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Biomedical subjects

E Tani

Publications and source records attributed to E Tani.

At least 55 records · Page 3Linked to original sources
PubMed1998

Synthesis and pharmacochemical investigation of some novel 1,2,4-4H-triazoles with potential antiviral activity.

We report the synthesis of some mercaptotriazole derivatives in an effort to discover underlying structural requirements for antiviral activity. A preliminary antiviral study was performed and the contribution of the compounds to free radical processes was investigated. Because lipophilicity influences both biological activity and antioxidant potential we calculated lipophilicity and attempted to correlate this with antioxidant activity. Treatment of the N-(aryl)piperazineacetohydrazides (compounds 1) with 2,4-dichlorophenylisothiocyanate gave the N-(aryl)piperazinethiosemicarbazides (compounds 2) in good yield. Cyclization of these compounds after treatment with NaOH solution provided the corresponding 5-(4-aryl-1-piperazinylmethyl)-4-(2,4-dichlorophenyl)-4H-1,2,4-triazole- 3-thiols (compounds 3) in good yield. Reaction of compounds 3 with 2,4-dichloro- or 4-fluorobenzyl chloride in acetone in the presence of potassium carbonate gave the target compounds (compounds 4) in about 70% yield. The antioxidant effect of the compounds on non-enzymatic lipid peroxidation of rat hepatic microsomal membranes was studied. Most of the examined compounds were active at concentration of 0.1 mM and most were found to prevent dimethylsulphoxide oxidation moderately (20-50%) at a concentration tenfold less than that of dimethylsulphoxide. The interaction of the synthesized compounds with 1,1-diphenyl-2-picrylhydrazyl stable free radical was also studied. Correlation was found between the two expressions of calculated lipophilicity, antioxidant activity and the lipophilicity of the synthesized compounds, and a correlation was derived between antioxidant activity and delta logP, which expresses the compounds' hydrogen-bonding capacity.

Animals↗
PubMed1997

Up- and down-regulation of calpain inhibitor polypeptide, calpastatin, in postischemic hippocampus.

Based on our previous observation that transient forebrain ischemia induces calpain-catalyzed proteolysis in gerbil hippocampus in a region-specific manner, we examined the effect of ischemia on the quantity and localization of the endogenous calpain-specific inhibitor protein, calpastatin, in the tissue. Brief (5 min) forebrain ischemia followed by reperfusion induced an overall increase of calpastatin immunoreactivity in hippocampus, particularly in pyramidal cells, in 4 h as analyzed by Western blotting and immunohistochemistry. The amount of calpastatin, however, decreased to the preischemic level and lower in 24 h to 7 days due to proteolysis except in CA2 showing continuously elevated calpastatin immunoreactivity. Because calpastatin is not only a potent inhibitor but also a preferred substrate for calpain and because CA2 neurons are less vulnerable to ischemic stress than the adjacent CA1 neurons, these observations imply involvement of calpastatin in calpain regulation as a bait substrate and, possibly, in neuroprotection under ischemic conditions. Calpastatin may participate in the stress responses together with the previously known ischemia-induced stress proteins such as heat shock proteins.

Animals↗
PubMed1997

Proliferation of breast epithelial cells in healthy women during the menstrual cycle.

OBJECTIVE: Our objective was to assess proliferation in normal breast epithelial cells from healthy women during the follicular and luteal phases of the menstrual cycle. STUDY DESIGN: We analyzed the proliferation marker Ki-67/MIB-1 by immunocytochemical methods in breast epithelial cells procured through fine needle aspiration biopsy from 47 healthy volunteers. Differences were assessed by Wilcoxon rank sum tests, and correlations were determined by Spearman's rank correlation coefficient. RESULTS: The proportion of KI-67/MIB-1-positive cells was higher in the luteal phase (2.04%) than in the follicular phase (1.66%). The values in women aged < 35 years were 2.29% and 1.13%, respectively (p = 0.003). In ovulating women with two aspirates during the same menstrual cycle the percentage of proliferating cells increased from the follicular phase (1.3%) to the luteal phase (2.4%) (p < 0.04). Proliferation was positively correlated with serum progesterone levels the day of aspiration (r = 0.34, p < 0.05). CONCLUSION: The fine needle aspiration biopsy technique is a valuable tool for in vivo studies of cell proliferation in the normal breast. Data clearly suggest a proliferative action of progesterone.

Adolescent↗
PubMed1997

Generation of the catalytic fragment of protein kinase C alpha in spastic canine basilar artery.

In previous studies of topical application of calphostin C, a specific inhibitor of the regulatory domain of protein kinase C (PKC), and calpeptin, a selective inhibitor of calpain, to spastic canine basilar artery (BA) researchers have suggested that the catalytic fragment of PKC (known as PKM) is probably formed by a limited proteolysis of continuously activated mu-calpain, but there has been no direct evidence for PKM formation in vasospasm. The present immunoblot study with anti-PKCalpha antibody shows a significant decrease in cytosolic 80-kD PKCalpha and a concomitantly significant increase in membrane PKCalpha in the spastic canine BA. In addition, an immunoblot study in which cleavage site-directed antibodies were used demonstrated a significant increase in immunoreactive 45-kD PKM. The changes in membrane PKCalpha and PKM were enhanced with the lapse of time after subarachnoid hemorrhage. The cleavage site-directed antibodies distinguish the proteolyzed from the unproteolyzed forms of PKC for in situ analyses of enzyme regulation mediated by proteolysis. The data indicate that PKCalpha in spastic canine BA is translocated to the cell membrane, where PKCalpha is rapidly cleaved into PKM as a result of proteolysis of the isozyme by mu-calpain but not by m-calpain. The authors hypothesize that mu-calpain is continuously activated in spastic canine BA and produces PKM by limited proteolysis of PKCalpha.

Animals↗
PubMed1996

Analysis of O6-methylguanine-DNA methyltransferase mRNA in fine needle biopsies from human melanoma metastases by reverse transcription and polymerase chain reaction.

O6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein, which removes alkyl groups from the O6 atom of guanine residues. Tumour cells which lack MGMT are sensitive to cytostatic drugs such as dacarbazine (DTIC), whose active species bind to this site. To explore whether analyses of MGMT expression can be used as a predictive test for clinical sensitivity to DTIC in melanomas, we developed a method to assay MGMT mRNA levels in cells obtained by fine needle aspiration biopsies of metastases. cDNA was synthesised from mRNA prepared from biopsy material. Polymerase chain reaction was performed using primers complementary to MGMT cDNA and to beta-actin, which served as an internal control. Analyses of 44 biopsies from 35 patients showed a considerable variation in MGMT mRNA, with 15 samples (34%) lacking detectable mRNA. In 6 out of 8 patients in whom more than one tumour was analysed, separate metastases had different levels of MGMT mRNA. There was no correlation between MGTM activity studied by a biochemical assay and MGMT mRNA levels when these were compared in 10 surgical biopsies.

Adult↗
PubMed1996

Cytotoxic fragment of amyloid precursor protein accumulates in hippocampus after global forebrain ischemia.

We developed an antibody specific to beta-amyloid precursor protein (beta APP) fragments possessing the exact amino terminus of the beta-amyloid peptide and examined its induction in postischemic hippocampus. In control hippocampus, this APP fragment was lightly observed in pyramidal neurons of CA sectors and dentate granule cells. Transient forebrain ischemia enhanced accumulation of the APP fragment in CA1 pyramidal neurons. Seven days after the ischemia, while the APP fragment was still observed in dentate granule cells and CA3 neurons, it disappeared in dead CA1 neurons. While astrocytes did not show in any immunoreactivity throughout the experiment, those in the CA1 sector showed moderate immunoreactivity 7 days after the ischemia. The APP fragment has a cytotoxic effect on cultured neurons. These results suggest that the accumulation of the cytotoxic APP fragment in CA1 neurons may play a role in the development of delayed neuronal death after the ischemic insult.

Amyloid beta-Protein Precursor↗
PubMed1996

Gliomatosis cerebri: a case report.

Gliomatosis cerebri is a rare disease that thus far was usually diagnosed at the time of autopsy. In this communication we report the case of a young woman with gliomatosis cerebri. Diagnosis was established on the basis of characteristic imaging findings and typical histopathological features of surgical specimens obtained by craniotomy.

Adult↗
PubMed1995

Diagnosis of lymphoma, leukemia, and metastatic tumor involvement of the cerebrospinal fluid by cytology and immunocytochemistry.

Fifty-five cerebrospinal fluid (CSF) specimens from 42 patients with suspected meningeal tumor involvement were reviewed. Cytology in conjunction with immunocytochemistry identified 26 CSF specimens as malignant. There were fifteen cases of lymphoma, four cases of leukemia, two cases of carcinoma, and two cases of melanoma. A monoclonal light chain expression was demonstrated in nine out of eleven B cell lymphomas. The three T-cell lymphomas all expressed pan T markers (CD 3) and two the T-helper antigen (CD 4). One patient had meningeal involvement of a true histiocytic lymphoma which was identified by its large atypical cells which were positive for alpha-1-anti-trypsin and muramidase. In four patients with a primary diagnosis of acute lymphoblastic leukemia, CSF involvement was confirmed by the demonstration of blasts with CD 10 (cALLA) or light chain restriction. Epithelial or melanocytic markers were demonstrated on the tumor cells in CSF from the remaining four patients. In 29 CSF specimens a diagnosis of reactive lymphocytosis was made using cytomorphology which mostly was characterized by macrophages mixed with small mature lymphoid cells. Immunologic evaluation showed that these mature cells were CD 10 negative T-cells and only few specimens contained polyclonal B-cells. The subsequent clinical course of these patients showed no evidence of CNS malignancy. It is concluded that cytology should be used in conjunction with immunocytochemistry to accurately evaluate CSF specimens from patients with possible malignant meningitis.

Adolescent↗
PubMed1995

Growth fraction in non-Hodgkin's lymphomas and reactive lymphadenitis determined by Ki-67 monoclonal antibody in fine-needle aspirates.

The fraction of proliferation cells was analysed in fine needle aspirates from a series of 448 non-Hodgkin's lymphomas and 199 reactive hyperplasias using an immunoperoxidase staining with monoclonal antibody Ki-67. There was a good correlation between proliferation fraction and cytologic assignment to high and low grade lymphomas. Thus high grade lymphomas had a high median percentage of Ki-67 positive cells with a figure of 82.1 for lymphoblastic, 60.0 for immunoblastic, and 59.7 for centroblastic lymphomas. For low grade lymphomas the figures were 17.1 and 11.1 percent for centroblastic/centrocytic and CLL/immunocytoma, respectively. The fraction of proliferation cells in reactive lymphadenitis varied between 1-50% with a median of 11.5%. Analysis of Ki-67 positivity can accordingly not be used to differentiate benign from neoplastic proliferations. Within all lymphoma subgroups but lymphoblastic lymphoma, there was a marked variation in fraction of Ki-67 positive cells, which resulted in a certain overlap between high and low grade lymphomas. The results show that cells procured through fine-needle aspiration can be used to analyse the fraction of proliferating cells which contributes information about the growth rate of the individual tumours that can not be obtained through cytologic classification.

Antibodies, Monoclonal↗
PubMed1995

Three distinct phases of fodrin proteolysis induced in postischemic hippocampus. Involvement of calpain and unidentified protease.

BACKGROUND AND PURPOSE: Fodrin, a neuronal cytoskeleton protein, is proteolyzed by calpain after ischemic insult. We examined proteolysis of fodrin induced by global forebrain ischemia in gerbil hippocampus in spatial terms by using the antibody specific to the calpain-proteolyzed form of fodrin. METHODS: In gerbils, a 10-minute forebrain ischemia was produced by occlusion of both carotid arteries. After recirculation, the hippocampus was processed for immunohistochemical and immunoblot study with the antibody against the calpain-proteolyzed form of fodrin. Additionally, short-term ischemia was studied to find the threshold of fodrin proteolysis. RESULTS: Three phases of fodrin proteolysis distinct in chronology and distribution arose: (1) an early predegeneration phase in the molecular layer and stratum oriens of the CA1 and CA3 sectors within the first 15 minutes, which lasted up to 4 hours; (2) a late predegeneration phase in the whole CA1 sector, except for the pyramidal cells, between 12 hours and 2 days; and (3) a postdegeneration phase in the cytoplasm of the CA1 neurons, which arose in 3 to 7 days. A 4-minute (not a 3-minute) forebrain ischemia induced the late predegeneration phase of fodrin proteolysis and delayed neuronal death in CA1. Immunoblotting showed that the primary product of calpain action was further proteolyzed by an unidentified protease. CONCLUSIONS: Calpain induced proteolysis of fodrin in ischemic hippocampus, and the late predegeneration phase of the proteolysis was closely associated with the delayed neuronal death in the CA1 sector. Calpain and another protease may play a role in the development of neuronal death after transient forebrain ischemia.

Animals↗
PubMed1995

Activity of smooth muscle phosphatases 1 and 2A in rabbit basilar artery in vasospasm.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage frequently leads to a long-term cerebral artery narrowing called vasospasm. Recently, the involvement of myosin light chain kinase has been found in experimental vasospasm in our laboratory. We therefore measured the activity of serine/threonine protein phosphatases 1 and 2A in the rabbit basilar artery in vasospasm and in vasocontraction to study their role, particularly in regard to vasospasm compared with vasocontraction. METHODS: Vasospasm was produced in the rabbit basilar artery by a two-hemorrhage method. Vasocontraction was induced by local application of KCl or serotonin to the rabbit basilar artery after a transclival exposure. The control animals were treated with saline instead of fresh blood. Serine/threonine protein phosphatase activity in the basilar artery was assayed with the use of [32P]phosphorylase-a as a substrate; protein phosphatase 1 activity was evaluated as protein phosphatase activity in the presence of 1 nmol/L okadaic acid, whereas protein phosphatase 2A activity was assessed as protein phosphatase activity inhibited by 1 nmol/L okadaic acid. RESULTS: Values of mean activity of protein phosphatase 1 in myofibrillar extract were 3.58 +/- 0.26 nmol/min per milligram in the control group, 3.22 +/- 0.12 nmol/min per milligram in the spastic group on day 2, and 3.01 +/- 0.16 nmol/min per milligram in the spastic group on day 4 (a significant decrease in protein phosphatase 1 activity in the spastic group on days 2 and 4). In contrast, these values did not show any significant changes in the KCl and serotonin groups. Values of mean activity of protein phosphatase 2A in cytosolic extract were 0.90 +/- 0.07 nmol/min per milligram in the control group, 0.75 +/- 0.10 nmol/min per milligram in the spastic group on day 2, and 0.62 +/- 0.17 nmol/min per milligram in the spastic group on day 4 (a significant reduction in protein phosphatase 2A in the spastic group on days 2 and 4). There was no evidence of significant changes of protein phosphatase 2A in cytosolic extract in the KCl and serotonin groups. CONCLUSIONS: Protein phosphatase 1 in myofibrillar extract is reported to catalyze the dephosphorylation of myosin light chain and calponin, whereas protein phosphatase 2A in cytosolic extract catalyzes the dephosphorylation of calponin and caldesmon. In addition, the phosphorylation of calponin and caldesmon results in the loss of their ability to inhibit smooth muscle contraction. Therefore, the significant decrease in activity of protein phosphatases 1 and 2A in vasospasm may result in uninterrupted vascular smooth muscle contraction by the preservation of phosphorylation of not only myosin light chain but also calponin and caldesmon.

Animals↗
PubMed1995

Effects of protein kinase C modulators on multidrug resistance in human glioma cells.

To identify the role of protein kinase C (PKC) in multidrug resistance, the effects of phorbol-12-myristate-13-acetate (PMA), a PKC activator, or calphostin C, a PKC inhibitor, on intracellular vincristine accumulation and expression of P-glycoprotein phosphorylation were studied in one multidrug-resistant and three multidrug-sensitive human glioma cell lines. Basal PKC activities and immunoreactivities of PKC-alpha and -zeta were higher in multidrug-resistant cells than in multidrug-sensitive cells. There was no significant difference in the immunoreactivity of PKC-delta between multidrug-resistant and -sensitive cells, and immunoreactive PKC-beta, -gamma, and -epsilon were not detected in either multidrug-resistant or -sensitive cells. The treatment of multidrug-resistant cells with 100 nM PMA for 2 hours resulted in the activation not of PKC-zeta but of PKC-alpha, with concomitant decrease in vincristine accumulation and increase in P-glycoprotein phosphorylation. The exposure of multidrug-resistant cells to 100 nM PMA for 24 hours induced down-regulation not of PKC-zeta but of PKC-alpha, with concurrent decrease in vincristine accumulation, and reduced but still increased P-glycoprotein phosphorylation. The treatment of multidrug-resistant cells with 100 nM calphostin C for 2 hours decreased immunoreactive PKC-zeta and not immunoreactive PKC-alpha, inducing increase in vincristine accumulation, with concomitant decrease in P-glycoprotein phosphorylation. There was no evidence of significant change in vincristine accumulation in multidrug-sensitive cells treated with PMA or calphostin C. This may suggest that at least two isozymes of PKC, PKC-alpha and -zeta, are involved in P-glycoprotein phosphorylation and that vincristine efflux function in multidrug-resistant human glioma cells is closely associated with P-glycoprotein phosphorylation and is decreased by PKC inhibitor.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Matrix metalloproteinases and tissue inhibitors of metalloproteinases in human gliomas.

The gene expression of five matrix metalloproteinases (MMPs) and two tissue inhibitors of metalloproteinases (TIMPs) was studied in human gliomas in vivo and in vitro to evaluate their roles in glioma invasion. Simultaneous expression of one to four MMP genes and two TIMP genes was found in 17 surgical glioma specimens, and one MMP (gelatinase A) gene and two TIMP genes were simultaneously expressed in tissue of three brains. The concomitant overexpression of gelatinase A, gelatinase B, and occasional matrilysin genes was associated with the malignancy of gliomas and accompanied by overexpression of the TIMP-1 gene. In five human glioma cell lines, gelatinase A, TIMP-1, and TIMP-2 genes were constitutively expressed in alll cell lines: the matrilysin gene in three cell lines; the stromelysin gene in two cell lines; and the interstitial collagenase gene in one cell line. There was a clear difference in the expression of gelatinase B and stromelysin genes between surgical glioma specimens and glioma cell lines: the gelatinase B gene was not expressed constitutively in vitro but was overexpressed in vivo, whereas the stromelysin gene was not expressed in vivo but was expressed in some cell lines. To find the cause of that difference in vivo and in vitro, the transcriptional regulations of MMP and TIMP genes by tumor promoter, growth factors, or cytokines were studied in vitro. Interstitial collagenase, gelatinase B, stromelysin, and TIMP-1 genes were upregulated in many cell lines by phorbol-12-myristate-13-acetate (PMA) and in some cell lines by epidermal growth factor, tumor necrosis factor-alpha, or interleukin-1 beta. Transforming growth factor-beta 1 (TGF beta 1) upregulated gelatinase A and matrilysin genes in some cell lines, and there were no clear responses from any MMP and TIMP genes to interleukin-6. Thus, the transcriptional modulation of MMP genes by these growth factors and cytokines seemed insufficient to explain the difference in gelatinase B and stromelysin gene expressions in vivo and in vitro and was suggestive of the genetic alteration of glioma cells in vitro, the heterogeneous cell population in glioma tissues, or both. Furthermore, the in vitro invasion of glioma cells through Matrigel in response to PMA, TGF beta 1, or TIMP-1 was assessed by chemoinvasion assay. In most cell lines, invasion was significantly stimulated by PMA or TGF beta 1 but suppressed by TIMP-1.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Inhibition by 5'-methylthioadenosine of cell growth and tyrosine kinase activity stimulated by fibroblast growth factor receptor in human gliomas.

Stimulation of three human glioma cell lines with basic fibroblast growth factor (bFGF) led to the enhancement of cell growth and the rapid tyrosine phosphorylation of cellular proteins, including major substrates of 90 kD. A methyltransferase inhibitor, 5'-methylthioadenosine (MTA), inhibited dose dependently the bFGF-stimulated cell growth and protein tyrosine phosphorylation in glioma cells by blocking both receptor autophosphorylation and substrate phosphorylation, as shown by immunoblotting with antiphosphotyrosine antibodies and cross-linking bFGF to receptors. The antiproliferative activity of MTA correlated quantitatively with its potency as an inhibitor of bFGF-stimulated protein tyrosine kinase activity. The methyltransferase inhibitor MTA had no effect on either epidermal growth factor- or platelet-derived growth factor-stimulated protein tyrosine phosphorylation in glioma cells, but inhibited specifically bFGF-stimulated protein tyrosine kinase activity. The concentration of MTA required for inhibition of protein methylation correlated well with the concentration required for inhibition of bFGF-stimulated cell growth and protein tyrosine phosphorylation. Because MTA had no effect on numbers and dissociation constants of high- and low-affinity bFGF receptors, the inhibition of bFGF-stimulated bFGF receptor tyrosine kinase activity is not likely to be the result of a reduction in bFGF receptor and bFGF binding capacity. In fact, MTA delayed and reduced the internalization and nuclear translocation of bFGF, and the internalized bFGF was submitted to a limited proteolysis that converted it to lower molecular peptides whose presence remained for at least 22 hours. The effect of MTA on bFGF-stimulated tyrosine phosphorylation was immediate and readily reversible.

Antibodies↗
PubMed1995

Apoptosis of human glioma cells in response to calphostin C, a specific protein kinase C inhibitor.

Calphostin C acts at the regulatory domain as a highly selective inhibitor of protein kinase C (PKC), and staurosporine acts at the catalytic domain as a nonspecific PKC inhibitor. The authors investigated the capacity of calphostin C and staurosporine to promote apoptotic fragmentation of DNA in four human glioma cell lines. The exposure of glioma cell lines to 100 nM calphostin C for 2 to 8 hours induced a decrease in particulate PKC activities and exposure for 16 to 24 hours produced a concentration-dependent increase in internucleosomal DNA cleavage on agarose gel electrophoresis. In addition, the human glioma cells showed the classic morphological features of apoptosis: cell shrinkage, nuclear condensation, and the formation of apoptotic bodies. A 24-hour exposure to staurosporine failed to induce internucleosomal DNA fragmentation at concentrations generally used to achieve maximum inhibition of enzyme activity (50 nM) but promoted fragmentation at considerably higher concentration (more than 200 nM). Deoxyribonucleic acid fragments obtained from cells exposed to 100 nM calphostin C for 16 to 24 hours possessed predominantly 5'-phosphate termini, consistent with the action of a Ca++/Mg(++)-dependent endonuclease. Northern and Western blot analyses revealed that the exposure to 100 nM calphostin C for 4 hours failed to alter bcl-2 transcript and protein, but exposure for more than 8 hours decreased the amount of bcl-2 transcript and protein. Together, these observations suggest that calphostin C is capable of inducing apoptotic DNA fragmentation and cell death in a highly concentration dependent manner in human glioma cells and that the apoptosis is closely associated with the decrease in transcription and translation of bcl-2.

Alkaloids↗
PubMed1995

Effect of phenobarbital, spironolactone and pregnenolone-16 alpha-carbonitrile on rat hepatic beta-glucuronidase.

beta-Glucuronidase cleaves beta-glucuronides of drugs, steroids, as well as macromolecular compounds containing glucuronic acid bound with a beta-glycoside bond. Therefore, the study of induction of this enzyme by known microsomal enzyme inducers is of obvious interest. The effect of phenobarbital, spironolactone and pregnenolone-16 alpha-carbonitrle on the rat liver beta-glucuronidase was studied. These compounds augmented the activity of this enzyme, in the above increasing order. These results are discussed in view of the influence on pharmacokinetics of many drugs. Furthermore, they may lead to new therapeutic approaches for certain diseases.

Animals↗
PubMed1995

[Increased expression of gelatinases A and B, matrilysin and TIMP-1 genes in human malignant gliomas ].

Malignant glioma is a local invasive tumor in the central nervous system. The mRNA expression of five matrix metalloproteinases (MMPs) and two tissue inhibitors of metalloproteinases (TIMPs) was examined in surgical specimens of three brain tissues, two astrocytomas, four anaplastic astrocytomas and eleven glioblastomas, including recurrent one anaplastic astrocytoma and two glioblastomas. In the control brain tissues, mRNA expression was high for TIMP-2, low for gelatinase A and TIMP-1, and undetectable for gelatinase B, interstitial collagenase, stromelysin and matrilysin. Gelatinase B and TIMP-1 were concomitantly overexpressed in primary glioblastomas. In addition, the average expression level of gelatinase A increased 3.0 fold in astrocytomas and anaplastic astrocytomas and 6.0 fold in glioblastomas, compared to the brain tissues. Matrilysin was induced variably in more than half of the primary glioblastomas, and interstitial collagenase was slightly induced in some primary and recurrent glioblastomas. Stromelysin was characteristically not expressed in any gliomas, and the expression level of TIMP-2 did not significantly change in the gliomas. These results suggest that the concomitant increased expression of gelatinase A, gelatinase B and occasional matrilysin genes is associated with the malignancy of gliomas and accompanied by the increased expression of TIMP-1 gene.

Astrocytoma↗