TGF-β1/IL-11/MEK/ERK signaling mediates senescence-associated pulmonary fibrosis in a stress-induced premature senescence model of Bmi-1 deficiency.

ABSTRACT: To study whether TGF-β1/IL-11/MEK/ERK (TIME) signaling mediates senescence-associated pulmonary fibrosis (SAPF) in Bmi-1-deficient (Bmi-1^-/-) mice and determines the major downstream mediator of Bmi-1 and crosstalk between p16^INK4a and reactive oxygen species that regulates SAPF, phenotypes were compared among 7-week-old p16^INK4a and Bmi-1 double-knockout, N-acetylcysteine (NAC)-treated Bmi-1^-/-, Bmi-1^-/-, and wild-type mice. Pulmonary fibroblasts and alveolar type II epithelial (AT2) cells were used for experiments. Human pulmonary tissues were tested for type Ι collagen, α-smooth muscle actin (α-SMA), p16^INK4a, p53, p21, and TIME signaling by using enzyme-linked immunosorbent assay (ELISA). Our results demonstrated that Bm

SUBMITTER: Chen H 

PROVIDER: S-EPMC7000795 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature