Gene Expression Analysis of Galpha13-/- Knockout Mouse Embryos Reveals Perturbations in Galpha13 Signaling Related to Angiogenesis and Hypoxia.
- Author:
Ji Hwan PARK
1
;
Sangdun CHOI
Author Information
1. Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea. sangdunchoi@ajou.ac.kr
- Publication Type:Original Article
- Keywords:
angiogenesis;
gene expression;
G protein Galpha13;
G protein signaling;
hypoxia
- MeSH:
Animals;
Anoxia;
Cardiovascular System;
Cell Cycle;
Dissociative Disorders;
DNA Replication;
Embryonic Development;
Embryonic Structures;
Endothelial Cells;
Female;
Gene Expression;
GTP-Binding Proteins;
Mice;
Mice, Knockout;
Pregnancy
- From:Genomics & Informatics
2011;9(4):161-172
- CountryRepublic of Korea
- Language:English
-
Abstract:
Angiogenesis is regulated by a large number of molecules and complex signaling mechanisms. The G protein Galpha13 is a part of this signaling mechanism as an endothelial cell movement regulator. Gene expression analysis of Galpha13 knockout mouse embryos was carried out to identify the role of Galpha13 in angiogenesis signaling during embryonic development. Hypoxia-inducible response factors including those acting as regulators of angiogenesis were over expressed, while genes related to the cell cycle, DNA replication, protein modification and cell-cell dissociation were under expressed. Functional annotation and network analysis indicate that Galpha13 -/- embryonic mice were exposed to hypoxic conditions. The present analysis of the time course highlighted the significantly high levels of disorder in the development of the cardiovascular system. The data suggested that hypoxia-inducible factors including those associated with angiogenesis and abnormalities related to endothelial cell division contributed to the developmental failure of Galpha13 knockout mouse embryos.
