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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

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Published on: September 4, 2017

Validation for the function of protein C in mouse models.

Ya Liu¹, Maoping Cai¹, Yan Chen¹

¹Zhanjiang Institute of Clinical Medicine, Central People's Hospital of Zhanjiang, Guangdong Medical University, Zhanjiang, Guangdong, China.

|April 29, 2024

Summary

This summary is machine-generated.

Mice with a Protein C (PC) deficiency mutation showed altered blood clotting and organ damage, validating PC’s crucial role in anticoagulation and hemostasis.

Keywords:

CRISPR/Cas9 Mouse model Protein C deficiency Venous thromboembolism

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Area of Science:

Biochemistry
Genetics
Hematology

Background:

Protein C (PC) is a vital anticoagulant protein encoded by the PROC gene.
Understanding PC's function is crucial for managing thrombotic and bleeding disorders.
Mouse models are essential for studying human genetic diseases.

Purpose of the Study:

To create and characterize a mouse model of autosomal recessive Protein C deficiency (PCD).
To investigate the in vivo function of Protein C using gene editing technology.
To validate the PROC c.1198G>A (p.Gly400Ser) mutation in a mammalian model.

Main Methods:

CRISPR/Cas9 gene editing was employed to introduce the specific PROC mutation in mice.
Genotyping, phenotypic analysis, and blood coagulation tests were performed on heterozygous and wild-type mice.
Histopathological examination (H&E staining) and immunohistochemistry were used to assess organ damage and fibrin deposition.

Main Results:

Heterozygous mice for the PC mutation exhibited prolonged clotting times (PT, APTT, TT) and decreased fibrinogen levels.
Reduced Protein C activity was observed in heterozygous mice, indicating impaired anticoagulant function.
Histopathology revealed liver steatosis, renal tubule damage, splenic hemorrhage, and significant fibrin deposition in multiple organs.

Conclusions:

The developed mouse model successfully recapitulates key features of Protein C deficiency.
The study validates the critical role of Protein C in maintaining hemostasis and preventing thrombosis.
The findings highlight the potential for organ damage secondary to PC deficiency.