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242 results on '"Ezaki, Taichi"'

2. Pericytes in Cutaneous Wound Healing

Author

Morikawa, Shunichi, Iribar, Haizea, Gutiérrez-Rivera, Araika, Ezaki, Taichi, Izeta, Ander, COHEN, IRUN R., Editorial Board Member, LAJTHA, ABEL, Editorial Board Member, LAMBRIS, JOHN D., Editorial Board Member, PAOLETTI, RODOLFO, Editorial Board Member, REZAEI, NIMA, Editorial Board Member, and Birbrair, Alexander, editor

Published
2019
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11. リンパ・リンパ管・リンパ組織の謎

Author

EZAKI, Taichi and KOTANI, Masahiko

Subjects
lymphatic vessel, fat, lymph, lymphatic system, lymphoid tissue
Abstract

日本語訳あり 臨時増刊1号東京女子医科大学医学部解剖学・発生生物学講座 講座主任 江﨑太一教授退任記念特別号

Published
2019

13. 転載:新生仔マウス高濃度酸素暴露肺障害モデルにおける肺胞微小血管障害の形態学的特徴

Author

NAKANISHI, Hidehiko, MORIKAWA, Shunichi, KITAHARA, Shuji, YOSHII, Asuka, UCHIYAMA, Atsushi, KUSUDA, Satoshi, and EZAKI, Taichi

Subjects
newborn, bronchopulmonary dysplasia, pulmonary hypertension, hyperoxia, pulmonary microvascular disease
Abstract

臨時増刊1号東京女子医科大学医学部解剖学・発生生物学講座 講座主任 江﨑太一教授退任記念特別号

Published
2019

44. Phenotypic changes and possible angiogenic roles of pericytes during wound healing in the mouse skin

Author

Morikawa, Shunichi and Ezaki, Taichi

Subjects
Wound healing, Angiogenesis, Pericytes, humanities, 61 - Medicina
Abstract

Pericytes (PCs) are attracting increasing attention as a crucial target for anti-angiogenic therapy. In this study, we sought to determine the functional significance of PCs during angiogenesis by using a skin wound healing model in which different angiogenic stages are identifiable. Angiogenesis was first observed on Day 3 after wounding and increased greatly on Day 5. On Day 5, the leading edge of the regenerating vessels (vascular advancing front; VAF) appeared to be composed of immature vessels, and was further divided into “tip” and “following” regions according to maturational differences. PCs distributed in regenerating vessels showed phenotypic differences according to different regions. PCs that expressed PDGFR-ß alone and lacked vascular basement membrane (BM) were predominant in the tip region of the VAF, while PCs that expressed both PDGFR-ß and NG2 with their BM coating were numerous in the following regions toward the rear of the VAF. Moreover, PCs in the VAF expressed VEGF-A and associated with most proliferating endothelial cells (ECs). VEGF-A expression of PCs and the proliferating ECs totally disappeared in the region toward the rear of the VAF. We conclude that PCs can differ in their phenotype according to the stage of angiogenesis during wound healing. They may promote angiogenesis at the initial stage but might in turn stabilize the newly formed vessels at the later stage.

Published
2011

48. Foxc2 influences alveolar epithelial cell differentiation during lung development.

Author

Tsuji, Mayoko, Morishima, Masae, Shimizu, Kazuhiko, Morikawa, Shunichi, Heglind, Mikael, Enerbäck, Sven, Ezaki, Taichi, and Tamaoki, Jun

Subjects
TRANSCRIPTION factors, CONGENITAL heart disease, YELLOW nail syndrome, GENE knockout, PROGENITOR cells, LUNG development, GENETICS
Abstract

FOXC2, a forkhead transcriptional factor, is a candidate gene for congenital heart diseases and lymphedema-distichiasis syndrome and yellow nail syndrome; however, there are no reports on Foxc2 and the development of the lung. We have identified lung abnormalities in Foxc2-knockout embryos during investigation of cardiac development. The aim of this study was to clarify the morphological characteristics during lung development using ICR- Foxc2 knockout lungs. Mutant fetuses at embryonic days 10.5-18.5 were obtained from mating of Foxc2 +/− mice and then analyzed. Notably, Foxc2-knockout lungs appeared parenchymatous and much smaller than those of the wild-type littermates. In the Foxc2 knockout lungs, the capillary beds remained distant from the alveolar epithelium until the late stages, the number of type2 alveolar cells per alveolar progenitor cell was lower and the type1 alveolar cells were thicker in Foxc2 knockout mice. In contrast, Foxc2 expression was only detected in the mesenchyme of the lung buds at E10.5, and it disappeared at E11.5 in Foxc2-LacZ knockin mice. Furthermore, the expression of Lef1 was significantly inhibited in E11.5 lungs. All of these results suggest that the abnormalities in Foxc2 knockout mice may involve maldifferentiation of alveolar epithelial cells and capillary vessel endothelial-alveolar epithelial approach as well as lymph vessel malformation. This is the first report about relationship between Foxc2 and lung development. This animal model might provide an important clue for elucidating the mechanism of lung development and the cause of respiratory diseases. [ABSTRACT FROM AUTHOR]

Published
2017
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