P16 ^INK4a Deletion Ameliorated Renal Tubulointerstitial Injury in a Stress-induced Premature Senescence Model of Bmi-1 Deficiency.

ABSTRACT: To determine whether p16 ^INK4a deletion ameliorated renal tubulointerstitial injury by inhibiting a senescence-associated secretory phenotype (SASP) in Bmi-1-deficient (Bmi-1 ^-/-) mice, renal phenotypes were compared among 5-week-old Bmi-1 and p16 ^INK4a double-knockout, and Bmi-1 ^-/- and wild-type mice. Fifth-passage renal interstitial fibroblasts (RIFs) from the three groups were analyzed for senescence and proliferation. The effect of Bmi-1 deficiency on epithelial-to-mesenchymal transition (EMT) was examined in Bmi-1-knockdown human renal proximal tubular epithelial (HK2) cells, which were treated with concentrated conditioned medium (CM) from the fifth-passage renal interstitial fibroblasts (RIFs) of above three group mice or with exogenous T

SUBMITTER: Jin J 

PROVIDER: S-EPMC5548892 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature