen and hTERT gene transfer. 1640

In vitro approaches have extensively been developed to study reparative dentinogenesis. While dental pulp is a source of unidentified progenitors able to differentiate into odontoblast-like cells, we investigated the effect of two media; MEM (1.8 mM Ca and 1 mM Pi) and RPMI 1640 (0.8 mM Ca and 5 mM Pi) on the behaviour of human dental pulp cells. Our data indicate that MEM significantly increased cell proliferation and markedly enhanced the proportion of alpha-smooth muscle actin positive cells, which represent a putative source of progenitors able to give rise to odontoblast-like cells. In addition, MEM strongly stimulated alkaline phosphatase activity and was found to induce expression of transcripts encoding dentin sialophosphoprotein, an odontoblastic marker, without affecting that of parathyroid hormone/parathyroid hormone related protein-receptor and osteonectin. In conclusion, these observations demonstrate that not only proliferation but also differentiation into odontoblast-like cells was induced by rich calcium and poor phosphate medium (MEM) as compared to RPMI 1640. This study provides important data for the determination of the optimal culture conditions allowing odontoblast-like differentiation in human pulp cell culture.
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PMID:Culture medium modulates the behaviour of human dental pulp-derived cells: technical note. 1648 35

Follicular dendritic cells (FDC) are involved in the presentation of native Ags to B cells during the secondary immune response. Some authors consider FDC to be hemopoietic cells, whereas others believe them to be mesenchymal cells. The low proportion of FDC in the lymphoid follicle, together with technical difficulties in their isolation, make these cells difficult to study. We show that Fibroblast Medium can be used successfully to isolate and maintain FDC lines. In this culture medium, we obtained 18 FDC lines from human tonsils, which proliferated for as long as 18 wk and showed a stable Ag phenotype as detected by flow cytometry and RT-PCR. FDC lines were CD45-negative and expressed Ags associated to FDC (CD21, CD23, CD35, CD40, CD73, BAFF, ICAM-1, and VCAM-1) and Ags specific for FDC (DRC-1, CNA.42, and HJ2). These cell lines were also able to bind B cells and secrete CXCL13, functional activities characteristic of FDC. Nevertheless, the additional expression of STRO-1, together with CD10, CD13, CD29, CD34, CD63, CD73, CD90, ICAM-1, VCAM-1, HLA-DR, alkaline phosphatase, and alpha-smooth muscle actin (alpha-SM actin) indicated that FDC are closely related to bone marrow stromal cell progenitors. The expression of alpha-SM actin also relates FDC with myofibroblasts. Like myofibroblasts, FDC lines expressed stress fibers containing alpha-SM actin and were able to contract collagen gels under the effect of TGFbeta1 and platelet-derived growth factor. These findings suggest that FDC are a specialized form of myofibroblast and derive from bone marrow stromal cell progenitors.
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PMID:Follicular dendritic cells are related to bone marrow stromal cell progenitors and to myofibroblasts. 1678 23

Histological modulations in tumor cells treated with anti-cancer drugs have been reported. The histogenesis of malignant fibrous histiocytoma (MFH) remains elusive. To investigate cellular characteristics and alterations, therefore, we derived cisplatin-resistant MFH cell lines (MT-PR and MT-10R) from MT-P and MT-10, respectively, and compared them with MT-10, a non-cisplatin-resistant MFH line (MT-10 was isolated as a clone cell line from MT-P, and MT-P was originally established from a rat spontaneous MFH). Immunohistochemically, MT-10 reacted to vimentin, alpha-smooth muscle actin (a marker of myofibroblasts), ED1/ED2 (rat macrophage/histiocyte-specific antibodies), and A3 (rat MFH-specific antibody) in varying degrees, indicating that MFH cells have features of both fibroblasts and histiocytes. However, MT-10R and MT-PR reduced ED1-positive cell numbers. MT-10 developed tumors of a storiform pattern, while MT-10R and MT-PR tumors comprise round or polygonal cells arranged in a compact sheet. Additionally, MT-PR tumors included ossifying areas. MT-10R and MT-PR, and their tumors showed a reaction to alkaline phosphatase (ALP), a marker of osteoblasts. RT-PCR revealed that mRNAs of bone morphogenetic protein (BMP)-2, BMP-6 and osteopontin were significantly increased in MT-10R and MT-PR tumors. Neoplastic cells in these tumors were immunoreactive to BMP-2 and BMP-6, while MT-10 tumors were not. Cisplatin-resistant MFH cells had potential to differentiate into osteogenic tissues by producing osteogenic factors, suggesting that MFH histology may be altered under anti-cancer drug treatments. Recently, cancer differentiation-based therapy, that could be induced by anti-cancer drugs, has been implied. MT-10R and MT-PR become useful experimental systems for studies on cellular differentiation provoked by anti-cancer drugs.
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PMID:Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines. 1726 96

Our objective was to establish the role of fibroblasts in medial vascular calcification, a pathological process known to be associated with elastin degradation and remodeling. Rat dermal fibroblasts were treated in vitro with elastin degradation products and transforming growth factor (TGF)-beta1, factors usually present in deteriorated matrix environments. Cellular changes were monitored at the gene and protein level by reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay, immunofluorescence, and von Kossa staining for calcium deposits. By 21 days, multicellular calcified nodules were formed in the presence of elastin degradation products and TGF-beta1 separately and to a significantly greater extent when used together. Before mineralization, cells expressed alpha-smooth muscle actin and large amounts of collagen type I and matrix metalloproteinase-2, characteristic features of myofibroblasts, key elements in tissue remodeling and repair. Stimulated cells expressed increased levels of core-binding factor alpha1, osteocalcin, alkaline phosphatase, and osteoprotegerin, representative bone-regulating proteins. For most proteins analyzed, TGF-beta1 synergistically amplified responses of fibroblasts to elastin degradation products. In conclusion, elastin degradation products and TGF-beta1 promote myofibroblastic and osteogenic differentiation in fibroblasts. These results support the idea that elastin-related calcification involves dynamic remodeling events and suggest the possibility of a defective tissue repair process.
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PMID:Osteogenic responses in fibroblasts activated by elastin degradation products and transforming growth factor-beta1: role of myofibroblasts in vascular calcification. 1759 59

When rat bone marrow stromal (BMS) cells were seeded on aligned type I collagen scaffolds and cultured in osteogenic media, they underwent simultaneous maturation and differentiation into osteogenic and vascular cell lineages. In addition, these cells produced mineralized matricellular deposits. BMS cells were seeded in Petri dish or the collagen scaffold, cultured in osteogenic media for 3, 6, and 9 d and subsequently processed for immunohistochemical and cytochemical analysis. Immunolocalization of lineage-specific proteins were visualized using confocal microscopy and mRNA transcript analysis was performed by real-time quantitative polymerase chain reaction (RT-qPCR). The alkaline phosphatase activity and calcium content significantly increased over the observed period of time in an osteogenic medium. Sheets of abundant Pecam (CD31), Flk-1 (VEGFR-2), tomato lectin (TL/LEL), and alpha-smooth muscle actin (alpha-SMA) positive cells were observed in the collagen scaffolds. Nascent capillary-like vessels were also seen amidst the osteoblasts in osteogenic culture, augmenting the maturation and differentiation of BMS cells into osteoblasts. In our in vitro study, concurrent differentiation of BMS cells, a heterogeneous cell population with multilineage differentiation potential, to osteogenic and vascular lineages demonstrated that the substrates (three-dimensional (3-D), collagen type I, aligned fibrils) had a profound effect on guiding the differentiation pathway of BMS cells.
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PMID:Concurrent differentiation of marrow stromal cells to osteogenic and vasculogenic lineages. 1794 Nov 11

Silymarin, a standardized extract of the milk thistle (Silybum marianum), has a long tradition as a herbal remedy, and was introduced as a hepatoprotective agent a few years ago. However, the therapeutic effects of silymarin remain undefined. Carbon tetrachloride (CCl4) is a xenobiotic used extensively to induce oxidative stress and is one of the most widely used hepatic toxins for experimental induction of liver fibrosis in the laboratory. In this study, we investigated the restoration of the CCl4-induced hepatic fibrosis by high dose of silymarin in rats. After treatment with oil (as normal group; n = 6) or CCl4 [as model (n = 7) and therapeutic (n = 7) groups] by intragastric delivery for 8 weeks for the induction of liver fibrosis, the rats in the normal and model group were administered orally normal saline four times a week for 3 weeks whilst the therapeutic group received silymarin (200 mg/kg). The histopathological changes were observed with Masson staining. The results showed that the restoration of the CCl4-induced damage of liver fibrosis in the therapeutic group was significantly increased as compared to that in the model group. Moreover, silymarin significantly decreased the elevation of aspartate aminotransferase (AST), alanine aminotransferase, and alkaline phosphatase in serum, and also reversed the altered expressions of alpha-smooth muscle actin in liver tissue. Therefore, these findings indicated that silymarin may have the potential to increase the resolution of the CCl4-induced liver fibrosis in rats.
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PMID:Effects of silymarin on the resolution of liver fibrosis induced by carbon tetrachloride in rats. 1839 25


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