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Updated: May 3, 2026

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation
Published on: June 21, 2021
Postconditioning leads to an increase in protein S-nitrosylation
Guang Tong1, Angel M Aponte, Mark J Kohr
1Department of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou, Guangdong Province, China;
Nitric oxide-mediated S-nitrosylation (SNO) protects the heart after ischemia. This study identified 77 S-nitrosylated proteins involved in postconditioning (PostC) cardioprotection, revealing key signaling pathways.
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Molecular Medicine
Background:
- Nitric oxide (NO) and S-nitrosylation (SNO) are implicated in postconditioning (PostC) cardiac protection.
- Specific SNO-modified proteins and sites following PostC remain unidentified in the myocardium.
Purpose of the Study:
- To investigate the role of SNO signaling in PostC-induced cardioprotection.
- To identify specific SNO-modified proteins and sites in the heart after PostC.
Main Methods:
- Utilized a Langendorff-perfused mouse heart model subjected to ischemia-reperfusion (I/R) with PostC.
- Employed two biotin switch-based techniques: 2D CyDye-maleimide DIGE and SNO-resin-assisted capture (SNO-RAC).
- Investigated the effect of NO synthase inhibition (l-NAME) on PostC-induced protection and SNO signaling.
Main Results:
- PostC significantly reduced infarct size and improved contractile function compared to I/R controls.
- PostC-induced protection was abolished by l-NAME, indicating NO dependence.
- 2D DIGE revealed a PostC-induced increase in SNO for several proteins, blocked by l-NAME.
- SNO-RAC identified 77 unique SNO-modified proteins in PostC hearts.
Conclusions:
- NO-mediated SNO signaling plays a crucial role in PostC-induced cardioprotection.
- This study provides the first comprehensive list of candidate SNO proteins involved in PostC.
- These findings elucidate novel molecular mechanisms underlying cardiac protection during reperfusion.
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