Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of trophic factor receptors stimulates tyrosine phosphorylation on proteins and supports neuronal survival. We report that in the recovery phase following reversible cerebral ischemia, tyrosine phosphorylation increases in the membrane fraction of the resistant hippocampal CA3/dentate gyrus (DG) region, whereas in the sensitive CA1 region or striatum, tyrosine phosphorylation is less marked or decreases. In the cytosolic fractions, a 42-kDa protein, identified as mitogen-activated protein (MAP) kinase, is markedly phosphorylated and activated immediately following ischemia, in particular in CA3/DG, but not in striatum. In the CA1 region, phosphorylation of MAP kinase is less intense and decreases later during reperfusion, which could explain the delay of neuronal degeneration in this structure. The data suggest that in ischemia-resistant neurons the growth factor receptor-coupled signaling cascade is stimulated and, through its effects on DNA transcription and mRNA translation, supports neuronal survival.
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PMID:Tyrosine phosphorylation and activation of mitogen-activated protein kinase in the rat brain following transient cerebral ischemia. 751 Jul 79

It has been suggested that the portal vein should be occluded during intermittent hepatic dearterialization in order to induce a more complete ischemia of the tumor. In this experiment the influence of portal branch ligation in combination with repeat dearterializations on a liver tumor was investigated. Twenty-seven rats were randomly allocated to sham treatment (n = 6); portal branch ligation (PBL) (n = 7); 120 min of repeat dearterialization (n = 7); and portal branch ligation (PBL) in combination with 50 min of repeat dearterialization (n = 7) (once a day during 5 days). The results showed that portal branch ligation alone did not alter the tumor growth compared with sham treatment (P > 0.05), nor did portal branch ligation in combination with repeat dearterializations for 50 min (P > 0.05). However, tumor growth delay was achieved following 120 min of repeat dearterializations without occlusion of the portal branch (P < 0.01 versus all the other groups). There was a significant weight loss of the lobe undergoing PBL, whether dearterialization was added or not (P < 0.001). The liver nucleotide/DNA and RNA/DNA ratio significantly decreased as well. Histological examination showed that > 50% of tumor cells became necrotic after repeat dearterializations for 2 hr indicating a significant damage to tumor tissue. In contrast, PBL in combination with repeat dearterializations for 50 min induced extensive liver necrosis without having any influence on tumor growth.
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PMID:Influence of portal branch ligation on the outcome of repeat dearterializations of an experimental liver tumor in the rat. 751 73

Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.
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PMID:[An evaluation of the plastic function of the cardiomyocytes by silver staining of the nucleoli in patients operated on for ischemic heart disease]. 752 67

The amounts of mRNAs for 72 kDa (HSP72) and 73 kDa (HSC73) heat shock proteins were measured semiquantitatively with competitive polymerase chain reaction (PCR) techniques after reverse transcription (RT) using a heterologous DNA fragment (PCR mimic) as an internal standard. The changes of signal intensities of PCR products were well correlated with the amount of mRNA in rat brain measured as optical densities of Northern blot. Thus, an analysis with mimic RT-PCR technique provides a rapid, semiquantitative, and safe method to detect changes of HSP72 and HSC73 mRNAs after brain ischemia.
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PMID:Rapid and semiquantitative analysis of HSP72 and HSC73 heat shock mRNAs by mimic RT-PCR. 755 61

Renal tubular cells do not proliferate under normal intact conditions, whereas a marked regeneration is evident when tubular cells are injured by renal toxins or by ischemia. In case of compensatory renal growth too, hyperplasia of renal proximal tubular cells is observed. Various growth factors, including epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) seem to be involved in renal regeneration, however, the physiological role of these growth factors for the natural course of the renal regeneration have yet to be established. Hepatocyte growth factor (HGF), a potent mitogen for cultured renal tubular cells, may function as a renotropic factor, which enhances regeneration of the kidney. Once renal tubular cells are damaged by some agents, HGF mRNA, HGF activity and DNA synthesis of renal tubular cells are sequentially increased. Since both HGF mRMA and HGF protein are localized in renal interstitial cells, HGF seems to act on the tubular cells as a paracrine mediator. In addition to these results, HGF has multiple biological functions. This suggests that HGF possesses biological activities essential for renal regeneration.
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PMID:[Hypertrophy and hyperplasia of renal tubular interstitial cells--regulatory factors]. 756 25

Involvement of the IEGs in brain injury and ischemia is under intensive investigation (Gubits et al., 1993). There are several families of the IEGs. They include the fos, jun, and zinc finger genes that encode transcription factors. Products of the fos family (c-fos, fra-1, fra-2, and fos B) bind to members of the jun family (c-jun, jun B, jun D) via leucine zippers, and this dimer then binds to the AP-1 site (consensus sequence -TGACTCA-) in the promoter of target genes, which in turn regulate the expression of late response genes that produce long-term changes in cells. For example, c-fos may regulate the long-term expression of preproenkephalin, nerve growth factor, dynorphin, vasoactive intestinal polypeptide, tyrosine hydroxylase and other genes with AP-1 sites in their promoters (Curran and Morgan, 1987; Sheng and Greenberg, 1990). It is likely that the c-fos gene up-regulation observed in ischemic astrocytes leads to the changes observed in the expressions of hsp and cytoskeleton protein genes in this experimental model. This is supported by the findings of Sarid (1991) and Pennypacker et al. (1994) who have shown that AP-1 DNA binding activity in hippocampus recognized an AP-1 sequence from the promoter region of the GFAP which is a potential target gene. van de Klundert et al. (1992) also suggested the involvement of AP-1 in transcriptional regulation of vimentin. IEGs can be induced within minutes by extracellular stimuli including transmitters, peptides, and growth factors. In this study, we have shown that c-fos induction by ischemia was rapid and transient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gene expression in astrocytes during and after ischemia. 756 84

The mechanisms behind tumour regression during ischaemic therapy of liver malignancy are not thoroughly elucidated. Ischaemia-reperfusion injury and release of free radicals is one mechanism suggested. The aim of the present study was to explore whether inhibition of hydroxyl radicals, by complex binding Fe with desferrioxamine (DFO), counteracted the retardation in tumour growth rate after HAL and whether DFO in itself had an effect on tumour growth in 2 experimental rat liver tumours. Rats with a hepatoma or an adenocarcinoma were subjected to HAL or to a sham procedure with or without additional injections of DFO daily for 2 or 7 days. HAL had an inhibitory effect on tumour growth rate. The effect of HAL was not counteracted by DFO, while DFO alone caused a decrease in tumour volume. There was an additive effect of DFO and HAL on tumour growth rate in both tumour systems. In vitro there was a growth inhibitory effect of DFO in both tumours, more pronounced in the hepatoma than in the adenocarcinoma. Our findings indicate that the effect of HAL is not mediated by release of oxygen free radicals. In the adenocarcinoma system, an additive effect of DFO and HAL was seen. As a rate-limiting enzyme for DNA synthesis is dependent on iron, depletion of iron can decrease mitotic activity, a mechanism that could explain the effect of DFO on tumour growth.
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PMID:Influence of hepatic artery occlusion and desferrioxamine on liver-tumour growth. 759 Dec 71

To clarify the pathogenesis and molecular basis of ischemia-related nerve cell death, we examined the occurrence of DNA fragmentation as a hallmark of apoptotic cell death following incomplete ischemia in the rat brain by means of in situ end labeling of fragmented DNA. Incomplete ischemia was produced by permanently occluding one carotid artery, while temporarily occluding the other. The condensed nuclei of ischemic neurons in the neocortex, and in the subiculum and CA1 area of the hippocampus were positively stained 24 h and 3 days following vessel occlusion, respectively, and their morphology was typically apoptotic. The ischemic neurons with condensed nuclei gradually increased in number and were clearly stained for fragmented DNA in these areas. The labeled nuclei in the neocortex became pyknotic 72 h later, and in the hippocampus 7 days later incomplete ischemia. After attaining a peak, the number of labeled nuclei decreased with the duration of recovery in all areas. These results suggest that an apoptotic process plays, at least primarily, a role in the degeneration of neurons associated with incomplete forebrain ischemia in rat.
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PMID:Detection of DNA damage induced by apoptosis in the rat brain following incomplete ischemia. 760 99

To investigate how cardiac myocytes recover from a brief period of ischemia, we used a metabolic inhibition (MI) model, one of the in vitro ischemic models, of chick embryo ventricular myocytes, and examined the induction of immediate-early (IE) genes mRNAs and the activity of mitogen-activated protein (MAP) kinase. We performed Northern blot analysis to study the expression of c-jun, c-fos, and c-myc mRNAs during MI using 1 mM NaCN and 20 mM 2-deoxy-d-glucose, and also during the recovery from MI of 30 min. The c-fos mRNA was induced transiently at 30 and 60 min during the recovery. The expression of c-jun mRNA was significantly augmented at 30, 60, 90, and 120 min during the recovery (3.0-, 4.7-, 2.4-, and 1.9-fold induction, respectively) and so did the expression of c-myc mRNA (1.4-, 1.7-, 1.8-, and 2.0-fold induction, respectively). In contrast, the levels of these mRNAs remained unchanged during MI. The electrophoretic mobility shift assay revealed that AP-1 DNA binding activity markedly increased at 120 min during the recovery. When the cells were pretreated with protein kinase C (PKC) inhibitors, 100 microM H-7 or 1 microM staurosporine, the induction of c-jun mRNA at 60 min during the recovery was markedly suppressed (95 or 82% reduction, respectively). The c-jun induction was partially inhibited when the cells were treated with 2 mM EGTA during MI and the recovery (42% reduction). MAP kinase activity quantified with in-gel kinase assay was unchanged during MI, but significantly increased at 5, 10, and 15 min during the recovery (3.0-, 4.1-, and 3.4-fold increase, respectively). S6 kinase activity was also augmented significantly at 15 min during the recovery. Thus, these data suggest that IE genes as well as MAP kinase may play roles in the recovery process of cardiac myocytes from MI, and that the augmentation of c-jun expression needs the activation of PKC and to some extent, [Ca2+]i.
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PMID:Immediate-early gene induction and MAP kinase activation during recovery from metabolic inhibition in cultured cardiac myocytes. 761 38

Transient focal ischemia-reperfusion in the cerebral cortex caused regional alteration of DNA-binding activities of transcription factors AP-1, CREB, Sp-1, and NF-kB. The changes were time-dependent. During the first 24 hr of reperfusion after 90 min ischemia, there was an increase in the binding activity of AP-1 only in the region surrounding the ischemic cortex. Five days after ischemia, an increase in the binding activities of CREB, Sp-1, and NF-kB, but not AP-1, was noted in the ischemic cortex, and to a lesser extent, Sp-1 and NF-kB, in the surrounding region. The binding activities of these transcription factors were reduced by hydrogen peroxide but could be restored by dithiothreitol and 2-mercaptoethanol. These results are the first demonstration of ischemia-induced differential regulation of transcription factor binding activities which are time-, region-, and redox state dependent.
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PMID:Alteration of transcription factor binding activities in the ischemic rat brain. 762 34


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