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Endogenous Natural Complement Inhibitor Regulates Cardiac Development.

Simon A Mortensen¹, Louise L Skov², Kasper Kjaer-Sorensen²

¹Department of Biomedicine, Aarhus University, DK-8000 Aarhus C, Denmark.

Journal of Immunology (Baltimore, Md. : 1950)

|March 5, 2017

Summary

Mannan-binding lectin-associated protein (MAp)44 regulates cardiac development by influencing neural crest cell migration. This immune molecule

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Area of Science:

Immunology
Developmental Biology
Cardiology

Background:

Congenital heart defects (CHDs) are a leading cause of perinatal mortality with unknown etiology in many cases.
Immune molecules play critical roles in fetal development and adult homeostasis.
Mannan-binding lectin (MBL)-associated protein (MAp)44 is an endogenous complement inhibitor.

Purpose of the Study:

To investigate the function of MAp44 in cardiac development.
To elucidate the role of MAp44 in regulating the MBL-associated serine protease (MASP)-3/collectin-L1/K1 complex.
To understand the impact of MAp44 on cardiac neural crest cell migration.

Main Methods:

Utilized zebrafish as a model organism for observing heart function and development.
Employed knockdown and rescue strategies to study the effects of MAp44.
Analyzed neural crest cell behavior and cardiac parameters like heart rate and output.

Main Results:

Knockdown of embryonic MAp44 resulted in impaired cardiogenesis, reduced heart rate, and decreased cardiac output.
Aberrant neural crest cell migration was observed in MAp44 knockdown embryos.
MAp44 was found to compete with MASP-3 for pattern recognition molecule interaction.
Overexpression of wild-type MAp44 rescued the observed developmental defects.

Conclusions:

MAp44 is crucial for normal cardiac development.
Immune molecules are integral to the orchestration of cardiac tissue formation.
MAp44's function in regulating MASP-3 complex composition impacts cardiac neural crest cell migration.