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:1.2.1.13 (glyceraldehyde-3-phosphate dehydrogenase)
6,511 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the temporal and spatial patterns of expression of mRNA encoding uterine extracellular matrix (ECM) proteins were determined during the peri-implantation period. Northern blot hybridization of cDNAs corresponding to laminin (LM) B1, LM B2, entactin, fibronectin, collagen (CL) type IV alpha 1, and CL IV alpha 2 was performed on RNA extracted from either whole mouse uteri or endometrial explants between Day 4, i.e., the day of implantation, and Day 7 of pregnancy, when the decidual response is well established. These analyses revealed a dramatic increase in LM B2, CL IV alpha 1, and CL IV alpha 2 mRNA expression by Day 7 of pregnancy. Relative levels of the mRNA encoding other ECM components, including LM B1, were not altered when compared to changes in the relative level of expression of glyceraldehyde-3-phosphate dehydrogenase mRNA. The differential expression of the B chains of LM appeared to be limited to the stromal cells of the endometrium. In situ hybridization of uterine sections with cRNA probes corresponding to LM B1, LM B2, and CL IV alpha 1 demonstrated that LM B1 was expressed temporally in high amounts in the primary decidual zones (PDZ) and persisted throughout PDZ degeneration. LM B2 mRNA was expressed in both primary and secondary decidual zones and persisted through Day 8 of pregnancy. CL IV alpha 1 mRNA expression mimicked that of LM B2. Oviduct ligation on Day 2 of pregnancy was used to prevent embryo transport to one uterine horn, whereas decidualization and embryo implantation were permitted in the contralateral horn. This experiment demonstrated that the increases in uterine ECM mRNA expression were not due solely to the changing hormonal milieu of the uterus. ECM components, including CL IV, have been shown to bind growth factors such as transforming growth factor-beta (TGF-beta) in an insoluble but biologically active form. The remarkable similarity between the pattern of CL IV and LM B2 expression and previously reported TGF-beta deposition (Tamada et al., Mol Endocrinol 1990; 4:965-972) prompted examination of the effects of this growth factor on blastocyst development in vitro. TGF-beta 1 was tested for its ability to alter embryo outgrowth on LM-coated tissue culture surfaces; however, significant differences in the rate or extent of outgrowth in the presence of TGF-beta were not detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential temporal and spatial expression of mRNA encoding extracellular matrix components in decidua during the peri-implantation period. 139 7

Total cellular RNA was extracted from bone cells of three different femoral compartments of 2-mo-old rats. The intact femora were first incubated with collagenase to obtain periosteal cells. The bisected periosteum-free diaphyses and metaphyses were then incubated with collagenase to obtain enriched populations of endosteal and cancellous bone cells, respectively. The total cellular RNA from these three tissues was separated by size using agarose gel electrophoresis, transferred to nylon filters, hybridized to 32P-labeled cDNA probes for glyceraldehyde-3-phosphate dehydrogenase (GAP), pre-pro-alpha (I) type I collagen (collagen), osteocalcin (BGP), and alkaline phosphatase (AP), and the cDNA/mRNA hybrids were visualized by radioautography. Bone matrix deposition was measured in each tissue compartment by tetracycline-based dynamic bone histomorphometry. The bone formation and apposition rates were greatest in the periosteum and least in metaphysis. Mean mRNA levels for collagen and BGP were positively correlated with mean bone formation and mineral apposition rates. Interestingly, mean AP mRNA levels were not correlated with indexes of bone formation. These results demonstrate that the steady-state mRNA levels for bone matrix proteins in femora show pronounced site specificity and correlate with the rates of bone matrix deposition.
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PMID:Tissue-specific expression of bone proteins in femora of growing rats. 141 91

Glucocorticoids modulate various cellular functions such as proliferation, energy metabolism and the synthesis of proteins. In the present study, the response of collagen genes to dexamethasone in different stages of chick embryo development was studied in tendon and heart using Northern blot analysis and specific cDNA probes. The changes in collagen gene expression were compared to alterations in two reference mRNAs: actin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The levels of specific mRNAs measured per ribosomal RNA in tendon and heart varied markedly during normal development. In tendon the relative levels of alpha 1(I), alpha 2(I) and alpha 1(III) collagen mRNAs were highest between days 14-16 when also the synthesis of matrix proteins is most active. In heart the levels of these mRNAs peaked at day 12. In addition, qualitative differences were observed in the expression of actin genes between tendon and heart. Dexamethasone in high dose decreased collagen mRNA levels in tendons, while in heart a stimulatory effect was noted. Dexamethasone also decreased GAPDH mRNA levels in tendons. The alterations in gene expression after dexamethasone treatment in tendon and heart did not correlate with the level of specific glucocorticoid receptors, which varied markedly during the development of chick embryos. The cDNA for pro alpha 1(I) collagen hybridized to two transcripts corresponding to 6.2 and 5.1 kb in tendon and heart. During normal development of chick embryos the ratio of 6.2/5.1 kb mRNAs decreased markedly in heart, but no such change was observed in tendons. Dexamethasone, however, decreased the ratio of 6.2/5.1 kb transcripts in tendons. There was a significant correlation between the ratio 6.2/5.1 kb transcripts and total alpha 1(I) mRNA both in tendon and heart, suggesting that the 6.2 kb transcript may be associated with the rate of synthesis of type I collagen.
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PMID:Comparison on collagen gene expression in the developing chick embryo tendon and heart. Tissue and development time-dependent action of dexamethasone. 202 46

The effects of glucocorticoids and retinoids on connective tissue biosynthesis were studied in cultured human skin fibroblasts (HSFs). More specifically attention was paid to the effects of dexamethasone and 13-cis-retinoic acid (RA) on total protein and collagen synthesis and on collagen and fibronectin mRNA levels. The results indicated that dexamethasone reduced the relative collagen synthesis and collagen mRNA levels in HSFs and increased the total incorporation of proline into proteins, the latter effect being due to increased activity in the intracellular proline pool. 13-cis-RA did not affect collagen synthesis at the concentration studied (10(-7) M) but it did reduce the corresponding mRNA levels. Simultaneous addition of both dexamethasone and 13-cis-RA or etretinate resulted in the largest decrease in type I and type III procollagen mRNA levels, indicating that retinoids do not oppose the effect of glucocorticoids on collagen synthesis in cultured HSFs. For comparison the effects of dexamethasone and 13-cis-RA on the mRNA levels of another extracellular matrix component, fibronectin, and of a constitutive enzyme, glyceraldehyde-3-phosphate dehydrogenase, were also studied. The results indicated, that dexamethasone treatment did not alter fibronectin mRNA levels in HSFs, while 13-cis-RA did so to a marked extent. Both dexamethasone and 13-cis-RA also reduced the mRNA level of glyceraldehyde-3-phosphate dehydrogenase, indicating that glucocorticoids and retinoids have both similar and different effects on gene expression in HSF.
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PMID:Comparison of the effects of dexamethasone and 13-cis-retinoic acid on connective tissue biosynthesis in human skin fibroblasts. 247 83

Platelet-derived growth factor (PDGF)-BB stimulates fibroblast-mediated contraction of collagen gels, as well as migration of fibroblasts through collagen-coated membranes. In the present study we examined effects of PDGF-BB stimulation on the synthesis of collagen-binding beta 1 integrins by human diploid fibroblasts (AG 1518). PDGF-BB stimulation led to an increase in the rare of integrin alpha 2-subunit synthesis. In contrast, synthesis of the integrin alpha 1- or alpha 3-subunits were not affected by PDGF-BB stimulation. Furthermore, levels of alpha 2-subunit mRNA relative to levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA increased after PDGF-BB stimulation. The latter finding is compatible with PDGF-BB stimulating transcription of the alpha 2-subunit gene. PDGF-BB stimulation did not influence the relation between levels of integrin beta 1-subunit mRNA and GAPDH mRNA. In addition, the rate of synthesis or post-translational processing of the integrin beta 1-subunit were not, or only marginally, affected by PDGF-BB stimulation. It is likely that the motility response elicited in fibroblasts by PDGF-BB involves such alterations in the synthesis of the alpha 2-subunit of the alpha 2 beta 1 collagen-binding integrin.
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PMID:Platelet-derived growth factor-BB stimulates synthesis of the integrin alpha 2-subunit in human diploid fibroblasts. 752 96

Fibrosis, characterized by the accumulation of collagen, is a late result of thoracic irradiation. The purpose of this study was to determine if extracellular matrix protein and transforming growth factor beta mRNA expression are altered late in the course of pulmonary fibrosis after irradiation, and then to determine if these changes differ between two strains of mice which vary in their sensitivity to radiation. Radiation-sensitive (C57BL/6) and radiation-resistant (C3H/HeJ) mice were irradiated with a single dose of 5 or 12.5 Gy to the thorax. Total lung RNA was prepared and immobilized by Northern and slot blotting and hybridized with radiolabeled cDNA probes for collagens I, III and IV, fibronectin, and transforming growth factor beta 1 and beta 3. Autoradiographic data were quantified by video densitometry and results normalized to a control probe encoding for glyceraldehyde-3-phosphate dehydrogenase. Alterations in mRNA abundance were observed in the sensitive mice at all times, while levels in the resistant mice were unaffected until 26 weeks after irradiation. The relationship between extracellular matrix protein per se and increased mRNA abundance suggests that late matrix protein accumulation may be a function of gene expression. Differences in levels of transforming growth factor beta mRNA may lead to strain-dependent variation in fibrotic response and may also contribute to the radiation-induced component of pulmonary fibrosis.
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PMID:Differences in correlation of mRNA gene expression in mice sensitive and resistant to radiation-induced pulmonary fibrosis. 772 35

We have previously found that the restoration of cartilage matrical proteoglycans is preceded by markedly increased activity of uridine diphosphoglucose dehydrogenase (UDPGD), an enzyme directly associated with glycosaminoglycan (GAG) synthesis, and by increased activity of enzymes of the major energy yielding pathways (glucose-6-phosphate dehydrogenase (G6PD), glyceraldehyde-3-phosphate dehydrogenase (GAPD) and succinate dehydrogenase (SDH)). We did not find an increase in lactate dehydrogenase (LDH). In the present longitudinal study of rabbits (from 5 weeks to 42 months of age), we looked for age related changes in the activity of these enzymes in auricular chondrocytes, as well as for collagen and GAG content. Collagen content (micrograms/wet weight) increased up to 12 months and remained stable; total GAG content (micrograms/wet weight) reached its maximal value at growth and then declined gradually, reducing the GAG/collagen ratio dramatically from 36 to 8. At any age LDH was two to three times more active than either G6PD, aldolase, or GAPD. SDH and UDPGD activities were even lower. The age related changes varied: (1) LDH and GAPD were stable and did not change with either growing or aging; (2) G6PD and aldolase reached their maximal activity at 3-9 months, followed by a sharp drop at 12 months. G6PD remained stable, while aldolase continued to decline, although more slowly; (3) Maximal activity of SDH and UDPGD was measured at 5 weeks. Thus, the changes in enzyme activity in chondrocytes with age were specific for each enzyme. The significant decline in G6PD, aldolase, the rate-limiting enzymes of the pentose shunt and classic glycolysis, and SDH markedly reduced the ability of chondrocytes to generate energy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential decline of rabbit chondrocytic dehydrogenases with age. 778 68

The effect of low M(r) heparin fragments (CY222) and fetal calf serum (FCS) on the level of fibronectin and fibrillar collagen mRNAs was investigated in smooth muscle cells (SMC) in culture. In the absence of FCS, addition of CY222 (100 micrograms/10(6) cells) to postconfluent early passage SMC resulted in a decrease in mRNA level of type III collagen. In contrast, mRNA levels coding for type I collagen, fibronectin and GAPDH (used as control of cellular activity) were not modified. Addition of 5% FCS (without CY222) to the culture medium did not affect mRNA levels of type I and type III collagens nor that of GAPDH. The level of fibronectin mRNA, however, increased in the presence of 5% FCS. In the presence of both 5% FCS and CY222, we observed a decrease in type III collagen mRNA and fibronectin mRNA levels (this level remained, however, above the control value without FCS and the level with CY222 alone). Our results demonstrate that low M(r) heparin fragments can modulate the steady-state levels of type III collagen and fibronectin mRNAs.
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PMID:Expression of fibronectin and interstitial collagen genes in smooth muscle cells: modulation by low molecular weight heparin fragments and serum. 788 80

Fibrosis, characterized by the accumulation of collagen, is a consequence of a chronic inflammatory response. The purpose of this study was to determine if tumor necrosis factor alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA expression are altered acutely after irradiation, during the so-called "latent" phase of pulmonary injury, and to examine if these alterations persist through the development of pneumonitis and fibrosis. Further, we wished to determine if these changes differ between two strains of mice which vary in their sensitivity to radiation. Fibrosis-sensitive (C57BL/6) and fibrosis-resistant (C3H/HeJ) mice were irradiated with a single dose of 5 or 12.5 Gy to the thorax. Total lung RNA was prepared and immobilized by slot blotting and hybridized with radiolabeled cDNA probes encoding for TNF-alpha, IL-1 alpha and IL-1 beta. Autoradiographic data were quantified by video densitometry and results normalized to a control probe encoding for glyceraldehyde-3-phosphate dehydrogenase. It was found that TNF-alpha mRNA levels were increased in C57BL/6 mice at days 1 and 7 postirradiation after 5 Gy and day 14 postirradiation after both 5 and 12.5 Gy, and IL-1 alpha mRNA levels were increased in C57BL/6 mice at days 56, 112 and 182 postirradiation after both 5 and 12.5 Gy, and IL-1 beta mRNA levels in the C3H/HeJ mice were increased at days 56 and 182 postirradiation after 12.5 Gy. In summary, these studies demonstrated early and persistent alterations in TNF-alpha, IL-1 alpha and IL-1 beta mRNA levels even at the lower dose (5 Gy). The temporal relationship between the elevation of these cytokines and the strain-dependent variation in fibrosis response suggests that IL-1 alpha and TNF-alpha contribute to the radiation-induced component of pulmonary fibrosis, whereas IL-1 beta may have a protective function.
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PMID:Early and persistent alterations in the expression of interleukin-1 alpha, interleukin-1 beta and tumor necrosis factor alpha mRNA levels in fibrosis-resistant and sensitive mice after thoracic irradiation. 864 37

X-Linked Alport syndrome is caused by mutations in the COL4A5 gene encoding the Type IV collagen alpha 5 chain (alpha 5(IV)). The authors' recent immunohistochemical study demonstrated abnormal expression of alpha 3(IV) and alpha 4(IV), as well as of alpha 5(IV), in patients with this syndrome, and a correlation between abnormal alpha 3(IV) and alpha 4(IV) expression and severity of the disease. The mechanism linking alpha 5(IV) mutations with abnormal alpha 3(IV) and alpha 4(IV) expression is unknown. To examine alpha 3(IV) and alpha 4(IV) mRNA expression in renal cortical tissues of patients with X-linked Alport syndrome, a nonradioisotopic, semiquantitative reverse transcription-polymerase chain reaction assay (alpha 3(IV) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), alpha 4(IV), and GAPDH coamplification) was performed. There were no significant differences among severely affected male (N = 3), mildly affected male (N = 2), and female (N = 1) X-linked Alport patients and control subjects (N = 2) with respect to alpha 3(IV) and alpha 4(IV) mRNA expression in renal cortical tissue. These findings indicate that alpha 3(IV) and alpha 4(IV) transcription is not turned off in X-linked Alport syndrome and suggest that abnormal expression of alpha 3(IV) and alpha 4(IV) proteins in this syndrome may be the result of failure of incorporation of alpha 3(IV) and alpha 4(IV) into the glomerular basement membrane.
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PMID:Expression of type IV collagen alpha 3 and alpha 4 chain mRNA in X-linked Alport syndrome. 879 4


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