Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effects of X irradiation on activation of the promoter of the human HSP70B gene, which is activated only after heat shock. The HSP70B promoter was ligated to the bacterial beta-galactosidase (beta-gal) gene, and the reporter plasmid was transfected into NCI-H1299 carcinoma cells. The expression of the reporter gene was determined by an immunological assay using an anti-beta-gal monoclonal antibody. There was no expression of beta-gal protein in the control cells, and neither 2 cGy nor 6 Gy of X rays activated the HSP70B promoter. Heat-shock treatment at 43 degrees C for 2 h induced beta-gal expression, and this level was increased significantly by irradiation with 2 cGy of X rays 5 h before heat-shock treatment. This stimulative effect was not observed when cells were pretreated with 10 or 50 cGy of X rays. Furthermore, irradiation of cells with 6 Gy of X rays before or immediately after heat-shock treatment did not affect the level of beta-gal expression. In situ staining of beta-gal-positive cells using X-gal as substrate revealed that low-dose irradiation did not increase the overall level of induction of beta-gal but increased the number of cells capable of inducing beta-gal in response to heat shock. Since preirradiation with 2 cGy of X rays did not alter either the constitutive level or the induced level of HSP72, another member of the HSP70 family, the effect of low-dose irradiation may not be obvious if the promoter is already active. Thus these results indicate that pretreatment with low doses of ionizing radiation may enhance the susceptibility of cells to various stresses, which would then facilitate the activation of gene transcription in response to a subsequent insult.
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PMID:Effect of low-dose preirradiation on induction of the HSP70B-LacZ fusion gene in human cells treated with heat shock. 945

The effect of overexpression of heat shock protein (HSP)72 on apoptosis induced by different stimuli in human umbilical vein endothelial cells (HUVECs) and the angiogenic cell line, ECV304, was studied. Transient overexpression of HSP72 was achieved using an adenoviral vector (Advhsp72) and apoptosis was induced by heat shock, tumour necrosis factor (TNF)-alpha with cycloheximide (CHX), lipopolysaccharide (LPS) with TNF-alpha and verocytotoxin (VT). Apoptosis induced by heat shock was reduced by HSP72 expression. However, HSP72 expression in HUVECs increased apoptosis induced by TNF-alpha/CHX, LPS and VT measured by flow cytometric analysis of propidium iodide (PI)-stained permeabilized cells. In contrast, apoptosis in ECV304 induced by the same stimuli was reduced by HSP72 expression. No difference was seen in cells transduced with a control adenoviral vector expressing beta-galactosidase. These data imply that induction of HSP72 in cells modulates responses to apoptotic stimuli, but that the nature of the response varies with the cell type. However, it is clear that in situations where apoptosis may be part of a pathological process, HSP72 induction, for example by reperfusion injury, may exacerbate the process.
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PMID:Contrasting effects of HSP72 expression on apoptosis in human umbilical vein endothelial cells and an angiogenic cell line, ECV304. 1105 88

We investigated whether HSV gene transfer of HSP72 in vivo and in vitro: (1) protected cornu ammonis 1 region of the hippocampus neurons from global cerebral ischemia; and (2) affected Bcl-2 expression. HSV vectors expressing HSP72 and beta-galactosidase (reporter) or beta-galactosidase only (control vector) were injected into cornu ammonis 1 region of the hippocampus 15 hours before induction of global cerebral ischemia (n = 10) and sham-operated rats (n = 8). HSP72 vector-treated rats displayed significantly more surviving transfected neurons (X-gal-positive, 31 +/- 8) compared with control vector-treated rats (10 +/- 4) after global cerebral ischemia. Sham-operated rats displayed similar numbers of X-gal-positive neurons (HSP72 vector 18 +/- 8 vs control vector 20 +/- 7). The percentage of beta-galactosidase and Bcl-2 coexpressing neurons in HSP72-treated rats after global cerebral ischemia (84 +/- 4%) was greater than that in control vector-treated rats (58 +/- 9%). The percentage of beta-galactosidase and Bcl-2 coexpressing neurons in sham-operated rats was similar in HSP72 (93 +/- 7%) and in control vector-treated rats (88 +/- 12%). HSP72 vector transfection led to 12 times as much Bcl-2 expression as the control vector in uninjured hippocampal neuronal cultures. In injured (oxygen-glucose deprivation) hippocampal neuron cultures, HSP72 vector transfection led to 2.8 times as much Bcl-2 expression as control vector. We show that HSP72 overexpression protects cornu ammonis 1 region of the hippocampus neurons from global cerebral ischemia, and that this protection may be mediated in part by increased Bcl-2 expression.
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PMID:Gene transfer of HSP72 protects cornu ammonis 1 region of the hippocampus neurons from global ischemia: influence of Bcl-2. 1221 Jul 85