Authors

LIN FAN1, HEYU MENG2, YUSHUANG YANG3, KAIYAO SHI3, DONGNA LIU3, FANBO MENG3*

Departments

1Postgraduated student of Department of Cardiovascular Medicine, China-Japan Union Hospital of Jilin University, now work in Echocardiography Department, First Affiliated Hospital of Soochow University, Suzhou 215006, China - 2Medical College of Yanbian University, Yanji 133000, China - 3Department of Cardiovascular Medicine, China-Japan Union Hospital of Jilin University, Jilin 130033, China

Abstract

Introduction: It has been accepted that gene play a role in the evolution of acute myocardial infarction (AMI). We found protein kinase C iota (PRKCI) gene had different expression in the peripheral leukocytes of patients with AMI through gene chip.

Materials and methods: 20 AMI patients were randomly selected and set as the AMI group, and 20 healthy people were selected as the control group. The clinical data of all study subjects were recorded. 6 ml of venous blood was sampled from both two groups for ribonucleic acid (RNA) and protein extraction; reverse transcription polymerase chain reaction (RT-PCR) and Western blot were then performed to detect the expression of PRKCI gene using glyceraldehyde -3 -phosphate dehydrogenase (GAPDH) and β- actin as the internal reference, respectively.

Results: There existed significant differences in low-density lipoprotein (LDL-ch) and high-density lipoprotein (HDL-ch) between the two groups. At the RNA level, the relative expression of PRKCI gene in the AMI group to the control group was 0.62 ± 0.11 (P=0.032); at the protein level, the PRKCI protein expression in the AMI group was also significantly reduced than the control group.

Conclusions: The low expression of PRKCI gene takes part in the development of AMI. PRKCI gene may be used as a molecular marker for the diagnosis of AMI, even treated as a therapeutic target for the clinical diagnosis and treatment of AMI patients.

Keywords

Acute myocardial infarction, PRKCI gene, RNA, PRKCI protein, molecular labeling

DOI:

10.19193/0393-6384_2018_2_50