مجله دانشگاه علوم پزشکی گرگان (Jan 2019)

Effect of gestational diabetes on expersion of desmocollin 2 and collagen structural genes in C57BL mouse embryo heart

  • Sara Pasban Bovanlo,
  • Masoud Golalipour,
  • Kamran Haidari,
  • Mohammad Jafar Golalipour

Journal volume & issue
Vol. 20, no. 4
pp. 31 – 35

Abstract

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Background and Objective: Gestational diabetes (GDM) is a metabolic disorder which is caused by insufficient secretion of insulin. GDM is a risk factor for embryo during pregnancy and it is possible leads to congenital heart defects (CHD). Some of these defects may be due to a change in the expression of some of the important structural genes in the heart. Desmocollin 2 and collagen structural genes have important role in the cell adhesion of the cardiomyocytes.This study was done to determine the effect of gestational diabetes on expersion of desmocollin 2 and col5a2 structural genes in C57BL mouse embryo heart. Methods: In this experimental study, 12 adult female and six adult male C57BL mice were used.After mating of the animals and observation of the vaginal plug, the female mice with vaginal plug were randomly divided into diabetic and control groups. At the first day of pregnancy, Induction of gestational diabetes mellitus in dams in the diabetic group was performed by the intraperitoneal (IP) injection of Streptozotocin with a dose of 150 mg / kg body weight per day in GD1. While in the control group, only citrate buffer was injected.Cesarean Surgery was done at E11.5 and embryo's heart was extracted from the body.Extraction of RNA, cDNA, and quantitative measurements of the amount of RNA were performed using Real -Time PCR. Results: Induction of gestational diabetes increased the expersion of desmocollin 2 and col5a2 structural genes in compared to controls, althought only the expersion of desmocollin 2 gene was significant (P<0.05). Conclusion: We suggest that the induction of DM lead to upregulation of structural genes primarily including desmocollin 2 and col5a2 in embryos heart development.

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