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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

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Decrease in calcium-sensing receptor in the progress of diabetic cardiomyopathy

Shu-zhi Bai1, Jian Sun, Hao Wu

  • 1Department of Pathophysiology, Harbin Medical University, Harbin 150086, China.

Diabetes Research and Clinical Practice
|December 6, 2011
PubMed

Insights

Diabetic cardiomyopathy (DCM) involves reduced myocardial calcium-sensing receptor (CaSR) expression, impairing calcium handling. Spermine, a CaSR agonist, may prevent DCM progression by restoring calcium homeostasis.

Area of Science:

  • Cardiology
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetic cardiomyopathy (DCM) is a cardiac complication of diabetes mellitus (DM).
  • The role of the calcium-sensing receptor (CaSR) in DCM pathogenesis is not fully understood.
  • Intracellular calcium ([Ca(2+)](i)) dysregulation is a hallmark of cardiac dysfunction.

Purpose of the Study:

  • To investigate the dynamic expression of CaSR in the myocardium of diabetic rats.
  • To explore the role of CaSR in the development and progression of DCM.
  • To examine the effect of spermine, a CaSR agonist, on cardiac function in diabetic rats.

Main Methods:

  • Type 2 DM model induced by streptozotocin (STZ) in Wistar rats.
  • Echocardiography for cardiac function assessment.
  • Western blot for protein expression analysis (CaSR, PKC-α, PLN, SERCA, RyR).
  • Measurement of intracellular calcium concentration ([Ca(2+)](i)).

Main Results:

  • Diabetic rats showed decreased myocardial CaSR, RyR, and SERCA/PLN expression over time.
  • Increased intracellular calcium ([Ca(2+)](i)), PKC-α, and PLN levels were observed in diabetic rats.
  • Cardiac structure and function (systolic and diastolic) were impaired in diabetic rats.
  • Spermine treatment attenuated cardiac dysfunction and structural abnormalities.

Conclusions:

  • Myocardial CaSR expression is reduced during DCM progression.
  • Impaired intracellular calcium homeostasis is a key mechanism in DCM.
  • CaSR modulation may represent a therapeutic target for diabetic cardiomyopathy.

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