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Autotaxin overexpression causes embryonic lethality and vascular defects
Hiroshi Yukiura1, Kuniyuki Kano1, Ryoji Kise1
1Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Aoba, Aramaki, Aoba-ku, Sendai, 980-8578, Japan.
Plos One
|May 21, 2015
Summary
Autotaxin (ATX) overexpression causes severe embryonic vascular defects and lethality. Neonatal ATX excess leads to retinal vascular abnormalities, highlighting the need for precise ATX regulation in vascular development.
Area of Science:
- Biochemistry
- Developmental Biology
- Physiology
Background:
- Autotaxin (ATX) is a key enzyme in lysophosphatidic acid (LPA) production.
- Elevated ATX levels are observed in various pathophysiological states.
- The precise role of elevated ATX in vivo remains unclear.
Purpose of the Study:
- To investigate the consequences of ATX overexpression on vascular development.
- To elucidate the impact of excess LPA signaling mediated by ATX.
Main Methods:
- Generation of conditional transgenic (Tg) mice overexpressing ATX.
- Utilized the Cre/loxP system for temporal control of ATX overexpression.
- Analyzed vascular formation during embryonic and neonatal periods.
Main Results:
- Embryonic ATX overexpression led to severe vascular defects and embryonic lethality around E9.5.
- Neonatal ATX overexpression significantly increased plasma LPA levels.
- Resulting retinal vascular defects included abnormal vascular plexus formation and increased regression.
Conclusions:
- Autotaxin levels require strict regulation for proper vascular development.
- Excessive ATX-mediated LPA signaling disrupts embryonic and neonatal vascular formation.
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