Cargando…

Potential Influence of Age and Diabetes Mellitus Type 1 on MSH2 (MutS homolog 2) Expression in a Rat Kidney Tissue

Background: Homeostasis of proliferating tissues is strongly dependent on intact DNA. Both neoplastic and non-neoplastic diseases have been associated with MSH2 (MutS homolog 2, a mismatch repair protein) deficiency. In this study, we examined how age and diabetes mellitus influence the expression o...

Descripción completa

Detalles Bibliográficos
Autores principales: Babić, Paško, Filipović, Natalija, Hamzić, Lejla Ferhatović, Puljak, Livia, Vukojević, Katarina, Benzon, Benjamin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9222930/
https://www.ncbi.nlm.nih.gov/pubmed/35741815
http://dx.doi.org/10.3390/genes13061053
Descripción
Sumario:Background: Homeostasis of proliferating tissues is strongly dependent on intact DNA. Both neoplastic and non-neoplastic diseases have been associated with MSH2 (MutS homolog 2, a mismatch repair protein) deficiency. In this study, we examined how age and diabetes mellitus influence the expression of MSH2 in the kidney. Methods: To study the effect of age, three groups of healthy rats were formed: 2 months, 8 months, and 14 months old. Two groups of diabetic rats were formed: 8 months old and 14 months old. Expression of MSH2 in the kidney was studied by quantifying immunofluorescent staining. Results: Age was identified as the main factor that influences MSH2 expression in kidneys. The effect of age followed parabolic dynamics, with peak expression at 8 months of age and similar levels at 2 and 14 months. Diabetes had an age-dependent effect, which manifested as the increase of MSH2 expression in 14-month-old diabetic rats in comparison to healthy animals. Conclusions: Age influences MSH2 expression in the kidney more than diabetes mellitus. Since ageing is a risk factor for kidney neoplasia, downregulation of MSH2 in older rats might represent one of the pro-oncogenic mechanisms of ageing at a molecular level.