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P0977LOW EXPRESSION OF AUTOPHAGY-RELATED PROTEIN 5 (ATG5) LEADS TO SUPPRESSION OF AUTOPHAGY IN PATIENTS WITH DIABETIC NEPROPATHY AND RETINOPATHY

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Abstract Background and Aims Autophagy is a catabolic mechanism that involves lysosomal-dependent degradation of unnecessary or dysfunctional intracellular components. Autophagy plays role in many biological processes, including diabetic nephropathy (DN) and diabetic retinopathy (DR). Autophagy-related gene 5 (ATG5) is one of the most important participants in the autophagy mechanism. Deficiencies in ATG5 protein levels are associated with several diseases by influencing the level of autophagy pathway. Our study's aim was to investigate if aberrant expression of ATG5 protein or Atg5 gene is associated with DN or DR. Method The study included 120 human participants in 4 groups – Healthy, diabetic (DM), DN and DR; and 10 mice in 2 groups – healthy and DN. Western blot analyses of ATG5 and its downstream collaborator LC3B were performed on human white blood cell (WBC) lysates and murine renal lysates. Immunohistochemical analysis was performed on mice renal tissues. Quantitative real-time PCR analysis of ATG5 was performed on total mRNA isolated from human WBC. Results Conclusion
Title: P0977LOW EXPRESSION OF AUTOPHAGY-RELATED PROTEIN 5 (ATG5) LEADS TO SUPPRESSION OF AUTOPHAGY IN PATIENTS WITH DIABETIC NEPROPATHY AND RETINOPATHY
Description:
Abstract Background and Aims Autophagy is a catabolic mechanism that involves lysosomal-dependent degradation of unnecessary or dysfunctional intracellular components.
Autophagy plays role in many biological processes, including diabetic nephropathy (DN) and diabetic retinopathy (DR).
Autophagy-related gene 5 (ATG5) is one of the most important participants in the autophagy mechanism.
Deficiencies in ATG5 protein levels are associated with several diseases by influencing the level of autophagy pathway.
Our study's aim was to investigate if aberrant expression of ATG5 protein or Atg5 gene is associated with DN or DR.
Method The study included 120 human participants in 4 groups – Healthy, diabetic (DM), DN and DR; and 10 mice in 2 groups – healthy and DN.
Western blot analyses of ATG5 and its downstream collaborator LC3B were performed on human white blood cell (WBC) lysates and murine renal lysates.
Immunohistochemical analysis was performed on mice renal tissues.
Quantitative real-time PCR analysis of ATG5 was performed on total mRNA isolated from human WBC.
Results Conclusion.

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