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Single Cell Transcriptional Profiling of Adult Mouse Cardiomyocytes
Published on: December 28, 2011
Quantitative proteomics reveals PPAR signaling pathway regulates the cardiomyocyte activity of neonatal mouse heart
Xinyu Li1, Nannan Wang1, Minhui Gui1
1State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Key Laboratory of Molecular Medicine, Chemistry and Biomedicine Innovation Center, Medical School of Nanjing University, Nanjing, China.
Insights
Understanding cardiac development offers new hope for treating cardiovascular diseases (CVDs). Activating the peroxisome proliferator-activated receptor (PPAR) pathway shows promise for enhancing cardiomyocyte activity and potentially treating CVDs.
Area of Science:
- Proteomics and Cardiovascular Research
- Molecular Mechanisms of Cardiac Development
Background:
- Cardiovascular diseases (CVDs) are a leading cause of mortality globally, with current treatments having limitations.
- The postnatal development of the mouse heart, particularly a window of high cardiomyocyte activity, presents a potential therapeutic target for CVDs.
Purpose of the Study:
- To create a proteomic atlas of cardiac development in mice.
- To identify key molecular changes and pathways involved in cardiac maturation.
- To explore potential therapeutic strategies for CVDs based on developmental insights.
Main Methods:
- Quantitative proteomics using iTRAQ was performed on mouse ventricular tissues from embryonic day 18.5 to postnatal week 8.
- Analysis identified 3422 quantified proteins and characterized proteomic shifts during cardiac development.
- Bioinformatic analysis focused on dysregulated proteins and enriched signaling pathways.
Main Results:
- A comprehensive proteomic atlas of mouse cardiac development was established.
- Key developmental events, including the metabolic shift from glycolysis to beta-oxidation, were characterized by proteomic changes.
- Significantly dysregulated proteins associated with cardiac regeneration (e.g., Erbb2, Agrin, Hmgb) and the peroxisome proliferator-activated receptor (PPAR) signaling pathway were identified.
Conclusions:
- The peroxisome proliferator-activated receptor (PPAR) signaling pathway is significantly enriched during cardiac development.
- Activation of the PPAR pathway, using bezafibrate, enhanced cardiomyocyte (H9C2) activity by increasing Cpt1α expression.
- PPAR pathway activation represents a potential therapeutic strategy for treating cardiovascular diseases.
Abstract:
Cardiovascular diseases (CVDs) are among the most morbid and deadly types of diseases worldwide, while the existing therapeutic approaches all have their limitations. Mouse heart undergoes a very complex postnatal developmental process, including the 1-week window in which cardiomyocytes (CMs) maintain relatively high cell activity. The underlying mechanism provides an attractive direction for CVDs treatment. Herein, we collected ventricular tissues from mice of different ages from E18.5D to P8W and performed iTRAQ-based quantitative proteomics to characterize the atlas of cardiac development. A total of 3422 proteins were quantified at all selected time points, revealing critical proteomic changes related to cardiac developmental events such as the metabolic transition from glycolysis to beta-oxidation. A cluster of significantly dysregulated proteins containing proteins that have already been reported to be associated with cardiac regeneration (Erbb2, Agrin, and Hmgb) was identified. Meanwhile, the peroxisome proliferator-activated receptor (PPAR) signaling pathway (Cpt1α, Hmgcs2, Plin2, and Fabp4) was also found specifically enriched. We further revealed that bezafibrate, a pan-activator of PPAR signaling pathway markedly enhanced H9C2 cardiomyocyte activity via enhancing Cpt1α expression. This work provides new hint that activation of PPAR signaling pathway could potentially be a therapeutic strategy for the treatment of CVDs.
