Circulating S-Glutathionylated cMyBP-C as a Biomarker for Cardiac Diastolic Dysfunction
Xiaoxu Zhou1, Euy-Myoung Jeong2, Hong Liu1
1Division of Cardiology Department of Medicine The Lillehei Heart InstituteUniversity of Minnesota Minneapolis MN.
Insights
Elevated circulating S-glutathionylated Cardiac myosin binding protein-C (cMyBP-C) indicates diastolic dysfunction (DD). This finding suggests S-glutathionylated cMyBP-C may serve as a novel biomarker for detecting DD across species.
Area of Science:
- Cardiology
- Biochemistry
- Biomarker Discovery
Background:
- Cardiac myosin binding protein-C (cMyBP-C) is crucial for regulating heart muscle contraction and relaxation.
- Elevated S-glutathionylation of cMyBP-C in the heart muscle is linked to diastolic dysfunction (DD) in animal models.
Purpose of the Study:
- To investigate if circulating S-glutathionylated cMyBP-C can serve as a biomarker for diastolic dysfunction (DD).
Main Methods:
- Diastolic dysfunction (DD) was assessed using echocardiography in humans, African Green monkeys, and mice.
- Circulating levels of S-glutathionylated cMyBP-C were measured via immunoprecipitation in blood samples.
Main Results:
- Humans, monkeys, and mice with DD exhibited significantly elevated levels of circulating S-glutathionylated cMyBP-C compared to controls.
- A positive correlation was observed between circulating S-glutathionylated cMyBP-C and DD in human participants.
Conclusions:
- Circulating S-glutathionylated cMyBP-C is elevated in individuals with DD across multiple species.
- S-glutathionylated cMyBP-C shows potential as a novel biomarker for the presence of diastolic dysfunction.
Abstract:
Background cMyBP-C (Cardiac myosin binding protein-C) regulates cardiac contraction and relaxation. Previously, we demonstrated that elevated myocardial S-glutathionylation of cMyBP-C correlates with diastolic dysfunction (DD) in animal models. In this study, we tested whether circulating S-glutathionylated cMyBP-C would be a biomarker for DD. Methods and Results Humans, African Green monkeys, and mice had DD determined by echocardiography. Blood samples were acquired and analyzed for S-glutathionylated cMyBP-C by immunoprecipitation. Circulating S-glutathionylated cMyBP-C in human participants with DD (n=24) was elevated (1.46±0.13-fold, P=0.014) when compared with the non-DD controls (n=13). Similarly, circulating S-glutathionylated cMyBP-C was upregulated by 2.13±0.47-fold (P=0.047) in DD monkeys (n=6), and by 1.49 (1.22-2.06)-fold (P=0.031) in DD mice (n=5) compared with the respective non-DD controls. Circulating S-glutathionylated cMyBP-C was positively correlated with DD in humans. Conclusions Circulating S-glutathionylated cMyBP-C was elevated in humans, monkeys, and mice with DD. S-glutathionylated cMyBP-C may represent a novel biomarker for the presence of DD.
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