Influence of the Expression of Inflammatory Markers on Kidney after Fetal Programming in an Experimental Model of Renal Failure.

Carlos Donizete Pereira Júnior,Maria Aparecida Da Glória,Niels Olsen Saraiva Câmara,Aldo Rogelis Aquiles Rodrigues,Fernanda Rodrigues Helmo,Rosana Rosa Miranda Corrêa,Aline Cristina Souza Da Silva,Lenaldo Branco Rocha,Marlene Antônia Dos Reis,Juliana Reis Machado,Vicente De Paula Antunes Teixeira,Camila Souza De Oliveira Guimarães,Laura Penna Rocha

doi:10.1155/2016/9151607

Abstract

Objective. To evaluate the expression of inflammatory markers in experimental renal failure after fetal programming. Methods. The offspring aged two and five months were divided into four groups: CC (control dams, control offspring); DC (diabetic dams, control offspring); CFA (control dams, folic acid offspring, 250 mg/Kg); and DFA (diabetic dams, folic acid offspring). Gene expression of inflammatory markers MCP-1, IL-1, NOS3, TGF-β, TNF-α, and VEGF was evaluated by RT-PCR. Results. MCP-1 was increased in the CFA and DFA groups at two and five months of age, as well as in DC5 when compared to CC5. There was a higher expression of IL-1 in the CFA2, DFA2, and DC2 groups. There was a decrease in NOS3 and an increase in TNF-α in DFA5 in relation to CFA5. The gene expression of TGF-β increased in cases that had received folic acid at two and five months, and VEGF decreased in the CFA5 and DFA5 groups. DC5 showed increased VEGF expression in comparison with CC5. Conclusions. Gestational diabetes mellitus and folic acid both change the expression of inflammatory markers, thus demonstrating that the exposure to harmful agents in adulthood has a more severe impact in cases which underwent fetal reprogramming.

Highlights

IntroductionThe theory of fetal origins of adult disease (FOAD) proposed by Barker et al (1986) claims that physiological changes during intrauterine development would promote the restriction of development, as well as ultrastructural and physiological changes that would predispose to the early development of cardiovascular and metabolic diseases in adulthood [1,2,3].In a model of diabetes in pregnancy, it was demonstrated that hyperglycemia promotes oxidative stress in the offspring, affecting the balance between oxidant and antioxidant factors [4], an increase in inflammatory markers, and a reduction in the number of glomeruli with aging [5].The Streptozotocin (STZ) may cause mild or severe diabetes mellitus (DM) in the dam and lead to different effects in rat offspring [6]
This study aimed to demonstrate the influence of fetal programming on the development of Acute renal failure (ARF), as well as the prognostic evolution of individuals that develop the disease
Real-Time Polymerase Chain Reaction (RT-PCR) analysis showed an increase in gene expression for monocyte chemoattractant protein-1 (MCP-1) in the groups that had received folic acid (CFA2 and DFA2) in comparison with their respective control groups

Summary

Introduction

The theory of fetal origins of adult disease (FOAD) proposed by Barker et al (1986) claims that physiological changes during intrauterine development would promote the restriction of development, as well as ultrastructural and physiological changes that would predispose to the early development of cardiovascular and metabolic diseases in adulthood [1,2,3].In a model of diabetes in pregnancy, it was demonstrated that hyperglycemia promotes oxidative stress in the offspring, affecting the balance between oxidant and antioxidant factors [4], an increase in inflammatory markers, and a reduction in the number of glomeruli with aging [5].The Streptozotocin (STZ) may cause mild or severe diabetes mellitus (DM) in the dam and lead to different effects in rat offspring [6]. The theory of fetal origins of adult disease (FOAD) proposed by Barker et al (1986) claims that physiological changes during intrauterine development would promote the restriction of development, as well as ultrastructural and physiological changes that would predispose to the early development of cardiovascular and metabolic diseases in adulthood [1,2,3]. In a model of diabetes in pregnancy, it was demonstrated that hyperglycemia promotes oxidative stress in the offspring, affecting the balance between oxidant and antioxidant factors [4], an increase in inflammatory markers, and a reduction in the number of glomeruli with aging [5]. The Streptozotocin (STZ) may cause mild or severe diabetes mellitus (DM) in the dam and lead to different effects in rat offspring [6].

Methods

Results

Conclusion