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Defective vascular development in connexin 45-deficient mice
Development (Cambridge, England)
|September 8, 2000
Summary
Connexin 45 (Cx45) deficiency in mice disrupts vascular development, leading to embryonic lethality. Impaired blood vessel maturation, not initial formation, causes severe defects and apoptosis.
Area of Science:
- Developmental Biology
- Cellular Biology
- Genetics
Background:
- Gap-junction proteins, like connexin 45 (Cx45), are crucial for intercellular communication.
- The specific biological functions of Cx45 in mammalian development remain incompletely understood.
Purpose of the Study:
- To investigate the role of connexin 45 (Cx45) in embryonic vascular development using a mouse model.
- To elucidate the consequences of Cx45 deficiency on blood vessel formation and maturation.
Main Methods:
- Generation of Cx45-deficient mice by replacing the Cx45-coding region with a lacZ reporter gene.
- Analysis of embryonic development, vascular morphology, and apoptosis in Cx45-deficient embryos.
- Assessment of TGF-beta1 signaling in yolk sac tissues.
Main Results:
- Cx45-deficient embryos displayed severe vascular abnormalities and died between embryonic day 9.5 and 10.5.
- While initial endothelial cell differentiation was normal, subsequent vascular tree formation, placental vascularization, and arterial smooth muscle development were impaired.
- Decreased TGF-beta1 protein levels and massive apoptosis were observed in Cx45-deficient embryos.
Conclusions:
- Connexin 45 is essential for the post-vasculogenic maturation of blood vessels, not initial vasculogenesis.
- Cx45 deficiency leads to critical vascular defects, potentially linked to altered TGF-beta1 signaling, resulting in embryonic lethality.
- Impaired vascular development in Cx45-deficient embryos may be partially compensated by other connexins.
