10.  Summary
  • We disrupted the murine HCII gene by homologous recombination in embryonic stem cells and obtained HCII-deficient mice in a mixed 129/SvJ x C57Bl/6 genetic background.

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  • HCII antigen is absent from the plasma of HCII-/- mice.

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  • Plasma from HCII-/- mice does not inhibit thrombin in the presence of dermatan sulfate, confirming that HCII is the only dermatan sulfate cofactor in murine plasma.

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  • Plasma from HCII-/- mice contains normal amounts of a heparin-dependent factor Xa inhibitor (antithrombin).

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  • HCII+/-x HCII+/- crosses produce the expected number of HCII-/- offspring, indicating that HCII deficiency is not lethal in utero.

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  • HCII-/- mice are normal in appearance, growth, and survival at ~6 months of age.

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  • HCII-/- x HCII-/- crosses produce litters of normal size, indicating that HCII deficiency in both parents is compatible with normal gestation.

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  • The HCII knockout mouse will provide an important tool to assess the role of HCII in thrombosis, wound healing, atherogenesis, and inflammation.
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