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M L Katayama

Publications and source records attributed to M L Katayama.

12 recordsLinked to original sources
PubMed2001

Human semaphorin 6B [(HSA)SEMA6B], a novel human class 6 semaphorin gene: alternative splicing and all-trans-retinoic acid-dependent downregulation in glioblastoma cell lines.

We have identified a novel human gene related to the class 6 semaphorin family of axon guidance molecules, termed human semaphorin 6B or (HSA)SEMA6B. Two splicing variants of this gene were identified by RT-PCR: (HSA)SEMA6B.1 (short isoform) and (HSA)SEMA6B.2 (longer isoform). Computational analysis suggests that these isoforms correspond to putative secreted and transmembranous semaphorins, respectively. The levels of (HSA)SEMA6B expression were evaluated by Northern blot analysis in different tissues and in some pathological and pharmacological conditions. We observed that (HSA)SEMA6B is highly expressed in human brain and at lower levels in a variety of other tissues. Interestingly, the (HSA)SEMA6B transcript was downregulated in two different human glioblastoma cell lines (T98G and A172) upon prolonged treatment with all-trans-retinoic acid, an anti-tumor and differentiation-inducing agent.

Alternative Splicing↗
PubMed2000

Differential regulation of vitamin D receptor expression in distinct leukemic cell lines upon phorbol ester-induced growth arrest.

A close correlation between vitamin D receptor (VDR) abundance and cell proliferation rate has been shown in NIH-3T3 fibroblasts, MCF-7 breast cancer and in HL-60 myeloblastic cells. We have now determined if this association occurs in other leukemic cell lines, U937 and K562, and if VDR content is related to c-myc expression, which is also linked to cell growth state. Upon phorbol myristate acetate (PMA) treatment, cells from the three lineages (HL-60, U937 and K562) differentiated and expressed specific surface antigens. All cell lines analyzed were growth inhibited by PMA and the doubling time was increased, mainly due to an increased fraction of cells in the G0/G1 phase, as determined by flow cytometry measurements of incorporated bromodeoxyuridine and cell DNA content. C-myc mRNA expression was down-regulated and closely correlated to cell growth arrest. However, VDR expression in leukemic cell lines, as determined by immunofluorescence and Northern blot assays, was not consistently changed upon inhibition of cell proliferation since VDR levels were down-regulated only in HL-60 cells. Our data suggest that VDR expression cannot be explained simply as a reflection of the leukemic cell growth state.

Antibodies, Monoclonal↗
PubMed1998

Expression of vitamin D receptor (VDR) in HL-60 cells is differentially regulated during the process of differentiation induced by phorbol ester, retinoic acid or interferon-gamma.

The effects of three inducers of differentiation, phorbol myristate acetate (PMA), retinoic acid (RA) and interferon-gamma (IFN-gamma), on the temporal regulation of vitamin D receptor (VDR) expression in HL-60 cells were analyzed by Northern blotting and immunofluorescence assays. VDR, at the protein level, expressed by 81% of uninduced cells, was reduced to 57% after 48 h of PMA or 96 h of RA treatment, preceded by growth inhibition and cell differentiation, evaluated by CD11b expression. Sorted CD11b positive cells in G0/G1 phase exhibited 53% the VDR content of CD11b negative cells (distributed throughout the cell cycle). PMA also induced an increase in PKC beta and PKC alpha mRNA and protein. Simultaneous exposure to PMA and sphingosine blocked stimulation of CD11b and PKC expression without affecting growth arrest and VDR down regulation. Similar effects were observed during sphingosine treatment. In IFN-gamma differentiated cells, the proportion of cells in G0/G1 phase was unchanged and VDR protein was unaltered as compared to uninduced cells. Control cells in G0/G1 expressed less VDR than cells in S and G2/M phases (74% and 59% respectively). All results suggest that in HL-60 cells, reduction of VDR expression is related to growth inhibition rather than to the differentiation process.

Cell Cycle↗
PubMed1998

Eosinophil accumulation in rat uterus following estradiol administration is modulated by laminin and its integrin receptors.

Eosinophils accumulate into the uterus of ovariectomized rats, after treatment with estradiol (E2). We have investigated whether this feature is related to interactions of eosinophils with uterine extracellular matrix proteins: laminin (LM) and fibronectin (FN). Eosinophils isolated from the peritoneal cavity of ovariectomized rats displayed estrogen receptors measured at both binding activity and mRNA levels. An increased number of laminin binding sites, calculated by Scatchard analysis using iodinated LM was determined in E2-treated eosinophils (70,100 +/- 28,000 sites/cell vs 21,000 +/- 5,000 sites/cell in controls). Eo binding to 125I-LM- was inhibited by the E8-LM fragment. Estradiol up-regulated the expression in eosinophils of alpha 6 and beta 2 integrin subunits evaluated by flow-cytometry as well as by alpha 6 mRNA expression. After E2 treatment, eosinophils showed higher adhesiveness to LM-coated dishes (10 +/- 2 vs 56 +/- 3%) which was inhibited by monoclonal antibodies against alpha 6, beta 1 and beta 2 integrins and by the steroid antagonist tamoxifen. These monoclonal antibodies also blocked the attachment of stimulated eosinophils to uterine cryostat sections obtained from spayed rats previously treated with estradiol. We did not detect any apparent influence of E2 on basal eosinophil adherence or binding to FN although alpha 4 and alpha 5 integrin subunits were expressed in eosinophils. Expression of laminin and merosin in the uterus was determined immunohistochemically. Our results suggest that integrin-laminin interactions may contribute to the preferential eosinophil recruitment in vivo.

Animals↗
PubMed1994

Integrin receptors and TGF-beta expression in chronic myeloid leukemia cells.

To understand the relationship between transforming growth factor beta-1 (TGF-beta 1) and the integrin profile presented by chronic myeloid leukemia cells, we have studied, using Northern analysis, the expression of TGF-beta 1 messenger RNA (TGF-beta mRNA) in myeloid cell lines and in patients with acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). In addition we determined the positivity for alpha 4 and alpha 5 integrin molecules in those cells using specific monoclonal antibodies and flow cytometry. CML patients (N = 3) presented mean values of alpha 4 and alpha 5 higher (alpha 4: 60 +/- 20%; alpha 5: 70 +/- 41%) than AML (N = 10) blast cells (alpha 4: 25 +/- 23%; alpha 5: 18 +/- 16%). Northern analysis revealed an almost four-fold higher expression of TGF-beta mRNA in K562 (derived from a patient with chronic myeloid leukemia) compared to the myeloblastic cell line HL60. The highest TGF-beta mRNA levels were seen in the U937 lineage. CML leukemic cells (N = 3) showed high TGF-beta mRNA levels comparable to the levels expressed by K562 which was paralleled by high beta 1 integrin mRNA. AML blast cells presented a variable degree of expression of TGF-beta mRNA when compared to HL60. One patient with acute megakaryoblastic leukemia (FAB subtype M7), usually associated with myelofibrosis, presented the highest TGF-beta mRNA levels. We conclude that studying TGF-beta 1 and its mechanisms of action will help in understanding fibrosis in leukemic patients, and perhaps to design treatments for such conditions.

Humans↗
PubMed1993

Vitamin D3 binding activity during leukemic cell differentiation.

In this paper we report that differentiation of the human promyelocytic leukemia cell line, HL60, along the myelocytic pathway, induced by retinoic acid (RA), or monocytic pathway, induced by phorbol-myristate acetate (PMA) and gamma interferon (IFN), was accompanied by a significant decline in 1,25-dihydroxycholecalciferol (1,25(OH)2D3) binding (control: 30.3 +/- 3.0 fM/10(6) cells; RA treated: 6.8 + 2.5 fM/10(6) cells; PMA treated: 12.3 +/- 6.7 fM/10(6) cells and IFN treated: 16.0 +/- 5.0 fM/10(6) cells). When differentiation and proliferation were uncoupled, by incubation with IFN or by inhibition of proliferation by cell density saturation, 1,25(OH)2D3 binding was better related to differentiation than to proliferation. Additionally we have compared 1,25(OH)2D3 binding levels in blasts from acute lymphocytic leukemia (ALL) patients (25.4 +/- 18.1 fM/10(6) cells) and normal, mature lymphocytes (10.6 +/- 2.1 fM/10(6) cells). Receptor binding was significantly higher (p < 0.05) in the immature blasts. Our data suggest that 1,25(OH)2D3 receptor levels could be considered a marker of functional immaturity, in these cells.

Calcitriol↗
PubMed1993

Glucocorticoid receptors in mononuclear cells of patients with sepsis.

Glucocorticoid receptor (GR) hormone-binding activity was studied by a whole-cell method in mononuclear cells (MNC) from peripheral blood of 7 patients during the hemodynamic compensatory phase of sepsis. 4 patients were receiving dopamine, which did not affect the GR count. The patients' plasma cortisol concentrations were normal or slightly elevated. Despite a wide range, the mean GR count and affinity in MNC from septic patients did not differ from those in normal controls, suggesting that glucocorticoids could still be effective in the hemodynamic compensatory phase of sepsis.

Adult↗
PubMed1993

Differential expression of fibronectin receptors during myeloid differentiation and in marrow- and peripheral blood-derived leukemic cells.

A 125I-labeled 120-kDa fibronectin fragment (FN120) containing the RGD binding site was employed to assess FN120 receptor levels in control and dimethylsulfoxide (DMSO)-differentiated HL60 cells, as well as in leukemic peripheral and bone marrow blast cells from acute lymphoid (ALL) and myeloid (AML) patients. Fibronectin CS1 fragment receptor alpha 4 (VLA4-alpha) and RGD-dependent alpha 5 integrin subunits (VLA5-alpha) were characterized by specific monoclonal antibodies (MoAb). HL60 cells, induced along the granulocytic pathway with DMSO, displayed low FN120 binding level densities (36,070 +/- 5142 sites/cell (s/c) vs. 19,780 +/- 4564 s/c, P < 0.005), respectively, for untreated and treated cells) together with decreased VLA5-alpha expression. Granulocytes displayed low levels of FN120 receptors (3167 +/- 1165 s/c) with weak VLA5-alpha expression and absence of VLA4-alpha. Normal lymphocytes displayed 17,670 +/- 8,705 s/c FN120 receptors and VLA4-alpha and VLA5-alpha. The mean FN120 binding levels and mean VLA5-alpha expression were lower in peripheral blast cells, both in ALL and AML, than in the bone marrow leukemic cells. VLA4-alpha remained the same irrespective of cell localization. FN120 binding sites and differential expression of VLA4-alpha and VLA5-alpha integrin molecules on hemopoietic cells could be related to lineage characteristics or cell type distribution within hemopoietic tissue.

Adolescent↗
PubMed1991

Increased expression of laminin receptors during myeloid differentiation.

Variation of laminin receptor levels (LNR) during myeloid-cell differentiation and in acute leukemia were investigated by 125I-laminin-binding determination during HL60 cell differentiation and in cells of patients with different types of leukemia, characterized according to the FAB classification. LNR levels in HL60 cells increased during differentiation, being significantly higher in cells exposed to phorbol myristate acetate (PMA) and ethanol (55,391 +/- 27,845 and 29,314 +/- 6,435 sites/cell respectively) as compared with HL60 controls (8,549 +/- 4,000 sites/cell). The control cells do not adhere to laminin-coated surfaces, but differentiation with PMA results in their rapid adherence on this substratum. Short treatment with PMA does not increase the number of adherent cells or the receptor expression. Granulocytes also presented equally high LNR concentration (29,739 +/- 13,516 sites/cell). The lymphoid cells (lymphocyte, acute lymphoid leukemia and chronic lymphocytic leukemia) shared low LNR numbers (less than 6,500 sites/cell). Myeloid cells displayed a wide range of LN receptors with higher levels being associated with the more differentiated FAB subgroups. 125I-laminin binding to lymphoid or myeloid leukemic cells was mainly inhibited by P1 fragments, whereas granulocytes and differentiated HL60 cells displayed a dual binding pattern for laminin fragments P1 and E8. These results were confirmed by assays using 125I-labelled P1 and E8 fragments. We conclude that magnitude of LNR levels and variation in expression of P1 and E8 receptors appear to be linked to lineage and maturation status in hematopoietic cells.

Adolescent↗
PubMedDate not supplied

Correction of Stahl's Ear.

Stahl's ear is a rare congenital anomaly difficult to correct surgically. This report presents the experience of the Division of Plastic Surgery, University of São Paulo Medical School for managing this anomaly. From January 1994 to September 1999, 15 patients underwent surgery (17 ears). Ages ranged from 7 to 22 (mean 15 years). Six patients were female. Four subjects were of Oriental descent, four were Negroes, and seven were Caucasians. Deformities included two bilateral, four on the left ear, and nine on the right one. Different methods were utilized for correction depending on the elasticity of the cartilage. In the presence of an elastic cartilage, sutures only are employed, otherwise the cartilage is repositioned, as described by Sugino et al. No standard characteristics were noted regarding gender or race, however, there were more unilateral cases and more on the right ear. The results were adequately satisfactory, with the two methods enabling us to recommend these surgical techniques for correction of Stahl's ear.

Ear, External↗
PubMedDate not supplied

Effects of retinoic and glycolic acids on neoangiogenesis and necrosis of axial dorsal skin flaps in rats.

Retinoic acid (RA) and glycolic acid (GA) are frequently used in the treatment of acne and skin aging, as well as improving skin healing after dermabrasion and in photoaged skin. Examples of histologic alterations caused by these substances are vascularization increase and interference with inflammatory as well as regenerative skin processes. The objective of this study was to evaluate the possible decrease of skin flap necrosis areas in rats, by applying both substances to the skin 14 and 30 days before surgery, and analyzing histopathologic skin alterations after treatment. Fifty Wistar rats were divided into five groups of 10 animals each. They received daily retinoic acid application for 14 and 30 days, daily glycolic acid application for 14 and 30 days, and vehicle application (control group) for 14 days. After treatment, each rat was submitted to random dorsal skin flap (10 x 3 cm) elevation; flaps were sutured back in place over isolating plastic strips. The rats were sacrificed after 7 days and flap necrosis areas were measured through transparency and then analyzed using computer scanning. Statistical analysis was carried out using monocaudal nonpaired t tests and histopathologic examination was performed in all cases. Compared with the control group, treatment with both acids did not decrease average flap necrosis areas. Though groups RA 30 days and GA 14 days presented larger necrosis area averages (p < 0.05), groups RA 14 days and GA 30 days showed no statistically significant difference (p > 0.05) when compared to the control group. Both substances caused spongiosis, stratum corneum thickening, and vascularization increase, with GA inducing greater granulomatous reaction and RA more spongiosis and queratinization. Group RA 30 days showed the most significant dermo-epithelial (including vascular) regenerative and proliferative effects. Retinoic and glycolic acid treatment led to significant and well-known skin alterations, with group RA 30 days showing most notable dermo-epithelial proliferative effects. In our experimental model, preoperatory RA and GA application did not decrease rat dorsal skin flap necrosis area when compared to the control group.

Animals↗