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Structural basis for the mutation-induced dysfunction of human CYP2J2: a computational study.

Shan Cong¹, Xiao-Tu Ma, Yi-Xue Li

¹Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, China.

Journal of Chemical Information and Modeling

|May 8, 2013

Summary

This summary is machine-generated.

CYP2J2 enzyme metabolizes arachidonic acid to protective epoxyeicosatrienoic acids (EETs). Specific mutations (T143A, N404Y) impair this function by altering enzyme structure and substrate binding, impacting cardiovascular health.

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Area of Science:

Biochemistry
Molecular Biology
Cardiovascular Research

Background:

Arachidonic acid is a crucial inflammatory intermediate.
Cytochrome P450 2J2 (CYP2J2) metabolizes arachidonic acid into cardioprotective epoxyeicosatrienoic acids (EETs).
CYP2J2 polymorphisms, T143A and N404Y, are linked to reduced arachidonic acid metabolism and cardiovascular disease.

Purpose of the Study:

To elucidate the structural mechanisms behind reduced arachidonic acid metabolism by CYP2J2 mutants (T143A and N404Y).
To provide insights into the role of CYP2J2 dysfunction in coronary artery disease and hypertension.

Main Methods:

Construction of three-dimensional structural models for wild-type CYP2J2 and its T143A and N404Y mutants using computational approaches (coordinate reconstruction, ab initio modeling) with CYP2R1 as a template.
Analysis of structural differences and their impact on the active site, substrate binding, and catalytic activity.

Main Results:

The T143A mutation destabilizes the C helix, closing the water access channel and hindering catalytic processes.
The N404Y mutation disrupts a critical hydrogen bond between Leu(378) and arachidonic acid, impairing substrate recognition and orientation.
Wild-type CYP2J2 exhibits a typical cytochrome P450 fold with a deeply buried heme group.

Conclusions:

Structural alterations caused by T143A and N404Y mutations provide a mechanistic explanation for impaired arachidonic acid metabolism by CYP2J2.
Understanding these structural-functional relationships is vital for investigating the pathogenesis of cardiovascular diseases associated with CYP2J2 dysfunction.