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Biomedical subjects

Y Kitajima

Publications and source records attributed to Y Kitajima.

At least 37 records · Page 2Linked to original sources
PubMed2001

Cyclic changes in expression of mRNA of vascular endothelial growth factor, its receptors Flt-1 and KDR/Flk-1, and Ets-1 in human corpora lutea.

OBJECTIVE: To evaluate the expression of mRNA of vascular endothelial growth factor (VEGF), its receptors Flt-1 and KDR/Flk-1, and Ets-1 in human corpora lutea. DESIGN: Prospective laboratory study. SETTING: University hospital in Japan. PATIENT(S): Women with regular menstrual cycles who underwent hysterectomy. INTERVENTION(S): Fifteen corpora lutea were obtained during hysterectomy (5 in the early luteal phase, 5 in the mid-luteal phase, and 5 in the late luteal phase). MAIN OUTCOME MEASURE(S): Expression of VEGF, Flt-1, KDR/Flk-1, and Ets-1 in human corpora lutea on northern blot analysis or immunohistochemistry. RESULT(S): Human corpora lutea in early luteal phase and mid-luteal phase had high VEGF mRNA expression. Expression of VEGF mRNA was significantly reduced in the late luteal phase. Immunohistochemistry showed that VEGF protein was expressed mainly in granulosa lutein cells and faintly in thecal lutein cells. Staining of VEGF protein was decreased in human corpora lutea in the late luteal phase. Expression of Flt-1 and KDR/Flk-1 mRNA was increased in the early luteal phase and mid-luteal phase and decreased in the late luteal phase. Immunohistochemistry showed that Flt-1 and KDR/Flk-1 proteins were expressed mainly in granulosa lutein cells and faintly in thecal lutein cells and endothelial cells in the early luteal phase and mid-luteal phase; their protein staining was reduced in the late luteal phase. Expression of Ets-1 mRNA changed similarly to VEGF and its receptor mRNA in human corpora lutea during the luteal phase. CONCLUSION(S): Levels of mRNA of VEGF and its receptors Flt-1 and KDR/Flk-1 in human luteal cells may be related to luteal function.

Blotting, Northern↗
PubMed2001

Transient translocation of hemidesmosomal bullous pemphigoid antigen 1 from cytosol to membrane fractions by 12-O-tetradecanoylphorbol-13-acetate treatment and Ca2+-switch in a human carcinoma cell line.

We previously showed that 12-O-tetradecanoylphorbol-13-acetate (TPA) and Ca2+-switch from low (0.07 mM) to normal (1.87 mM) concentration in culture medium, which were also linked to activation of protein kinase C (PKC), lead to phosphorylation of 180 kDa-bullous pemphigoid antigen (BPAG) 2, but not of 230 kDa-BPAG1, and possibly to its disassembly from hemidesmosomes in a human squamous cell carcinoma cell line (DJM-1). In this study, we examined the effects of TPA and Ca2+-switch on intracellular localization of BPAG1 by immuno-blotting and immuno-fluorescence microscopy with monoclonal antibodies to the antigen after sub-cellular fractionation. In DJM-1 cells cultured in low Ca2+ medium, BPAG1 was detected as phosphate buffered saline-soluble (cytosolic), Triton X-100 soluble (roughly membrane-associated) and Triton X-100 insoluble (cytoskeleton-bound) forms, whereas in normal Ca2+-grown cells only as cytosolic and cytoskeleton-bound forms. In normal Ca2+-cultured cells, TPA (50 nM) caused a complete translocation of BPAG1 from cytosol to membrane fractions within 10 min, that was inhibited by pretreatment with H7 (a selective PKC inhibitor) at 40 microM. After 30 min and 4 h of TPA-treatment, BPAG1 was exclusively detected in cytoskeleton fractions. Morphologically, immuno-fluorescence microscopy showed that treatment caused a marked reduction of BPAG1 from the cytoplasm and generated a linear pattern at cell-cell contacts, suggesting translocation of BPAG1 from the cytosol to the plasma membrane. In contrast, the Ca2+-switch from low to normal caused a prominent increase of BPAG1, both in cytosolic and membrane-associated forms after 4 h, that was inhibited both with H7 and cycloheximide (an inhibitor of protein synthesis) at 70 microM, suggesting a role for PKC and BPAG1 synthesis in these Ca2+-induced effects. These results suggest that TPA and Ca2+-switch induced BPAG1 translocation to membrane fractions possibly mediated by PKC-activation. Furthermore, whereas TPA affects the redistribution of BPAG1 among their pools without inducing their synthesis, Ca2+-switch induces both membrane translocation and synthesis of BPAG1, suggesting involvement of signaling other than PKC pathways in control of BPAG1 synthesis.

Autoantigens↗
PubMed2001

"Apocrine" poroma: review of the literature and case report.

BACKGROUND: "Apocrine" poroma has recently been proposed as a new term to designate a distinctive benign skin neoplasm with differentiation toward the folliculosebaceous-apocrine unit. CASE REPORT: In support of alternative differentiation, a case of apocrine poroma is reported in a 73-year-old man. A nodule on the right upper abdomen, which was thought clinically to be seborrheic keratosis or basal cell epithelioma, was excised. HISTOLOGY: Histologically, this neoplasm heterogeniously consisted of poroma-like, sebaceous and follicular epithelial components. Since these components share the common embryologic origin of the folliculosebaceous-apocrine unit, this histologic pattern indicates apocrine differentiation of the tumor. CONCLUSION: This is an additional case to support the term "apocrine" poroma as a diagnosis.

Acrospiroma↗
PubMed2001

Chemotherapy induces or increases expression of multidrug resistance-associated protein in malignant melanoma cells.

BACKGROUND: Human malignant melanoma is notoriously resistant to chemotherapeutic agents. Melanoma-derived cell lines are often markedly chemoresistant, suggesting that cellular mechanisms mediate generation of the multidrug resistance (MDR) phenotype. This phenotype is often due to P-glycoprotein (Pgp) and the MDR-associated protein (MRP), which are drug transporter proteins associated with resistance to a broad spectrum of lipophilic drugs. OBJECTIVES: To determine the relationships between the expression of the MDR gene MDR-1 (the product of which is Pgp) or the MRP gene, and clinical chemoresistance of malignant melanoma. METHODS: We examined changes in the expression of MDR-1 and MRP genes at the mRNA level before and after chemotherapy by reverse transcription-polymerase chain reaction (RT-PCR) analysis using formalin-fixed, paraffin-embedded sections of 18 specimens taken from eight melanoma patients. mRNA expression of the MDR-1 and MRP gene-specific PCR products was quantitatively determined by densitometry and compared with that of an internal standard (beta-actin). RESULTS: Five of seven primary melanomas were found to express the MRP gene to a certain extent even before chemotherapy. After first and second courses of chemotherapy, six patients had an increased ratio of MRP mRNA to beta-actin mRNA compared with the prechemotherapy levels in the same patients. None of the cases of melanoma expressed MDR-1. CONCLUSIONS: These results suggest that a significant mRNA level of MRP gene was intrinsically present in malignant melanoma even before exposure to chemotherapeutic drugs and increased in its expression after chemotherapy, suggesting that MRP plays a part in increasing the chemoresistance of malignant melanoma during chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

An extremely severe case of cutaneous calcinosis with juvenile dermatomyositis, and successful treatment with diltiazem.

A case of cutaneous calcinosis associated with juvenile dermatomyositis is described. The patient was a 3-year-old girl who had been diagnosed as having dermatomyositis at age 1 year. She was treated with prednisolone, but developed multiple calcified nodules in the subcutaneous tissues and intermuscular fascia. These nodules gradually increased in size despite continual therapy with steroids and aluminium hydroxide. Treatment with diltiazem completely suppressed the development of calcinosis.

Calcinosis↗
PubMed2001

Phosphatidylinositol-specific-phospholipase C cleaves urokinase plasminogen activator receptor from the cell surface and leads to inhibition of pemphigus-IgG-induced acantholysis in DJM-1 cells, a squamous cell carcinoma line.

We showed previously that pemphigus IgG enhanced both the activity of urokinase plasminogen activator (uPA) in cultured cells and the expression of its receptor (uPAR) on uPA-binding keratinocytes. In the present study, to clarify whether uPAR and uPA-activated plasmin are actually involved in the blistering process after pemphigus IgG binding to the cell surface, we examined the effects of the following on uPAR expression and on cell-cell detachment in DJM-1 cells, a squamous cell carcinoma line: (i) phosphatidylinositol-specific phospholipase C (PI-PLC) - which releases uPAR from the membrane surface into the culture medium by cleaving the glycosylphosphatidylinositol anchor thus inhibiting uPAR activity, and (ii) uPA inhibitors (tranexamic acid, aprotinin, p-aminobenzonic acid and dexamethasone). Preincubation with PI-PLC decreased dramatically the pemphigus IgG-induced uPAR expression in a dose-dependent manner, and inhibited pemphigus IgG-induced cell-cell detachment at 10 microg/mL. On the other hand, tranexamic acid (15 mM) inhibited pemphigus IgG-induced cell-cell detachment without reduction of uPAR expression, although aprotinin, p-aminobenzonic acid and dexamethasone failed to alter either of these parameters. Although uPAR expression on the pemphigus IgG-bound cell surface and uPA activation may contribute significantly to the pathogenesis of acantholysis in pemphigus, the mechanisms are complicated and should be defined further.

Acantholysis↗
PubMed2001

TBP-interacting protein TIP120A is a new global transcription activator with bipartite functional domains.

BACKGROUND: We previously identified a TBP (TATA-binding protein)-interacting protein 120A (TIP120A) from rat liver nuclear extracts. TIP120A is thought to be a unique global transcription factor that can interact with TBP and can stimulate all classes of eukaryotic transcription. RESULTS: We produced various truncation proteins of TIP120A to delineate its functional domains. TIP120A binds to TBP in the acidic amino acid-rich N-terminal region and in the leucine-rich C-terminal region. These regions exhibited an ability to stimulate basal transcription in vitro. In addition, these two regions overlap with domains that facilitate nonspecific DNA-binding of RNA polymerase II. The sequences of these two regions are significantly conserved among TIP120A homologues of eukaryotes. CONCLUSIONS: TIP120A is a bipartite transcription factor, and both N-terminal and C-terminal regions exhibit TBP-binding activity and stimulate the basal transcription ability.

Amino Acid Sequence↗
PubMed2001

Lysyl oxidase and MMP-2 expression in dehydroepiandrosterone-induced polycystic ovary in rats.

Polycystic ovary syndrome (PCOS) is characterized by cystogenesis; however, the cause of this cystogenesis is unknown. At ovulation, preovulatory collagenolytic activities in the ovarian follicles increase and various proteinases are needed to degrade the tissues surrounding the follicles. To clarify the roles of enzymes in collagen degradation of the follicular wall of polycystic ovary (PCO) in relation to the cystogenesis, we examined expression of lysyl oxidase (LOX), which initiates cross-link formation of the collagen and elastin in the extracellular matrix, and expression of matrix metalloproteinases (MMPs) in ovaries of model rats with PCO induced by dehydroepiandrosterone (DHEA) compared with MMP expression in control rats. DHEA treatment increased LOX mRNA expression to more than three times the control value (P: < 0.01). MMP-2 mRNA expression in control rats was threefold greater than that in the DHEA-induced group (P: < 0.05). Expression of both latent and active forms of MMP-2 in controls was more than twice that in the DHEA-induced group (P: < 0.05) as shown by Western blotting, and expression of the active form of MMP-2 was also twice as high in the controls as in the DHEA-treated group (P: < 0.05) as shown by zymography. Our results suggest that depression of MMP-2 activity and increased LOX expression may be one of the causes of the cystogenesis of PCO.

Androstenedione↗
PubMed2001

Surfactant protein D (SP-D) and systemic scleroderma (SSc).

We measured serum levels of SP-D in collagen diseases (110 cases) such as systemic scleroderma (SSc), scleroderma spectrum disorders (SSD), systemic lupus erythematodes (SLE), Sjogren syndrome (Sjs), dermatomyositis (DM), rheumatoid arthritis (RA), and dermatitis (DE) (109 cases) as a control. Additionally, we performad a correlation analysis to determine how these levels were related to pulmonary fibrosis and function test (vital capacity, %DLco). The serum levels of SP-D increased in SSc patients with Barnett type III more than in SSc patients with Barnett type I or II, while they increased slightly in SSD (incomplete type of SSc) patients. The differences in these figures were statistically significant between the SSc (SSc & SSD) and non-SSc (SLE, DM, Sjs & RA) groups (p<0.005). The serum levels of SP-D in SSc patients with anti-topoisomerase I antibodies were statistically higher than those in SSc patients with other types of anti-nuclear antibodies. There was a statistically significant correlation between the severity of pulmonary fibrosis and the serum levels of SP-D, and a statistically negative correlation between SP-D levels and vital capacity or %DLco, but there was no proportional correlation with the forced expiatory volume (FEV1.0%). There was no statistical relationship between pre- and post-therapy with photopheresis; however, there was a statistical correlation between the serum levels of SPD and KL-6. In the group of collagen diseases, plasma levels of SP-D were higher than serum levels of SP-D. Patients with SSc possess higher levels of SP-D than do those with other collagen diseases and dermatitis, which may correspond to the severity of pulmonary fibrosis.

Adolescent↗
PubMed2001

The number and distribution of Merkel cells in rudimentary polydactyly.

BACKGROUND: Rudimentary polydactyly histologically reveals a marked neural proliferation in the dermis and a large number of Meissner corpuscles in the dermal papillae. OBJECTIVE: Our study was performed to determine whether this neural proliferation is related to Merkel cells. METHOD: Using an antibody to cytokeratin 20, we examined the number and distribution of Merkel cells in 5 cases of rudimentary polydactyly, including an immature case without Meissner corpuscles. RESULTS: Only the case without Meissner corpuscles had a markedly large number of Merkel cells and some dermal Merkel cells. CONCLUSION: The normal number of Merkel cells in the mature cases suggests that abundant Merkel cells may appear at first and disappear after the development of neural proliferation. Merkel cells may be associated with the generation of cutaneous nerve plexus and nerve endings in the upper dermis, and possibly with the development of Meissner corpuscles, at the early stage of rudimentary polydactyly.

Adult↗
PubMed2001

Successful extracorporeal shock wave lithotripsy for sibling pancreatic duct stones.

We present a case of 2 brothers with idiopathic chronic pancreatitis associated with pancreatic duct stones which could be successfully disintegrated by extracorporeal shock wave lithotripsy (ESWL). An obvious etiology for the pancreatolithiasis, like alcohol or biliary disease, was lacking and point mutations of the cationic trypsinogen gene exons 2 and 3 were not detected in the long arm of the 7th chromosome. However, a hereditary etiology could not be precluded since pancreatolithiasis occurred in the siblings. There has been no recurrence of pancreatic stones during 42 months of follow-up periods, for both. ESWL, the least invasive therapy, appeared applicable and effective for pancreatolithiasis in the present cases.

Adult↗
PubMed2001

[Ultrastructure and molecular biochemistry on pathogenic fungal cells: the architecture of septal cell walls of dermatophytes].

This review provides abstracts of our research for which the year 2000 prize of The Japanese Society for Medical Mycology was awarded. The study consists of 4 fields: 1)Ultrastructure and biochemistry of the cell walls of dermatophytes. 2) Freeze-fracture electron microscopic study on the membrane systems of pathogenic fungi. 3) Action mechanisms of antifungal agents in terms of membrane structure and functions. 4) Dimorphism and virulence of pathogenic fungi in terms of molecular biology of membrane lipids. Since the detailed contents of these studies were reported in my previous review article (Jpn J Med Mycol 41: 211-217, 2000), I would like to mention these studies only briefly here, together with a detailed review of the septal cell wall architecture of dermatophytes, which I did not cover in my earlier articles.

Antifungal Agents↗
PubMed2001

Exogenous expression of E-cadherin in gallbladder carcinoma cell line G-415 restores its cellular polarity and differentiation.

E-cadherin (E-cad) is critical for the development and maintenance of polarity and differentiation of epithelial cells. Our previous study revealed gallbladder (GB) cancer cell lines expressing E-cadherin could form cystic or spheroid-like structures in a 3-D matrix. This differentiated phenotype was disrupted by addition of anti-E-cad antibody. By extrapolation, we postulated that E-cad might directly regulate epithelial morphogenesis in GB carcinoma. In the present study, we introduced an expression plasmid harboring mouse E-cad cDNA (pBATEM2) into an undifferentiated GB cancer cell line (G-415) which did not express E-cad. We systemically compared differences including cell phenotype, morphogenesis, and ultrastructure between the parental G-415 cells (parental-cells) and E-cad transfected cells (E-cad-cells) under various conditions such as monolayer culture, 3-D gel culture as well as inoculation of nude mice. In contrast to parental-cells, E-cad-cells presented a typical epithelial shape with tight intercellular connections in monolayer culture. They developed round multicellular cystic structures in 3-D gel. The cysts secreted mucous substances via the apical surface into the cystic lumen, in which the substances were positively stained by alcian blue (pH 2.5). Ultrastructural sections of gel/xenograft tumor revealed re-establishment of adherens junctions and restoration of cell polarization. Immunohistochemical and immunofluorescent staining showed exogenous E-cad primarily accumulated at the extended cell-cell contact sites. Moreover, the membranous translocation of alpha-, and beta-catenin from cytoplasm was also found in 3-D matrix and xenograft tumor sections. Histopathologic examination revealed papillary adenocarcinoma features in the central region of the xenograft tumors. Our results demonstrate that exogenous expression of E-cad in undifferentiated GB cancer G-415 cells reverses differentiated characteristics in spatial growth conditions. Simultaneous translocation of alpha-, beta-catenin to membrane following functional E-cad expression may be a critical event for this process.

Adenocarcinoma, Papillary↗
PubMed2000

Establishment and characterization of human hilar bile duct carcinoma cell line and cell strain.

We established and characterized a human hilar bile duct carcinoma (HBDC) cell line from cells isolated from the ascites of a 75-year-old Japanese woman. Histopathological findings were confirmed to be poorly differentiated adenocarcinoma (pat BsrlCm according to the Japanese Society of Biliary Surgery General rules for surgical and pathological studies on cancer of the biliary tract, 4th edn.). Using a semi-agarose method, a daughter-cell strain was also established. Both the cell line and the strain were transplanted into scid or nude mice with a 100% inoculation rate. The population doubling times of the cell line and the strain were 32.25 and 35.78 h, respectively. The cell line and strain strongly expressed human epithelial antigen (HEA)-125 and cytokeratin (CK)-19 but did not express desmin and partly expressed vimentin. High values tumor markers (carbohydrate antigen [CA19-9], Span-1, KMO-1) were detected in culture supernatants from both the cell line and the cell strain and the concentrations paralleled the patient's serum data. DNA analysis revealed that the cell strain was diploid, whereas the cell line was aneuploid, with a DNA index (DI) of 0.85. Chromosomal analysis of the cell line and the strain revealed a range of numerical abnormalities (76-93 and 74-88, respectively) as well as structural abnormalities. The establishment of this HBDC cell line and strain may provide some benefit for fundamental biological research.

Adenocarcinoma↗
PubMed2000

Loss of heterozygosity of adenomatous polyposis coli gene in cutaneous tumors as determined by using polymerase chain reaction and paraffin section preparations.

It has been suggested that an alteration in the adenomatous polyposis coli (APC) gene, which is a tumor suppressor gene, is one of the earlier events in carcinogenesis of some adenocarcinomas. We undertook this study to determine the prevalence of loss of heterozygosity (LOH) of the APC gene in several kinds of cutaneous tumors. Fifty-seven unrelated Japanese patients were examined for analysis of the APC gene. The 57 cases consisted of extramammary Paget's disease, squamous cell carcinoma (SCC), eccrine poroma and porocarcinoma, metastatic tumor of rectal adenocarcinoma and malignant melanoma. DNA was extracted from the tumor and normal portions dissected from the formalin-fixed paraffin-embedding sections and amplified with the use of the PCR. The amplified DNA was examined for LOH in the APC gene. Seven samples of 32 heterozygous persons of APC gene (three out of seven eccrine poromas, two eccrine porocarcinomas and two metastatic tumors of rectal adenocarcinoma) showed for LOH in the APC gene. None of the heterozygous samples from the extramammary Paget's disease (11), SCC (five) and melanoma (five) showed LOH. These results suggest that tumor or tumor suppressor genes, other than the APC gene, may be responsible for extramammary Paget's disease and SCC and that LOH involving APC may have some relevance to the formation and progression of eccrine tumors as in rectal tumors.

Adenomatous Polyposis Coli Protein↗
PubMed2000

Assembly pathway of desmoglein 3 to desmosomes and its perturbation by pemphigus vulgaris-IgG in cultured keratinocytes, as revealed by time-lapsed labeling immunoelectron microscopy.

To determine the assembly pathway of desmoglein 3 (Dsg3) into desmosomes and the subsequent effects of pemphigus vulgaris immunoglobulin G (PV-IgG) on such, we employed a time-lapsed labeling for FITC/Rhodamine (Rod) double-stained immunofluorescence and 5-nm/10-nm gold double-stained immunoelectron microscopy by using PV-IgG, which was confirmed to react specifically Dsg3. Cells from a human squamous cell carcinoma cell line (DJM-1) were first treated briefly with PV-IgG (3 min), then incubated in either anti-human IgG-FITC or 5-nm gold antibody-containing medium (5 min), followed by a 60-minute chase in normal medium without antibodies. The same cells were reincubated with PV-IgG medium for 3 minutes, followed by either anti-human IgG-Rod or 10-nm gold antibodies for 5 minutes. Using this method, FITC and 5-nm gold particles show the fate of Dsg3-PV-IgG complexes during the following 60-minute chase. IgG-Rod or 10-nm gold particles, which are bound during the last 5 minutes of the chase, show Dsg3 molecules newly expressed on the cell surface during the 60-minute-chase period. Initially, Dsg3 formed two types of small clusters on the nondesmosomal plasma membrane, ie, either half-desmosome-like clusters with keratin intermediate filament (KIF) attachment or simple clusters without KIF attachment. The PV-IgG binding to Dsg3 caused the internalization of the simple clusters into endosomes, but not the half-desmosome-like clusters. After the 60-minute-chase period, both types of cell surface Dsg3 clusters were labeled with only 10-nm gold, suggesting that new Dsg3 molecules were being delivered to the cell surface. Desmosomes were labeled with both 5-nm gold and 10-nm gold, whereas the half-desmosome-like clusters were labeled with only 10-nm gold, suggesting that the desmosomes themselves were not split. These results suggest that Dsg3 first forms simple clusters, followed by KIF-attachment, and then becomes integrated into desmosomes, and that PV-IgG-induced internalization of the nondesmosomal simple clusters of Dsg3 may represent the primary effects of PV-IgG on keratinocytes.

Autoantigens↗