Mol. Cells 2013; 36(5): 465-471
Published online November 8, 2013
https://doi.org/10.1007/s10059-013-0228-1
© The Korean Society for Molecular and Cellular Biology
The hyaloid vessel is a transient vascular network that nourishes the lens and the primary vitreous in the early developmental periods. In hyaloid vessels devoid of the support of astrocytes, we demonstrate that tight junction proteins, zonula occludens-1 and occludin, are regularly expressed at the junction of endothelial cells. To figure out the factor influencing the formation of tight junctions in hyaloid vessels, we further progress to investigate the interactions between endothelial cells and pericytes, two representative constituent cells in hyaloid vessels. Interestingly, endothelial cells interact with pericytes in the early postnatal periods and the interaction between two cell types provokes the up-regulation of transforming growth factor beta 1. Further in vitro experiments demonstrate that transforming growth factor beta 1 induces the activation of Smad2 and Smad3 and the formation of tight junction proteins. Taken together, in hyaloid vessels, pericytes seem to regulate the formation of tight junctions by the interaction with endothelial cells even without the support of astrocytes. Additionally, we suggest that the hyaloid vessel is a valuable system that can be utilized for the investigation of cell-cell interaction in the formation of tight junctions in developing vasculatures.
Keywords endothelial cells, hyaloid vasculature, pericytes, tight junction, transforming growth factor beta 1
Mol. Cells 2013; 36(5): 465-471
Published online November 30, 2013 https://doi.org/10.1007/s10059-013-0228-1
Copyright © The Korean Society for Molecular and Cellular Biology.
Dong Hyun Jo, Jin Hyoung Kim, Jong-Ik Heo, Jeong Hun Kim, and Chung-Hyun Cho
1Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul 110-744, Korea, 2Department of Biomedical Sciences, 3Ischemic/Hypoxic Disease Institute, 4Department of Pharmacology, 5Department of Ophthalmology, College of Medicine, Seoul National University, Seoul 110-744, Korea
The hyaloid vessel is a transient vascular network that nourishes the lens and the primary vitreous in the early developmental periods. In hyaloid vessels devoid of the support of astrocytes, we demonstrate that tight junction proteins, zonula occludens-1 and occludin, are regularly expressed at the junction of endothelial cells. To figure out the factor influencing the formation of tight junctions in hyaloid vessels, we further progress to investigate the interactions between endothelial cells and pericytes, two representative constituent cells in hyaloid vessels. Interestingly, endothelial cells interact with pericytes in the early postnatal periods and the interaction between two cell types provokes the up-regulation of transforming growth factor beta 1. Further in vitro experiments demonstrate that transforming growth factor beta 1 induces the activation of Smad2 and Smad3 and the formation of tight junction proteins. Taken together, in hyaloid vessels, pericytes seem to regulate the formation of tight junctions by the interaction with endothelial cells even without the support of astrocytes. Additionally, we suggest that the hyaloid vessel is a valuable system that can be utilized for the investigation of cell-cell interaction in the formation of tight junctions in developing vasculatures.
Keywords: endothelial cells, hyaloid vasculature, pericytes, tight junction, transforming growth factor beta 1
Minji Lee, Yeonhwa Song, Inhee Choi, Su-Yeon Lee, Sanghwa Kim, Se-Hyuk Kim, Jiho Kim, and Haeng Ran Seo
Mol. Cells 2021; 44(1): 50-62 https://doi.org/10.14348/molcells.2020.0212Suji Kim, and Chang-Hoon Woo
Mol. Cells 2018; 41(11): 964-970 https://doi.org/10.14348/molcells.2018.0111Da-Hye Lee, Jungsul Lee, Jongwook Jeon, Kyung-Jin Kim, Jang-Hyuk Yun, Han-Seok Jeong, Eun Hui Lee, Young Jun Koh, and Chung-Hyun Cho
Mol. Cells 2018; 41(8): 771-780 https://doi.org/10.14348/molcells.2018.0207