M

M Shirao

Kurume University

Publishes on T-cell and Retrovirus Studies, Viral-associated cancers and disorders, Cell Adhesion Molecules Research. 12 papers and 1.3k citations.

12Publications
1.3kTotal Citations

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IL-6 increases endothelial permeability in vitro.
N Maruo, Ikuo Morita, M Shirao et al.|Endocrinology|1992
Cited by 366

The effect of interleukin 6 (IL-6) on endothelial permeability was examined by measuring fluorescein isothiocyanate-labeled albumin flux across an endothelial cell monolayer. Bovine vascular endothelial cells (BVEC) were cultured up to confluency on collagen-coated polycarbonate micropore filters and then the filters were mounted on modified Boyden chambers. Treatment of the BVEC with IL-6 at 100 ng/ml for 21 h caused a remarkable increase in the permeability of fluorescein isothiocyanate-labeled albumin across the endothelial monolayer. This effect of IL-6 was concentration dependent, in the range from 10-200 ng/ml of IL-6. The effect of IL-6 was also time dependent, the maximal level being reached at 21 h from the beginning of the treatment. This stimulatory effect of IL-6 on albumin clearance was completely abolished by the addition of anti-IL-6 antibody. Light microscopic observation of a cross-section of a monolayer showed that the IL-6-induced increase in the permeability was correlated with changes in cell shape and rearrangement of intracellular actin fibers. IL-6 did not show any cytotoxicity toward or growth inhibition of endothelial cells, even at more than 200 ng/ml. The enhancing effect of IL-6 on the increase in the permeability was reversible; when IL-6 was removed by a medium change and the cells were incubated for a further 24 h without IL-6, the permeability was restored to the control level. These results suggest that IL-6 can induce an increase in endothelial permeability in vitro by rearranging actin filaments and by changing the shape of endothelial cells.

HTLV‐I Uveitis: A Distinct Clinical Entity Caused by HTLV‐I
Manabu Mochizuki, Toshiki Watanabe, Kazunari Yamaguchi et al.|Japanese Journal of Cancer Research|1992
Cited by 293

Seroepidemiological, clinical and virological studies were carried out in an HTLV-I endemic area to find out if HTLV-I caused an intraocular inflammatory disorder, uveitis. The seroprevalence in patients with uveitis without defined etiologies (62/175, 35.4%) was significantly higher than that in patients with non-uveitic ocular diseases (42/261, 16.1%) or in patients with uveitis with defined etiologies (8/78, 10.3%). Moreover, the seroprevalence in young adults (20-49 years) with uveitis without defined etiologies was 30/67 (44.8%), whereas it was only 10/107 (9.3%) in the other two groups. The uveitis in HTLV-I carriers was characterized clinically by a moderate inflammation of the vitreous body accompanied by a mild iritis and retinal vasculitis. The proviral DNA of HTLV-I was detected by polymerase chain reaction from the inflammatory cells in the anterior chamber in 9 out of 9 seropositive patients with the uveitis, but not in any of the tested patients with other types of uveitis. These data, thus, indicate that HTLV-I causes a specific type of intraocular inflammation, uveitis.

Uveitis Associated with Human T Lymphotropic Virus Type I: Seroepidemiologic, Clinical, and Virologic Studies
Manabu Mochizuki, Toshiki Watanabe, K Yamaguchi et al.|The Journal of Infectious Diseases|1992
Cited by 136

Journal Article Uveitis Associated with Human T Lymphotropic Virus Type I: Seroepidemiologic, Clinical, and Virologic Studies Get access Manabu Mochizuki, Manabu Mochizuki Reprints or correspondence: Dr. Manabu Mochizuki, Department of Ophthalmology, Kurume University School of Medicine, 67 Asahimachi, Kurume (830). Japan. Search for other works by this author on: Oxford Academic PubMed Google Scholar Toshiki Watanabe, Toshiki Watanabe Search for other works by this author on: Oxford Academic PubMed Google Scholar Kazunari Yamaguchi, Kazunari Yamaguchi Search for other works by this author on: Oxford Academic PubMed Google Scholar Kazuo Tajima, Kazuo Tajima Search for other works by this author on: Oxford Academic PubMed Google Scholar Koichi Yoshimura, Koichi Yoshimura Search for other works by this author on: Oxford Academic PubMed Google Scholar Shunsuke Nakashima, Shunsuke Nakashima Search for other works by this author on: Oxford Academic PubMed Google Scholar Makoto Shirao, Makoto Shirao Search for other works by this author on: Oxford Academic PubMed Google Scholar Shinji Araki, Shinji Araki Search for other works by this author on: Oxford Academic PubMed Google Scholar Norio Miyata, Norio Miyata Search for other works by this author on: Oxford Academic PubMed Google Scholar Shigeo Mori, Shigeo Mori Search for other works by this author on: Oxford Academic PubMed Google Scholar ... Show more Kiyoshi Takatsuki Kiyoshi Takatsuki Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 166, Issue 4, October 1992, Pages 943–944, https://doi.org/10.1093/infdis/166.4.943 Published: 01 October 1992

Characterization of rat LECAM‐1 (L‐selectin) by the use of monoclonal antibodies and evidence for the presence of soluble LECAM‐1 in rat sera
Takuya Tamatani, Fujiko Kitamura, Keisuke Kuida et al.|European Journal of Immunology|1993
Cited by 83

We have characterized the rat LECAM-1 (L-selectin) by the use of newly generated hamster anti-rat LECAM-1 monoclonal antibodies (mAb) (HRL1, HRL2, HRL3, HRL4), with respect to the biochemistry, cellular distribution and function, and developed an ELISA system to detect the soluble form of rat LECAM-1. In the rat, lymphocyte and neutrophil LECAM-1 have apparent molecular masses of 65 and 62 kDa, respectively, and differential glycosylation may account for the molecular heterogeneity. Readily detectable levels of LECAM-1 are expressed on peripheral blood lymphocytes and neutrophils, but not on thymocytes. Lymphocyte LECAM-1 is rapidly shed from the cell surface upon cell activation with PMA, but not with interleukin (IL)-8. In contrast, neutrophil LECAM-1 showed rapid shedding upon stimulation with phorbol 12-myristate 13-acetate (PMA) or IL-8. Concomitantly there is up-regulated expression of Mac-1 in PMA- and IL-8-stimulated neutrophils. Neutrophil rolling in mesenteric venules was significantly inhibited by administration of function-blocking anti-rat LECAM-1 mAb HRL3, but not by non-blocking HRL4, indicating that LECAM-1 plays a significant role in leukocyte rolling. Given that LECAM-1 is rapidly shed from the cell surface, we attempted to develop an ELISA system for detecting LECAM-1 is soluble form, and measured the levels in experimental autoimmune uveitis. The circulating levels of LECAM-1 increased from day 4, which preceded the appearance of clinical signs of uveitis and remained high until uveitis subsided, suggesting that soluble LECAM-1 is potentially a useful parameter to monitor certain types of inflammatory or immune disorders.