Biomedical subjects

Atsushi Yasui

Publications and source records attributed to Atsushi Yasui.

4 recordsLinked to original sources

PubMed2005

Prospective assessment of Y-chromosome microdeletions and reproductive outcomes among infertile couples of Japanese and African origin.

BACKGROUND: To compare the frequency of Y-chromosome microdeletions in Japanese and African azoospermic and oligozoospermic men and describe embryo characteristics and reproductive outcome following in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI). METHODS: Our study was performed prospectively at two centers, a private IVF clinic and a university hospital. Japanese and African (Tanzanian) men with nonobstructive azoospermia (NOA) and oligozoospermia (concentration < 5 x 10(6) /ml) were evaluated for Y-chromosome microdeletions (n = 162). Of the 47 men with NOA, 26 were Japanese and 21 were Africans. Of the 115 men with oligozoospermia, 87 were Japanese and 28 were Africans. Reproductive outcomes of patients with Y-chromosome microdeletions were then compared with those of 19 IVF+ICSI cycles performed on couples with Y-chromosome intact males/tubal factor infertility which served as a control group. RESULTS: Seven azoospermic and oligozoospermic patients had Y-chromosome deletions; the total number of deletions in the AZFc region was five. There was only one deletion in the AZFa region and one complete deletion involving all three regions (AZFa, b, and c) within AZF. In our study population, microdeletion frequency among Japanese men was 6.2% (95% CI, 4.25%-14.45%), whereas no deletions were identified in the African group (95% CI, 0.0%-7.27%). The difference between the two groups was not statistically significant, however. Embryos derived from ICSI utilizing sperm with Y-chromosome microdeletion showed reduced rates of fertilization, blastocyst development, implantation, and pregnancy compared to the Y-chromosome intact group, although these observed differences were not statistically significant. CONCLUSION: The observed frequency of Y-chromosome microdeletion was 6.2% among Japanese azoospermic and oligozoospermic males; no microdeletions were identified among our African study patients. In this population of couples undergoing IVF+ICSI, there was no statistically significant difference in embryo characteristics or pregnancy outcome between patients with Y-chromosome microdeletion and those with an intact Y-chromosome.

Journal Article↗

PubMed2004

Expression of splice variants of the human ADAM15 gene and strong interaction between the cytoplasmic domain of one variant and Src family proteins Lck and Hck.

OBJECTIVE: The aim of the present study was to show variant species of ADAM15 and unique Src homology 3 (SH3)-binding motifs, which strongly bound Src family proteins compared with ADAM15. METHODS AND RESULTS: RT-PCR using primers for the cytoplasmic domain revealed the presence of different species, designated ADAM15v1 and ADAM15v2, which had characteristic SH3-binding class I and class II motifs. The mRNA of ADAM15v1 and ADAM15v2 was mainly found in peripheral blood mononuclear cells, T lymphocytes and monocytic cell lines. ADAM15v2 protein interacted more strongly with the Src family proteins Lck and Hck than did ADAM15 protein, as examined by pull-down analysis and immunoprecipitation followed by immunoblot analysis. The binding with Lck and Hck was enhanced by the phosphorylation of ADAM15v2 protein. CONCLUSIONS: These results suggest that the cytoplasmic domain of ADAM15v2 strongly interacts with Lck and Hck and regulates leukocyte function.

ADAM Proteins↗

PubMed2003

Structure and expression of the murine ADAM 15 gene and its splice variants, and difference of interaction between their cytoplasmic domains and Src family proteins.

The murine cell surface antigen ADAM 15 is a transmembrane glycoprotein that is expressed in a variety of cells including monocytic and T cell lines and consists of a metalloprotease domain, a disintegrin domain, a cysteine-rich domain, and an epidermal growth factor (EGF)-like domain in the extracellular region. The cytoplasmic domain comprises 103 amino acids containing proline-rich endophilin I, Src homology 3 (SH3), and phox homology domain-containing protein (SH3PX1) binding motifs. The ADAM15 gene is composed of 21 exons and 20 introns and spans approximately 10 kb. The transcription initiation site of the ADAM15 gene was defined by an oligonucleotide-capping method. Reverse transcription (RT)-PCR using primers of the cytoplasmic domain of ADAM15 revealed the presence of different ADAM15 species designated ADAM15v1 and ADAM15v2, respectively, that had characteristic SH3-binding class I and/or class II motifs. The ADAM15v1 and ADAM15v2 genes consist of an extra one exon and two exons, respectively, which exist in intron 19 of the ADAM15 gene. The expression of ADAM15v1 and ADAM15v2 mRNA was found in T lymphocyte and monocyte lines. ADAM15v2 protein interacted more strongly with the Src family proteins Lck and Src than ADAM15 protein, when examined by pull-down and immunoprecipitation followed by immunoblot analysis using a T lymphocyte line. Phosphorylation of ADAM15v2 protein markedly enhanced the binding with Lck. These results suggest that the cytoplasmic domain of ADAM15v2 strongly interacts with Lck and plays an important role in T lymphocytes.

ADAM Proteins↗

PubMed2002

CD156 transgenic mice. Different responses between inflammatory types.

CD156 (ADAM8) is part of the ADAM family of proteins with the catalytic site consensus sequence of metalloprotease and disintegrins. To examine the role of CD156 in vivo, we generated mutant CD156 (eCD156) transgenic mice expressing the ectodomain of CD156 under the control of the alpha1-antitrypsin (AT) promoter. One of the transgenic mice designated ATMS2-TG18 expressed a 1.84 kb mRNA which was predicted to be a truncated CD156. The expression of the transgenic CD156 mRNA in ATMS2-TG18 mice was abundant in the liver and slight in kidney. Turpentine oil (TO) and lipopolysaccharide (LPS) markedly upregulated the expression. Soluble CD156 (sCD156) was produced constitutively, and increased after the treatment with TO. Casein-induced peritoneal leukocyte infiltration was significantly less extensive in ATMS2-TG18 than non-transgenic mice. The expression of L-selectin in neutrophils (PMN) from peripheral blood leukocytes (PBL) was more strongly downregulated in ATMS2-TG18 than non-transgenic mice, suggesting that L-selectin in PMN from ATMS2-TG18 mice was shed by sCD156. In contrast, oxazolone (Ox)-induced contact hypersensitivity reactions (CHR) were more marked in ATMS2-TG18 than non-transgenic mice. The expression of E-selectin mRNA was detected in inflammatory skin sites from ATMS2-TG18, but not non-transgenic mice, suggesting that sCD156 may activate the endothelial cells and lead to the upregulation of E-selectin. These results suggest that CD156 regulates leukocyte infiltration directly or indirectly.

ADAM Proteins↗