Presence of H Type 3/4 Chains of ABO Histo-blood Group System in Serous Cells of Human Submandibular Gland and Regulation of Their Expression by the Secretor Gene (<i>FUT2</i>)

Liu, Yuhua; Fujitani, Noboru; Koda, Yoshiro; Soejima, Mikiko; Kimurâ, Hiroshi

doi:10.1177/002215549904700706

Cited by 11 publications

(13 citation statements)

References 33 publications

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“…Similar Se gene-dependent expression of A/H type 3 chain in oral epithelium and salivary glands (Mandel et al 1991;Liu et al 1999) and secretor status-independent expression of type 3 chain A/H structures in erythrocyte membranes have been reported (Clausen et al 1985(Clausen et al ,1987.…”

Section: Discussionsupporting

confidence: 59%

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Nosaka

Ishida

Tanaka

et al. 2007

J Histochem Cytochem.

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Histo-blood group ABH antigens are widely distributed in human tissues. The epitopes of ABH antigens are carried by at least four different peripheral core isotypes of internal carbohydrate backbones (type 1–4). Each type of ABH antigen is expressed tissue specifically, and aberrant expression of ABH antigens is often observed during oncogenesis. We immunohistochemically examined the expression of A type 3 antigens in wounded and diseased skin tissues (A and AB blood groups). In uninjured skin, the expression of A type 3 antigens was restricted to the eccrine sweat gland. In addition to the sweat glands, A type 3 antigens were found in vascular endothelial cells of the wound sites. The extent of A type 3 antigens expression related to postinfliction intervals. A significantly higher expression rate of A type 3 antigens in endothelial cells was also observed in diseased skin, suggesting that inflammation might induce A type 3 antigen expression in endothelial cells. Double-color immunofluorescence staining of the specimens showed that von Willebrand factor (vWF) was a core-protein of A type 3 determinants aberrantly expressed in endothelial cells in inflamed tissues, suggesting that aberrant expression of A type 3 antigens is involved in stabilization of vWF in inflammation.

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Section: Discussionsupporting

confidence: 59%

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Nosaka

Ishida

Tanaka

et al. 2007

J Histochem Cytochem.

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“…Ken Furukawa and Shin Yazawa (Department of Legal Medicine, Gunma University School of Medicine). Although anti-H 1E3 has been demonstrated to be reactive with H Type 1-H Type 4 synthetic trisaccharides (Nakajima et al 1993), we demonstrated that anti-H MAb 1E3 is reactive predominantly with H Type 1 and H Type 2 antigens in situ in human submandibular glands (Liu et al 1998;Liu et al 1999). In addition, we demonstrated that anti-H 1E3 became specific for H Type 1 (Fuc ␣ 1-2Gal ␤ 1-3GlcNAc ␤ 1-) after absorption with red cell ghosts (Liu et al 1998).…”

Section: Methodsmentioning

confidence: 69%

“…Then the pretreated sections were immunostained using a streptavidin-biotin complex immunoperoxidase method as described previously (Liu et al 1998(Liu et al , 1999. Controls without the first antibody showed negative staining.…”

Section: Methodsmentioning

confidence: 99%

“…We have immunohistochemically determined the differences in the distribution of H Type 1, H Type 2, and H Type 3/4 antigens in human submandibular gland, using specific monoclonal antibodies (MAbs) (Liu et al 1998(Liu et al ,1999. The distribution of ABO and Lewis antigens in many normal or tumor tissues has been investigated by lectinor immunohistochemical methods (Mazzuca et al 1982;Yuan et al 1985;Cossu et al 1990;Ito et al 1990;Maritgnone et al 1993;Liu et al 1998Liu et al ,1999. However, the distribution of Type 1-Type 4 chains of blood group antigens in human respiratory epithelium is not yet reported (Alvarez-Fernandez, and Carretero-Albiñana 1991;Bals and Welsch 1997).…”

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confidence: 99%

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Distribution of H Type 1–4 Chains of the ABO(H) System in Different Cell Types of Human Respiratory Epithelium

Fujitani

Liu

Okamura

et al. 2000

J Histochem Cytochem.

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We used three anti-H monoclonal antibodies (MAbs) specific for H Type 1, H Type 2, and H Type 3/4 antigens to investigate the distribution of H Type 1-H Type 4 chains of the ABO(H) histo-blood group in the human respiratory system. Strong staining of H Type 1 chain and weak staining of H Type 2 chain were observed in mucous cells of submucosal glands of bronchial epithelium, which were dependent on the secretor status. No H Type 3/4 chains were detected in mucous cells. Serous cells of submucosal glands of respiratory system showed no staining by three anti-H antibodies. H Type 1 and H Type 3/4 antigens were detected heterogeneously in apical surfaces of bronchial epithelium from secretors but not from nonsecretors. In contrast, basal cells of bronchial epithelium expressed H Type 2 irrespective of the secretor status, probably regulated by the H gene. Some alveolar Type II cells contained only H Types 3/4, which were dependent on the secretor status, whereas alveolar Type I cells had no H antigens. Our results indicated that different cell types in respiratory epithelium expressed different types of carbohydrate chains of histo-blood group antigens under the control of the H or the Se gene.

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“…Two distinct α(1,2)fucosyltransferases are known to be present in human tissues. One is the H gene (FUT1)-encoded α(1,2)fucosyltransferase (H enzyme), which regulates the expression of the H antigen on erythrocyte membranes, and the other is the Secretor gene (FUT2)-encoded α(1,2) fucosyltransferase (Se enzyme), which regulates the expression of the H antigen in the secretory fluids and digestive mucosa (Oriol et al 1986;Clausen and Hakomori 1989;Liu et al 1998aLiu et al , 1999a. The frequency of H enzyme deficiency (Bombay and paraBombay phenotypes) is very low (e.g., 1 in 13,000 Indians and 1 in 312,081 Germans; Bhatia and Sanghvi 1962;Wagner and Flegel 1997).…”

Section: Introductionmentioning

confidence: 99%

An Alu -mediated large deletion of the FUT2 gene in individuals with the ABO-Bombay phenotype

Koda

Soejima

Johnson³

et al. 2000

Human Genetics

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Recently, we have found an allelic deletion of the secretor alpha(1,2)fucosyltransferase (FUT2) gene in individuals with the classical Bombay phenotype of the ABO system. The FUT2 gene consists of two exons separated by an intron that spans approximately 7 kb. The first exon is noncoding, whereas exon 2 contains the complete coding sequence. Since the 5' breakpoint of the deletion has previously been mapped to the single intron of FUT2, we have cloned the junction region of the deletion in a Bombay individual by cassette-mediated polymerase chain reaction. In addition, the region from the 3' untranslated region of FUT2 to the 3' breakpoint sequence has been amplified from a control individual. DNA sequence analysis of this region indicates that the 5' breakpoint is within a free left Alu monomer (FLAM-C) sequence that lies 1.3 kb downstream of exon 1, and that the 3' breakpoint is within a complete Alu element (AluSx) that is positioned 1.5 kb downstream of exon 2. The size of the deletion is estimated to be about 10 kb. There is a 25-bp sequence identity between the reference DNA sequences surrounding the 5' and 3' breakpoints. This demonstrates that an Alu-mediated large gene deletion generated by unequal crossover is responsible for secretor alpha(1,2)fucosyltransferase deficiency in Indian Bombay individuals.

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Presence of H Type 3/4 Chains of ABO Histo-blood Group System in Serous Cells of Human Submandibular Gland and Regulation of Their Expression by the Secretor Gene (FUT2)

Cited by 11 publications

References 33 publications

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Distribution of H Type 1–4 Chains of the ABO(H) System in Different Cell Types of Human Respiratory Epithelium

An Alu -mediated large deletion of the FUT2 gene in individuals with the ABO-Bombay phenotype

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