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Interacting proteins of BDH1 in heart by IP LC-MS/MS

ABSTRACT: Sepsis-induced myocardial dysfunction is associated with high mortality in sepsis. However, the underlying mechanisms of sepsis-induced myocardial dysfunction remain unclear. The heart is an energy-demanding organ. Under basal physiological conditions, cardiomyocytes rely primarily on energy provided by fatty acid oxidation. However, recent studies have revealed the important role of metabolic rearrangements in cardiomyocytes under some pathological conditions. 3-hydroxybutyrate dehydrogenase 1 (BDH1) is a key enzyme in ketone body metabolism, catalyzing the interconversion of acetoacetate and (R)-3-hydroxybutyrate. Previous studies have demonstrated the role of BDH1 in myocardial metabolic remodeling during acute fasting, but the expression patterns and functions of BDH1 in the septic heart are unknown. The aim of this study was to identify the interactors of BDH1 in H9C2 rat cardiomyocytes with or without lipopolysaccharide (LPS) treatment.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Tiening Zhang

PROVIDER: PXD056148 | iProX | Thu Sep 19 00:00:00 BST 2024

REPOSITORIES: iProX

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Project description:Background: Sepsis can lead to multiple organ damage, and the heart is one of the most vulnerable organs. Vagal nerve stimulation can reduce myocardial injury in sepsis and improve survival rate. However, the relative effect of disparate cell populations on sepsis induced myocardial dysfunction and the low-level tragus stimulation on it, remain unclear. Methods: We used the cardiac single-cell transcriptomic strategy to characterize the cardiac cell population and the network of cells that forms the heart. And we selected all cardiac macrophage from CD45+ cells using single-cell mRNA sequencing data. Then we used echocardiography performing, western blot and immunofluorescence and immunohistochemical technology to verify the data of the single-cell mRNA sequencing results. Results: In single-cell mRNA sequencing data, our analysis provides a comprehensive map of the cardiac cellular landscape uncovering multiple cell populations that contribute to sepsis induced myocardial dysfunction under low-level tragus stimulation. Pseudo timing analysis in single-cell sequencing showed that low level vagal nerve stimulation could induce the transformation of cardiac monocytes into M2 macrophages and play an anti-inflammatory role. After low-level tragus stimulation, the expression of α7nAChR in the heart tissue increased significantly. Echocardiography showed that low-level tragus stimulation could improve the cardiac function of septic myocardial injury of the mice. Comparing with the sepsis group, the expression of interleukin-1β in heart tissue of the mice in sepsis with low-level tragus stimulation group is significantly lower. Conclusion: Low-level tragus stimulation can improve sepsis-induced myocardial dysfunction by promoting cardiac monocytes to M2 macrophages. Goal of the study: In the present study, we aimed to screen macrophages, their crosstalk with other cells, and macrophages associated with cardiac injury and further verify their origins and roles in the septic myocardial injury process and low-level tragus stimulation (LL-TS) to treat septic myocardial dysfunction.

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Interacting proteins of BDH1 in heart by IP LC-MS/MS

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