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

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
 ...
PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69

MK-801 and ketamine are noncompetitive N-methyl-D-aspartate (NMDA) receptor blockers that decrease brain injury in animal models of focal and global ischemia. Recent reports, however, suggested that MK-801 itself can damage neurons. Here we show that MK-801 (0.1 to 5.0 mg/kg) and ketamine (40 to 100 mg/kg) typically induce heat shock protein HSP72 mainly in layer 3 neurons of the posterior cingulate and retrosplenial cortex of the rat. These HSP72-immunoreactive neurons contain abnormal cytoplasmic vacuoles visualized by electron microscopy. The HSP72 immunoreactivity is maximal at 24 hours with 1.0-mg/kg doses of MK-801 and disappears by 2 weeks. Based on these data, we propose: (1) MK-801 and ketamine injure selected neurons, which express HSP72 in response to that injury. (2) Since HSP72 is induced for 1 to 2 weeks, the prolonged psychological side effects of MK-801, ketamine, phencyclidine, and related drugs could be related to this injury. (3) The neuroprotective effect of MK-801 is probably not related to HSP72 induction. (4) HSP72 immunocytochemistry is useful for studying nonlethal neuronal injury from a wide variety of brain insults.
 ...
PMID:MK-801 and ketamine induce heat shock protein HSP72 in injured neurons in posterior cingulate and retrosplenial cortex. 183 80

The potential role of the nonconstitutive 72-kDa heat-shock protein (HSP72) in selective neuronal vulnerability to ischemia was studied in rats subjected to graded global ischemia. Immunocytochemistry using a monoclonal antibody against HSP72 was performed on tissue collected after 24 hr of reperfusion. The appearance of HSP72 immunoreactivity correlated in a graded fashion with those regions known to be selectively vulnerable in ischemia. That is, HSP72 was induced in only hilar interneurons and CA1 pyramidal cells following brief ischemia. After intermediate durations of ischemia, HSP72 was expressed in the CA3 neurons and cortical layers 3 and 5, and after the longest intervals, HSP72 appeared in dentate granule cells. Heat-shock protein expression preceded cell death (assessed with acid fuchsin staining) in all regions. This temporal profile suggests that the capability of neurons to express HSP72 is unlikely to account for selective vulnerability of different brain regions following ischemia; its role in neuroprotection during ischemic injury in vivo remains unknown.
 ...
PMID:The temporal profile of 72-kDa heat-shock protein expression following global ischemia. 200 65

Global ischemia was produced in adult rats by combining bilateral carotid artery occlusions with systemic hypotension for 5 or 10 minutes. Induction of the 72 kD heat shock protein (HSP72) in the hippocampus was examined immunocytochemically 18-24 hours later. Several patterns of HSP72-like immunoreactivity (HSP72LI) were observed. Five minutes of ischemia induced HSP72 in isolated columns of CA1a pyramidal neurons, or throughout CA1 pyramidal neurons and dentate hilar neurons. Ten minutes of ischemia induced marked HSP72LI in CA3 pyramidal neurons, moderate HSP72LI in dentate granule cells, and minimal HSP72LI in CA1 pyramidal, dentate hilar neurons, and hippocampal glia. Two hippocampi subjected to 10 minutes of ischemia exhibited marked HSP72LI in capillary endothelial cells but no neuronal or glial HSP72LI. It is proposed that (a) the induction of HSP72 in hippocampal sectors correlates with their vulnerability to global ischemia (CA1 greater than hilus greater than CA3 greater than dentate gyrus); (b) the induction of HSP72 in hippocampal cells correlates with their vulnerability to global ischemia in that mild ischemia induced HSP72 only in neurons, moderate ischemia in neurons and glia, and severe ischemia only in capillary endothelial cells; (c) the failure to induce HSP72 in hippocampal neurons in 2 cases of 10 min ischemia may be related to severe injury causing disruption of protein synthesis in these cells.
 ...
PMID:Induction of heat shock protein 72-like immunoreactivity in the hippocampal formation following transient global ischemia. 201 84

The expression of heat shock protein immunoreactivity in rat brain was evaluated in a model of neonatal hypoxia-ischemia. One-week-old rats were subjected to left carotid artery coagulation and exposure to 8% O2/92% N2 for 2 h (moderate injury) or 3.5 h (severe injury). Animals were sacrificed 1, 12 and 24 h after the hypoxic insult. Cells immunoreactive for the 72 kDa heat shock protein (HSP72) were observed in ipsilateral cortex as early as 1 h after the termination of the hypoxia. After 12 h, neurons in the ipsilateral hippocampus and cortex stained intensely for HSP72 immunoreactivity in the moderately injured group. In the severely injured brains, bilateral staining was observed in neurons and vessels of the hippocampus and cortex. Therefore, cells containing HSP72 immunoreactivity may serve as an early marker for neuronal injury from hypoxia-ischemia in the neonatal rat brain and more importantly may illustrate previously unrecognized areas of central nervous system vulnerability.
 ...
PMID:Hypoxia-ischemia induces heat shock protein-like (HSP72) immunoreactivity in neonatal rat brain. 235 Aug 81

Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. tau, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, tau, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased tau immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of tau, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective marker of ischemic insult.
 ...
PMID:Alterations in tau immunostaining in the rat hippocampus following transient cerebral ischemia. 751 35

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.
 ...
PMID:Rapid and semiquantitative analysis of HSP72 and HSC73 heat shock mRNAs by mimic RT-PCR. 755 61

Muscle necrosis has been frequently observed in cardiomyoplasty patients and in experimental animal studies. The purpose of this study was to determine if heat shock could provide protection to skeletal muscle as has been shown in cardiac muscle. A 15-minute heat shock at 42 degrees C resulted in an immediate increase in HSP72 mRNA and was followed within 3 hours by a two-fold increase in HSP72. Surgical dissection of the latissimus dorsi muscle (LDM) followed by an ischemic period resulted in a two-fold increase in HSP72 in control LDM, whereas the already high levels in the heat-shocked LDM increased only slightly with surgery and ischemia. Citrate synthase activity and tissue histology indicated that heat shock did not protect the LDM from the imposed surgical trauma and ischemia insults used in this study.
 ...
PMID:Cardiomyoplasty: preservation of the latissimus dorsi muscle. 777 73

Exposure of animals to transient hyperthermia causes the induction of highly conserved proteins, heat shock proteins (HSPs), which are thought to by cytoprotective against a variety of injuries, including ischemia. We tested the hypothesis that heating donor animals prior to harvest would improve pulmonary preservation. Anaesthetized New Zealand White rabbits underwent radiant heating to 42.5-43.5 degrees C (rectal) 8 h prior to harvest of the lungs. The lungs were harvested without flush and stored for 18 h at 4 degrees C. The left lung were perfused ex vivo with fresh blood for 10 min. Blood gases, pulmonary artery (Ppa) and airway (P(aw) pressures, and wet/dry ratios (W/D) were measured. Control animals were treated identically except without heating. All heated animals had HSP72 at lung harvest and 18 h later, whereas no control had detectable levels of HSP72 at either time. In Experiment 1 (n = 12, VT 20 ml, F1O2 0.21, 30 bpm, PEEP 0.5 cm H2O), PO2 in the heated group was 57.6 +/- 7.3 mmHg (mean +/- SEM) vs. 51.6 +/- 5.7 in the controls (NS). In Experiment 2 (n = 8, VT 15 ml, F1O2 0.21, 35 bpm, PEEP 2 cm H2O), PO2 of the heated group was 63.5 +/- 6.5 vs. 83.1 +/- 9.5 in the controls (NS). Ppa after 10 min was not significantly different in the heated group in Experiment 1 (16.7 +/- 0.9 mmHg vs. 24.2 +/- 3.7 in controls) or in Experiment 2 (19.5 +/- 1.8 vs. 11.3 +/- 2.9 in controls). Wet/dry ratios were not different in either Experiment 1 (6.4 +/- 0.4 vs. 5.8 +/- 0.2 in controls) or Experiment 2 (5.0 +/- 0.2 vs. 5.0 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effect of heat shock on immediate post-preservation lung function. 786 44

Vulnerability of aged hearts to ischemia may be due to defects in protective mechanisms provided by heat shock proteins (HSPs). To determine whether there is a defect in the induction of HSPs by ischemia in old hearts, HSP72 and HSP73 (inducible and constitutive HSP70, respectively) mRNA induction was examined in young (2-mo-old; n = 36) and old (18-mo-old; n = 32) rat hearts. Transient (10- or 20-min) ischemia was applied by tightening a snare placed around left coronary arterial branches 3 days before examination to avoid the effect of operation on induction. HSP72 mRNA was induced markedly in young hearts after 10-min ischemia, peaked at 2 h, but was induced only slightly in old hearts. HSP73 mRNA was also induced in young hearts, peaked at 4 h, but was not induced in old hearts. The mRNAs were markedly induced in old hearts as well after 20-min ischemia, which was accompanied by the induction of HSP72 protein. Thus the age-related modulation of HSP72 and HSP73 mRNAs suggests a defective sensing mechanism for ischemia in old hearts.
 ...
PMID:Diminished heat shock protein 70 mRNA induction in aged rat hearts after ischemia. 797 10


1 2 3 4 5 6 7 Next >>