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Biomedical subjects

K Matuoka

Publications and source records attributed to K Matuoka.

11 recordsLinked to original sources
PubMed1992

Cloning of ASH, a ubiquitous protein composed of one Src homology region (SH) 2 and two SH3 domains, from human and rat cDNA libraries.

The protein ASH (for abundant Src homology), composed of one Src homology region (SH) 2 and two SH3 domains, was cloned by screening human and rat cDNA libraries with an oligonucleotide probe directed to a consensus sequence of the SH2 domains. The rat-derived ASH peptide was comprised of 217 amino acids with a molecular mass of 25-28 kDa and was found to be ubiquitous in rat tissues. A human cDNA clone was also found to code for part of the same protein, suggesting that ASH is common to human and rat. The amino acid sequence of ASH was strikingly similar to Sem-5, the product of a nematode cell-signaling gene, and ASH is most probably a mammalian homologue of Sem-5. ASH bound in vitro to phosphotyrosine-containing proteins, including activated epidermal growth factor receptor, the ASH SH2 domain being responsible for the binding. Induced expression of an antisense ASH cDNA led to a reduction in cell growth. Considering these observations and the structural homology to Sem-5, ASH is likely to function as a ubiquitous signal transducer, possibly resembling Sem-5, which communicates between a receptor protein tyrosine kinase and a Ras protein.

Adaptor Proteins, Signal Transducing↗
PubMed1990

[A clinicopathological study of the spinal leptomeningeal dissemination from cerebral malignant gliomas without a recurrence of the primary lesions].

Reported are three cases of a spinal leptomeningeal dissemination from supratentorial malignant gliomas, in which the recurrence of the primary tumors of the intracranial leptomeningeal involvement was not observed clinicopathologically. All cases complained of spinal cord symptoms such as paraplegia or a sensory disturbance from time to time after the initial operation for their intracranial primary tumors. The duration between the first operation and the appearance of the spinal cord symptoms ranged from 11 to 17 months. In all cases, a computerized tomography scan demonstrated no recurrence of the primary tumor and no findings indicating intracranial leptomeningeal gliomatosis, such as a diffuse contrast enhancement of the ventricular wall or the subarachnoidal space, or hydrocephalus. Myelography showed a block or an irregular filling defect in two cases given immediate operations for spinal mass lesions. In one of these cases, a well-defined extramedullary tumor was removed at the level of the 7th-8th thoracic vertebrae. The pathological diagnosis was a glioblastoma multiforme, which was similar to the primary tumor. The patient survived for 18 months after total removal of the spinal tumor followed by postoperative spinal irradiation. All patients died of recurrent tumors from 3 to 18 months (mean: 8 months) after the appearance of the spinal cord symptoms. In the other case, an intramedullary tumor was found by a laminectomy. These two cases were autopsied. In one, an intramedullary tumor was found to extend from the lower medulla oblongata to the cervical cord, whereas the recurrence of the primary tumor was not seen and there was no intracranial leptomeningeal invasion nor any spinal subarachnoid seeding. The pathological diagnosis of this intramedullary tumor was a glioblastoma. In the other, there was a diffuse leptomeningeal dissemination of glioblastoma multiforme throughout the spinal cord, with an intramedullary invasion to almost all parts. A partial intracranial subarachnoid seeding of a malignant lower grade tumor than seen in the spinal lesion was found, though there was no recurrence of the primary tumor.

Adult↗
PubMed1989

Diacylglycerol, but not inositol 1,4,5-trisphosphate, accounts for platelet-derived growth factor-stimulated proliferation of BALB 3T3 cells.

Recently we found that an intracellular event related to phosphatidylinositol 4,5-bisphosphate (PIP2) is crucial for platelet-derived growth factor (PDGF)-induced mitogenesis in fibroblastic cells (Matuoka, K., et al.: Science 239:640-643, 1988). In the present study we examined the mitogenic effects of PIP2 and its hydrolysis products introduced into the cytoplasm of BALB 3T3 cells by micro-injection to confirm the role of PIP2 hydrolysis in PDGF stimulation of cell proliferation. Injection of 1,2-dioleylglycerol (diolein) into serum-deprived quiescent cells induced DNA synthesis with the same time course as that induced by exposure of the cells to PDGF and, in the presence of PDGF, caused no additional increase in the cell population entering S phase. The injection of PIP2, inositol 1,4,5-trisphosphate, or 1,2-dioleylphosphatidic acid into the cells did not induce mitogenesis. Consistent results were obtained in experiments in which the cells were exposed to 1-oleyl-2-acetylglycerol (OAG) and ionomycin; namely, OAG stimulated proliferation of BALB 3T3 cells, but ionomycin did not induce any mitogenesis. Desensitization of the protein kinase C pathway by prolonged exposure of the cells to phorbol ester abolished the induction of cell proliferation by subsequent injection of diolein or exposure to phorbol ester or OAG as well as by PDGF challenge. These findings strongly suggest that activation of the protein kinase C system following formation of diacylglycerol by PIP2 hydrolysis is mainly responsible for the mitogenic action of PDGF on BALB 3T3 cells.

Animals↗
PubMed1989

A decrease in hyaluronic acid synthesis by aging human fibroblasts leading to heparan sulfate enrichment and growth reduction.

Cultured normal human fibroblasts during in vitro aging exhibited increased proportions of heparan sulfate (HS; a glycosaminoglycan (GAG) species) in the cell-associated GAG pool, coincident with decreased cell growth activity. An analysis of GAG metabolism demonstrated that human fibroblasts during aging became relatively rich in HS due to an alteration in the profile of GAG synthesis. HS became relatively enriched and hyaluronic acid (HA) relatively depleted through a decrease in HA synthase activity. An experimental enrichment of human fibroblast cultures with exogenous HS brought about an arrest of the cells in the G0/G1 phase and a decrease in the rate of S phase entry, coincident with aged cell growth behaviour. These results suggest that the change in HA synthesis is responsible, at least to some extent, for the growth reduction during aging of normal human fibroblasts.

Cell Division↗
PubMed1989

[Milk of calcium renal stone: a case report].

A case of milk of calcium renal stone is presented. A 29-year-old woman complained of fever up and left lateral abdominal pain was diagnosis of milk of calcium renal stone. Ultrasonography showed hemispheric hypoechoic area and horizontal high echoic line with acoustic shadow. So-called "milk of calcium renal stone" is relatively uncommon and reports of ultrasonographic features are rare.

Acute Disease↗
PubMed1988

Mitogenesis in response to PDGF and bombesin abolished by microinjection of antibody to PIP2.

The turnover of phosphatidylinositol 4,5-bisphosphate (PIP2) is believed to constitute a crucial step in the signaling pathways for stimulation of cells by a variety of bioactive substances, including mitogens, but decisive evidence for the idea has not been obtained. In the present study, a monoclonal antibody to PIP2 was microinjected into the cytoplasm of NIH 3T3 cells before or after exposure to mitogens. The antibody completely abolished nuclear labeling with [3H]thymidine induced by platelet-derived growth factor and bombesin, but not by fibroblast growth factor, epidermal growth factor, insulin, or serum. The findings strongly suggest that PIP2 breakdown is crucial in the elicitation and sustaining of cell proliferation induced by some types of mitogens such as platelet-derived growth factor and bombesin.

Animals↗
PubMed1987

Hyaluronate synthetase inhibition by normal and transformed human fibroblasts during growth reduction.

To establish the relation of glycosaminoglycan synthesis to cell proliferation, we investigated the synthesis of individual glycosaminoglycan species by intact cells and in a cell-free system, using normal and transformed human fibroblasts under differing culture conditions. Reducing serum concentration brought about a marked decline in the synthesis of hyaluronate (HA) as well as cell proliferation on both normal and transformed cells. Both HA synthesis and proliferation decreased with increasing cell densities markedly (in inverse proportion to cell density) in normal cells but gradually in transformed cells. This noticeable congruity of the changes in HA synthesis and proliferation indicates that the change in HA synthesis is related primarily to cell proliferation rather than to cell density or cellular transformation. Examination of HA synthesis in a cell-free system demonstrated that the activity of HA synthetase also fluctuated in conjunction with cell proliferation. Furthermore, growth-reduced cells (except crowded transformed cells) inhibited cell-free HA synthesis and this inhibition was induced coincidentally with a decrease in both HA synthetase activity and proliferation. These findings suggest that the change in HA synthesis is significant in the regulation of cell proliferation.

Cell Division↗
PubMed1985

Cell surface changes in senescent and Werner's syndrome fibroblasts: their role in cell proliferation.

Cell surface is known to participate in the regulation of cell proliferation through interaction with adjacent cell surfaces or the extracellular matrix, or both. A clinical survey of the Werner syndrome suggests some disorders in glycosaminoglycan metabolism. Also, the skin fibroblasts derived from the patients with WS have a reduced proliferation capacity. We here examined, in vitro and in vivo, alterations of the cell-surface properties of WS cells and aging human fibroblasts. Cell-surface negative charges, examined by electrophoretic mobility of dispersed single cells in buffer, were seen to decline steadily as a function of cumulative population doublings. A strict linear relationship was found between electrophoretic mobility (micron/sec/V/cm) and number of cells harvested at each passage in all cell lines examined. The slope of this line in cells from donors of different ages indicated that WS fibroblasts resemble cells from much older normal controls. The same conclusion was drawn from our previous study of Con A-mediated red cell adsorption, which was confirmed as reflecting an alteration of cell-surface coat negative charge. Electrophoretic mobility after treatment of cell surface with degradative enzymes showed that the cell-surface negative charges were attributable to sialic acid, chondroitin sulphates, hyaluronic acid, and heparan sulphate. Two-dimensional electrophoresis of 3H-glucosamine incorporated glycosaminoglycans (GAGs) revealed that heparan sulphate was the main component of GAGs on the fibroblast cell surface and that the relative amount of heparan sulphate among GAGs on the cell surface increased in vitro with the number of passages. Growth kinetics of fibroblasts on sheets of fixed cells treated with a fixative (glutaraldehyde) and degradative enzymes were examined to elucidate the role of cell-surface GAGs in the regulation of cell proliferation. Cell growth was inhibited 40% when the fibroblasts were cultured on the fixed sheets of late passage cells. Treatment of the fixed cell sheets with heparitinase or nitrous acid resulted in complete recovery from the growth inhibition. Cell growth on sheets of fixed cells derived from young, middle, and senescent fibroblasts showed that the surface of the senescent cells had the greatest inhibitory effect. These inhibitory effects of fixed cell sheets correlated well with both the amount of heparan sulphate relative to the total GAGs on the surface and to the saturation density of cell growth at each passage. These findings strongly suggest that heparan sulphate, or its complex, on the cell surface is involved in the regulation of cell proliferation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

Growth-coupled changes in glucosaminoglycans (heparan sulfate and hyaluronic acid) in normal and transformed human fibroblasts.

Changes in glycosaminoglycans (GAGs) were investigated in relation to cell density, growth and transformation of human fibroblasts. Relative amounts (percentages of the total GAGs) of heparan sulfate (HS) increased and those of hyaluronic acid (HA) decreased in growth-reduced (serum-starved, exogenous HS-treated and dense) cultures of normal (WI-38) cells. In contrast, transformed (WI-38 CT-1) cells exerted such GAG changes only in serum-starved cultures, but not in HS-treated or dense cultures. These results indicate that the changes in glucosaminoglycans (G1cAGs) (HS and HA) is coupled exclusively with cell growth.

Animals↗
PubMed1985

Actions of exogenous heparan sulfate and hyaluronic acid on growth and thymidine incorporation of normal and transformed human fibroblasts. A comparison with the effects of high cell density and low serum concentration and a warning against thymidine incorporation as a measure of DNA synthesis.

Treatment of normal human (WI-38) cells with exogenous heparan sulfate (HS) reduced cell growth and incorporation of radio-isotope-labeled thymidine (TdR) into DNA. In spite that growth of their transformants (WI-38 CT-1) was enhanced by HS treatment, transformed cells also decreased in TdR incorporation thereby. This peculiar observation was explained by a reduction of TdR uptake, leading to a decrease in specific radioactivity of newly synthesized DNA. The changes in cell growth and TdR incorporation by HS treatment were revealed to be similar to the changes with increasing cell density rather than by serum starvation.

Biological Transport↗