The aggregation of platelets on the plaque rupture site on the coronary artery is reported to cause acute ischemic heart diseases (AIHD i.e. ACS, AMI, etc). Strokes are reported to occur due to thrombosis on the arteries of the brain. Dermcidin isoform 2 (dermcidin), an environmentally induced stress protein, was found to high in above mentioned diseases. The effect of this protein was investigated on the genesis of diabetes mellitus and hypertension, the two major atherosclerotic risk factors. The mechanism of dermcidin isoform-2 was investigated in the disease progression and its regulation.Design and Method:
Platelets aggregation was measured by aggregometer. Dermcidin protein was isolated by SDS-PAGE. Nitric Oxide (NO) was measured by methemoglobin method. Binding of stress protein was analyzed by Scatchard plot. Glucose Activated Nitric Oxide Synthase (GANOS) in liver cells and (r)-cortexin synthesis in the kidney cortex cells was determined by in-vitro translation of mRNA. Dermcidin in the Plasma of Hypertensive Patients was analyzed by immunoblot. Synthesis of (r)-cortexin was determined in the goat kidney cortex cells in the presence of low dose of aspirin.Results:
The level of dermcidin was found to five folds higher in AMI than ACS and forty folds higher than normal. The protein was also found in stroke patients. Dermcidin protein possessed a high affinity binding sites in AMI platelets. The NO and insulin level was found to very low in strokes. A specific and unique dose of aspirin and insulin was able to neutralize the effect of dermcidin in AMI and stroke. The plasma dermcidin and cortexin was found to higher and lower respectively in hypertensive patients. It was also found that aspirin could be able to increase the expression of (r)-cortexin.Conclusions:
Dabetes and hypertension might be inhibited by the regulation of dermcidin and (r)-cortexin and as a result heart disease and stroke could be restricted.