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Role of the calcium sensing receptor in cardiomyocyte apoptosis via mitochondrial dynamics in compensatory hypertrophied myocardium of spontaneously hypertensive rat
- Source :
- Biochemical and Biophysical Research Communications. 487:728-733
- Publication Year :
- 2017
- Publisher :
- Elsevier BV, 2017.
-
Abstract
- Calcium sensing receptor (CaSR) mediates pathological cardiac hypertrophy. Mitochondria maintain their function through fission and fusion and disruption of mitochondrial dynamic is linked to various cardiac diseases. This study examined how inhibition of CaSR by the inhibitor Calhex231 affected the mitochondrial dynamics in a hypertensive model in rats. Spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were used in this study. Cardiac function and blood pressure was evaluated at the end of the study. SHRs showed increases in the ratio of heart weight to body weight and the levels of CaSR; all of these increases were suppressed by Calhex231. Additionally, Calhex231 treatment of SHRs changed the expression of proteins involved in mitochondrial dynamics. Our results demonstrated that CaSR activation induced cardiomyocyte apoptosis through the mitochondrial dynamics mediated apoptotic pathway in hypertensive hearts.
- Subjects :
- 0301 basic medicine
Cardiac function curve
medicine.medical_specialty
Biophysics
Apoptosis
Blood Pressure
030204 cardiovascular system & hematology
Mitochondrion
Biology
Rats, Inbred WKY
Biochemistry
03 medical and health sciences
0302 clinical medicine
Spontaneously hypertensive rat
Rats, Inbred SHR
Internal medicine
medicine
Animals
Myocytes, Cardiac
Calcium Signaling
cardiovascular diseases
Molecular Biology
Cells, Cultured
Heart weight
Cell Biology
Mitochondria
Rats
030104 developmental biology
Endocrinology
Blood pressure
Hypertension
Calcium
Calcium-sensing receptor
Receptors, Calcium-Sensing
Cardiomyocyte apoptosis
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 487
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....0396eb876f2047692708c99066e55688