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Published on: February 1, 2018
Caspase-1 transcripts in failing human heart after mechanical unloading
Tommaso Prescimone1, Andrea D'Amico2, Chiara Caselli1
1CNR Institute of Clinical Physiology, Laboratory of Cardiovascular Biochemistry, Pisa, Italy.
Insights
Left Ventricular Assist Device (LVAD) implantation in heart failure patients alters Caspase-1 (Casp-1) signaling. This suggests inflammation may regulate Casp-1 and apoptosis, offering therapeutic insights for cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Inflammation Studies
Background:
- Caspase-1 (Casp-1) plays a key role in cardiovascular diseases (CVDs) by promoting inflammation and cardiomyocyte loss.
- Targeting Casp-1 is a potential strategy to prevent the progression of heart failure (HF).
Purpose of the Study:
- To investigate the impact of Left Ventricular Assist Device (LVAD) implantation on cardiac inflammation and apoptosis.
- To assess the modulation of Caspase-1 (Casp-1) expression levels following LVAD implantation.
Main Methods:
- Cardiac tissue samples were obtained from end-stage HF patients before and after LVAD implantation.
- Samples from heart transplant recipients (HTx) on medical therapy served as controls.
- Real-time PCR was used to evaluate the cardiac expression of Casp-1 and its inhibitors, COP and ICEBERG.
Main Results:
- Caspase-1 (Casp-1) expression was significantly elevated in patients pre-LVAD compared to HTx controls (p=0.006).
- ICEBERG levels were markedly reduced in pre-LVAD patients relative to HTx controls (p<0.001).
- No significant difference in COP expression was observed between groups.
Conclusions:
- LVAD implantation is associated with a distinct Caspase-1 (Casp-1) system profile in heart failure patients.
- Inflammation appears to be a critical factor in a negative feedback loop regulating Casp-1 signaling and downstream apoptosis.
Background:
Caspase (Casp)-1 has been indicated as a molecular target capable of preventing the progression of cardiovascular diseases, including heart failure (HF), due to its central role in promoting inflammation and cardiomyocyte loss. The aim of this study was to assess whether Left Ventricular Assist Device (LVAD) implantation modifies the inflammatory and apoptotic profile in the heart through the modulation of Casp-1 expression level.
Methods:
Cardiac tissue was collected from end-stage HF patients before LVAD implant (pre-LVAD group, n=22) and at LVAD removal (post-LVAD, n=6), and from stable HF patients on medical therapy without prior circulatory support (HTx, n=7) at heart transplantation, as control. The cardiac expression of Casp-1, of its inhibitors caspase recruitment domain (CARD) only protein (COP) and CARD family, member 18 (ICEBERG), was evaluated by real-time PCR in the three groups of patients.
Results:
Casp-1 was increased in the pre-LVAD group compared to HTx (p=0.006), while on the contrary the ICEBERG level was significantly decreased in pre-LVAD with respect to HTx patients (p<0.001); no difference in COP expression level was found.
Conclusions:
This study describes a specific pattern of the Casp-1 system associated with inflammation and apoptosis markers in patients who require LVAD insertion. The inflammation could be the key process regulating, in a negative loop, Casp-1 signaling and its down-stream effects, apoptosis included.
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