研究者詳細 - 平岡　佐規子

Complement regulatory proteins in normal human esophagus and esophageal squamous cell carcinoma 査読

K Shimo, M Mizuno, J Nasu, S Hiraoka, C Makidono, H Okazaki, K Yamamoto, H Okada, T Fujita, Y Shiratori

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY 19 ( 6 ) 643 - 647 2004年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：BLACKWELL PUBLISHING ASIA

Background: Altered expression of three complement regulatory proteins, decay-accelerating factor (CD55), membrane cofactor protein (CD46) and homologous restriction factor 20 (CD59) has been identified in human gastrointestinal malignancies, but their expression in esophageal cancer has not been described. Therefore the purpose of the present paper was to study the distribution of these proteins in human normal and malignant esophageal mucosa.
Methods and results: In the normal esophageal mucosa, CD55 predominantly stained on the cell membrane of squamous epithelium in the superficial and prickle cell layers, whereas CD46 most intensely stained on the cell membrane in the basal and parabasal cell layers. In contrast to this reciprocal expression of CD55 and CD46, CD59 was broadly distributed on the cell membrane in all layers. In the esophageal squamous cell carcinoma, CD55 staining was intense in the stroma but was negligible in the cancer cells. In contrast, CD46 and CD59 stained almost uniformly on the tumor cell membrane. There was a significant difference in the intensity of the staining of CD55 and CD46 among cells in various layers of normal esophageal mucosa and esophageal carcinoma cells, but not in the staining of CD59. Similar expression patterns of the three complement regulatory proteins in carcinoma cells and in normal epithelium in the basal and parabasal cell layers were observed.
Conclusions: These observations on the expression of the three complement regulatory proteins would help understanding of the host immune responses involving the complement system against esophageal squamous cell carcinoma. (C) 2004 Blackwell Publishing Asia Pty Ltd.

DOI： 10.1111/j.1440-1746.2003.03328.x

Increased serum concentrations and surface expression on peripheral white blood cells of decay-accelerating factor (CD55) in patients with active ulcerative colitis 査読

C Makidono, M Mizuno, J Nasu, S Hiraoka, H Okada, K Yamamoto, T Fujita, Y Shiratori

JOURNAL OF LABORATORY AND CLINICAL MEDICINE 143 ( 3 ) 152 - 158 2004年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：MOSBY, INC

Inflammatory stimuli induce expression and release of decay-accelerating factor (DAF), a complement-regulatory protein present on peripheral-blood cells. Therefore, in ulcerative colitis (UC), an inflammatory colonic disease in which activated leukocytes are involved, DAF may be released from leukocytes into the circulation. In this study we compared serum DAF concentrations and surface DAF expression on peripheral-blood cells in patients with UC with disease activity. Peripheral-blood samples were obtained from 60 patients with UC (30 with active and 30 with inactive disease) and 19 healthy volunteers. Serum DAF concentrations were determined by means of immunoassay, and surface DAF expression on blood cells was examined with the use of flow cytometry. Serum DAF concentrations in patients with active disease (mean 48.6 ng/mL) were significantly higher than those in patients whose disease was in remission (33.3 ng/mL; P = .0003) and those in healthy controls (32.3 ng/mL; P = .0007). Surface DAF expression on neutrophils, CD14+ monocytes, and subsets of lymphocytes in patients with active UC was significantly increased compared with that in patients with UC in remission and in healthy controls. The increased serum DAF concentrations and surface DAF expression on leukocyte fractions in patients with active disease fell to significantly lower levels when the disease had gone into remission after medical therapy. Serum DAF concentrations are increased in UC patients in relation to disease activity. The likely source of increased DAF concentrations is peripheral-blood leukocytes that have been activated as part of the UC disease process.

DOI： 10.1016/j.lab.2003.11.004

Difference in Ulex europaeus agglutinin I-binding activity of decay-accelerating factor detected in the stools of patients with colorectal cancer and ulcerative colitis 査読

H Okazaki, M Mizuno, J Nasu, C Makidono, S Hiraoka, K Yamamoto, H Okada, T Fujita, T Tsuji, Y Shiratori

JOURNAL OF LABORATORY AND CLINICAL MEDICINE 143 ( 3 ) 169 - 174 2004年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：MOSBY, INC

Expression of decay-accelerating factor (DAF, CD55), a complement-regulatory glycoprotein, is enhanced in colorretal-cancer (CC) cells and colonic epithelium in ulcerative colitis UC, and stools from these patients contain increased amounts of DAF. Carbohydrate chains of glycoproteins are often altered during malignant transformation or inflammation. In this study, we investigated whether DAF molecules in patients with CC and those with UC differ with respect to oligosacchadde side chains. We analyzed DAF in stools and homogenates of colonic-tissue specimens obtained from patients with CC or UC using solid-phase enzyme-linked assay and Western blotting for reactivity with the lectins Ulex europaeus agglutinin l (UEA-l), wheat-germ agglutinin, peanut agglutinin, and concanavalin A. UEA-l bound to DAF in stools from patients with UC but not in that from the stools of CC patients, as demonstrated on the solid-phase enzyme-linked assay (P < .05, Mann-Whitney U test) and Western blotting. Binding of UEA-l was specifically inhibited by the addition of fucose. The difference in LEA-l reactivity with DAF was observed also in colonic-tissue homogenates from patients with UC and those with CC. DAF expressed in the mucosa and excreted into the stools of UC patients is different from that expressed in CC with regard to UEA-l reactivity. Future studies should be directed toward determining whether a qualitatively unique isoform of DAF is present, of which sugar chains are specific to CC in UC patients.

DOI： 10.1016/j.lab.2003.11.005