Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion of microcrystals that nucleate in tubular fluid to the apical surface of renal tubular cells could be a critical step in the formation of kidney stones, 20% of which contain hydroxyapatite (HA). HA crystals bound rapidly to monolayer cultures of monkey kidney epithelial cells (BSC-1 line), used to model the surface of the nephron, in a concentration-dependent manner. Adhesion was blocked by diverse polyanions including heparin, pentosan polysulfate, polyaspartate, and polyglutamate, as well as many found in tubular fluid such as chondroitin sulfates A and B, heparan sulfate, citrate, nephrocalcin, and osteopontin. The polycations cetylpyridinium chloride and cationized ferritin, as well as the cationic dyes alcian blue, polyethylenimine, and brilliant blue R, also inhibited adhesion of HA crystals, as did specific lectins including Triticum vulgaris (wheat germ agglutinin). Anions that inhibited adhesion of crystals appeared to act on the crystal surface, whereas cations and lectins exerted their effect on the cell. Treatment of cells with neuraminidase inhibited binding of crystals, suggesting that anionic cell surface sialic acid residues function as HA crystal receptor sites that can be blocked by specific cations or lectins. Adherence of HA crystals to cells of another renal line (MDCK) and, to 3T3 fibroblasts was also inhibited by heparin, polyaspartate, alcian blue, and T vulgaris lectin, suggesting that these crystals bind to analogous molecules on the surface of different types of cells. These results suggests that the structure, quantity, and/or function of soluble anions in tubular fluid, as well as those anchored to the cell surface, could be critical determinants of HA crystal retention in the nephron and the subsequent formation of a renal stone.
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PMID:Adhesion of hydroxyapatite crystals to anionic sites on the surface of renal epithelial cells. 927 83

Tumors derived from rat C6 cell implants into rat brain exhibit similar morphological characteristics and degree of vascularization to human glioblastomas. To establish a molecular basis for C6 gliosarcoma malignancy, we have constructed a molecular profile of the most abundantly expressed genes, using serial analysis of gene expression (SAGE). Sequence tags (1168) representing 738 individual transcripts were collected and tag-to-gene mapping was carried out using the UniGene data set for rat. Differentially expressed C6 transcripts were identified by comparison of tags collected for C6 cells with a similar number (1002) of tags from a rat primary astrocyte library. Genes found to be expressed at increased levels in C6 cells are associated with cell surface interactions, migration, or metastasis formation and proliferation. These include the receptor for hyaluronan-mediated motility (RHAMM), S-100 related protein 42A, galectin I, preproenkephalin, osteopontin, autocrine motility factor, alpha-tubulin, ad1 antigen, and cofilin. In addition, a tag with no database match probably representing a previously uncharacterized transcript was differentially expressed in C6 cells. Transcripts showing reduced expression in C6 cells relative to astrocytes included the extracellular matrix glycoprotein osteonectin/SPARC (secreted protein, acidic, rich in cysteine), actin-binding proteins thymosins beta-4 and beta-10, the cysteine protease inhibitor cystatin C, the actin-gelling protein SM22/transgelin, and ferritin-H. SAGE results were confirmed by Northern blot for all transcripts tested, reaffirming the value of the SAGE technique for expression profiling in cancer biology.
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PMID:Growth and migration markers of rat C6 glioma cells identified by serial analysis of gene expression. 1100 14

About 10% of hip endoprostheses will loosen after 10 years. Prosthesis loosening is caused by two different pathomechanisms: aseptic loosening (AL) and septic loosening (SL). This study evaluated differences in gene expression in AL and SL. Eight hybridizations were performed on PIQOR cDNA arrays. Objects of the study were periprosthetic interface tissue samples from two patients with SL and three patients with AL. Tissue parts directly adjacent to the site of RNA isolation were analyzed immuno/histopathologically in order to overcome the problem of tissue heterogeneity. Thirty-three genes were found constantly differentially expressed, among which were cd11b, cd18, cd68, osteopontin and ferritin heavy-chain upregulated in AL and collagen types 1alpha-1, 3alpha-1, integrin alpha-1, thrombospondin2 and nidogen upregulated in SL. The most striking finding was the strong upregulation (from 20-fold to 323-fold) of megakaryocyte stimulating factor (msf) in all aseptic cases and one of the two septic cases, which was confirmed by real-time reverse transcription-polymerase chain reaction. In this study, msf is linked to prosthesis loosening for the first time. The upregulation in AL suggests an important pathogenetic role: the msf splice product lubricin is responsible for the lubrication of healthy joints, but its excellent lubrication ability may disturb the tight interaction between bone and prosthesis and thereby contribute to prosthesis loosening.
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PMID:Differential gene expression in the periprosthetic membrane: lubricin as a new possible pathogenetic factor in prosthesis loosening. 1278 22

About 5 to 12 % of hip endoprostheses will loosen after ten years. The periprosthetic membran between bone and prosthesis plays a crucial role in prosthesis loosening. Different pathomechanisms lead to the growth of such a membran, which can be discriminated by different histomorphologies: wear particle induced type, infectious type, combined type, indifferent type. 8 hybridizations were performed on PIQOR cDNA arrays. Objects of the study were periprosthetic interface tissue samples from 3 patients with particle induced and 2 patients with infectious prosthesis loosening. Tissue parts directly adjacent to the site of RNA-isolation were analyzed immuno-/ histopathologically in order to overcome the problem of tissue heterogeneity. 34 genes were found constantly differentially expressed, among which were cd9, cd11b, cd18, cd68, osteopontin, ferritin heavy-chain upregulated in the particle induced membrane and collagen types 1alpha-1, 3alpha-1, integrin alpha-1, thrombospondin 2 and nidogen upregulated in the infectious membrane. The most striking finding was the strong upregulation (from 20 fold to 323 fold) of megakaryocyte stimulating factor (msf) in all wear particle cases and 1 out of 2 infectious cases, which was confirmed by real-time RT-PCR. The upregulation of msf suggests an important pathogenetic role: The msf splice product lubricin is responsible for the lubrification of healthy joints, but its excellent lubrification ability may disturb the tight interaction between bone and prosthesis and thereby contribute to prosthesis loosening.
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PMID:[Differential gene expression in the wear particle induced and infectious periprosthetic membrane of loosened knee-endoprostheses]. 1688 14

Postmenopausal osteoporosis is characterized by an imbalance of bone resorption exceeding bone formation, resulting in a net loss of bone mineral density (BMD). Estrogen deficiency is known to promote bone resorption. However, the causative factors that impair bone formation have not been identified. Women after menopause experience not only estrogen deficiency but also iron accumulation as a result of cessation of menstruation. In this study we investigated whether increased iron plays a role in osteoporosis. By growing primary mouse osteoclast and osteoblast progenitor cells as well as immortalized cell lines in the presence of iron, we found that increased iron had minimal effects on osteoclast cell differentiation. Interestingly, iron, particularly in its inorganic form, and to a lesser extent ferritin and transferrin all suppressed alkaline phosphatase (ALP) activities in osteoblasts. Moreover, iron downregulated mRNA levels of several other osteoblastogenic markers such as Runx2, osterix, osteopontin, and osteocalcin. To further show that this in vitro finding is relevant to the in vivo condition, we demonstrated that iron-accumulated mice with intact ovaries exhibited a significant decrease in BMD. Although iron inhibited preosteoblast cell differentiation, it did enhance preosteoblast cell proliferation, as evidenced by increased cell growth and expression of cell cycle regulator genes such as CDK4, CDK6, cyclin D1, and cyclin D3 and G(2) /M phase cell population. Taken together, our results suggest that increased iron could be a factor that slows down bone formation in postmenopausal women.
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PMID:Inhibitory effects of iron on bone morphogenetic protein 2-induced osteoblastogenesis. 2130 72

Several biomolecules potentially serve as promoters or inhibitors of calcification in dialysis patients which include fetuin A, matrix gla protein, osteopontin, osteoprotegerin, etc. The primary aim was to compare the biomarkers of coronary artery calcification (CAC) and to study its role as predictors of CAC in hemodialysis (HD) patients. Of 126 patients undergoing chronic HD, 100 patients completed the study. Blood samples were drawn for serum creatinine, electrolytes, calcium, phosphorus, Vitamin D3, parathyroid hormone (PTH), lipid profile, high sensitivity C-reactive protein, ferritin, fetuin A, and fibroblast growth factor-23 (FGF-23). Non-contrast Computed Tomography scan of the coronary arteries was conducted on all participants. Participants who were positive for CAC (P group) were compared with those negative for CAC (N group) using two sample t-test. Multiple logistic regression analysis was conducted to determine the predictors of CAC. The prevalence of vascular calcification (VC) was 60% with higher prevalence seen in males (71%), older age group, patients with dialysis vintage >5 years (27%), and diabetic population (62%). Mean serum phosphorus was significantly higher (P <0.001) and fetuin A (P <0.001) was significantly lower in the P group. Age (OR: 1.2, P = 0.004), serum phosphorus (OR: 1.8, P = 0.024), and fetuin A (OR: 0.0006, P = 0.001) were found as predictors of CAC. CAC was more prevalent in males, patients with higher age group and in those with longer dialysis vintage and diabetic population. Participants with CAC exhibited significantly high phosphorus and low fetuin A levels. Age, phosphorus level, and fetuin A were found to be predictors of CAC in dialysis patients. FGF-23 could not predict CAC.
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PMID:Predictors of coronary calcification in Indian hemodialysis patients. 3015 18