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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Calcium-sensing receptor induces rat neonatal ventricular cardiomyocyte apoptosis
Yi-hua Sun1, Mei-na Liu, Hong Li
1Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Abstract:
The calcium-sensing receptor (CaSR) exists in many tissues, and its expression has been identified in rat cardiac tissue. However, the physiological importance and pathophysiological involvement of CaSR in homeostatic regulation of cardiac function are unclear. To investigate the relation of CaSR and apoptosis in cardiomyocytes, we examined the role of the CaSR activator gadolinium chloride (GdCl(3)) in rat neonatal ventricular cardiomyocytes. Expression of the CaSR protein was observed by Western blot. The apoptotic ratio of rat neonatal ventricular cardiomyocytes was measured with flow cytometry and immunofluorescence techniques. A laser scan confocal microscope was used to detect the intracellular concentration of calcium ([Ca(2+)](i)) in rat neonatal ventricular cardiomyocytes using the acetoxymethyl ester of fluo-3 (fluo-3/(AM)) as a fluorescent dye. The results showed that GdCl(3) increased the phosphorylation of extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal protein kinases (JNK), and p38. GdCl(3) also activated caspase 9 and increased apoptosis in myocyte by increasing [Ca(2+)](i). In conclusion, these results suggest that CaSR promotes cardiomyocyte apoptosis in rat neonatal ventricular cardiomyocytes through activation of mitogen-activated protein kinases and caspase 9 signaling pathways.
Insights
The calcium-sensing receptor (CaSR) promotes heart cell death (apoptosis) in rats. Activation of CaSR increases intracellular calcium, leading to cardiomyocyte apoptosis via specific signaling pathways.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- The calcium-sensing receptor (CaSR) is present in cardiac tissue, but its role in heart function and disease is not well understood.
- Investigating CaSR's involvement in cardiomyocyte apoptosis is crucial for understanding cardiac pathophysiology.
Purpose of the Study:
- To explore the relationship between CaSR and apoptosis in cardiomyocytes.
- To elucidate the signaling mechanisms by which CaSR influences cardiomyocyte apoptosis.
Main Methods:
- Western blot to detect CaSR protein expression.
- Flow cytometry and immunofluorescence to measure cardiomyocyte apoptosis.
- Laser scan confocal microscopy to quantify intracellular calcium levels ([Ca(2+)](i)).
Main Results:
- Gadolinium chloride (GdCl(3)), a CaSR activator, increased the phosphorylation of ERK, JNK, and p38.
- GdCl(3) activated caspase 9 and elevated intracellular calcium concentrations.
- These effects led to increased apoptosis in rat neonatal ventricular cardiomyocytes.
Conclusions:
- CaSR activation promotes cardiomyocyte apoptosis in neonatal rat ventricular cells.
- This process involves the activation of mitogen-activated protein kinases (MAPKs) and the caspase 9 signaling pathway.
- CaSR plays a significant role in the regulation of cardiomyocyte apoptosis, offering potential therapeutic targets.
