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Abstract: PO1392

PTEN-Induced Kinase 1 Has Association with Renal Aging in the Context of Inflammatory Response

Session Information

Category: Glomerular Diseases

  • 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix

Authors

  • Jeong, Hyeyun, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • Min Heui, Ha, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • Sung, Min ji, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • Lee, Yu ho, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • An, Hyun-Ju, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • Lim, Song Hee, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
  • Lee, So-young, CHA Bundang Medical Center, Seongnam, Gyeonggi-do, Korea (the Republic of)
Background

Among several changes of aging-related human organ system, functional and structural deterioration of kidney is the most dramatic phenomenon, and the role of mitophagy has recently considered important in pro-aging process in CKD patients. PTEN-induced kinase 1 (PINK1), known to be associated with age-related diseases regulates mitochondrial dysfunction. To enhance understanding the function of PINK-1 on aging, we compared whole-kidney RNA sequencing between naturally aging mice (24-month-old) and PINK1 knock out aging mice.

Methods

Kyoto Encyclopedia of Genes and Genomes pathway analysis and gene ontology analysis were performed for gene expression analysis. To investigate the role of PINK1 on aging, we used Pink1-deficient mice and PINK1-overexpressing HKC8.

Results

Compared to naturally aging kidneys, PINK1 knock out aging mice showed prominent expression of the genes related to cytokines, immune system response, and inflammation (Fig 1). We also investigated the function of PINK1 on PINK1 (-/-) aging mice. PINK1 deficiency showed aggravated tubulointerstitial fibrosis on PAS staining (Fig2A), and the Urinary Albumin-Creatinine Ratio increased more prominently according to aging in PINK1 (-/-) mice (Fig2B). The Quantitative PCR analysis validated that the expression of genes associated with aging, fibrosis, and inflammation increased in PINK1 (-/-) mice compared to age-matched controls (Fig2C). Under treatment with H2O2, the expression of aging and pro-inflammatory marker decreased in PINK1-overexpressing HKC8 compared to naturally aging mice (Fig2D).

Conclusion

In conclusion, our results suggest that PINK1 deficiency contributes to renal aging process via proinflammatory change in the kidney.

Fig 1

Fig 2