Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: UMLS:C0037116 (
silicosis
)
1,822
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Silicosis
is a progressive fibrotic disease of lung tissue caused by long-term inhalation of SiO
2
. However, relatively few studies of the direct effects of SiO
2
on lung fibroblasts have been performed.
PPP1R13B
is a major member of the apoptosis-stimulating proteins of the p53 family, but its role in pulmonary fibrosis is unclear. To elucidate the role of
PPP1R13B
in the pathological process of
silicosis
, we explored the molecular mechanisms related to
PPP1R13B
and the functional effects of proliferation and migration of fibroblasts. Through lentivirus transfection, Western blotting, and fluorescent
in situ
hybridization experiments, we found that SiO
2
downregulated circRNA-012091 (circ-012091) expression in lung fibroblasts and induced upregulation of downstream
PPP1R13B
. Transfection of L929 cells with
PPP1R13B
CRISPR NIC plasmid inhibited the upregulation of endoplasmic reticulum stress (ERS) and autophagy-related protein expression in lung fibroblasts treated with SiO
2
, and induced decreases in cell proliferation, migration, and viability. Transfection of L929 cells with the
PPP1R13B
CRISPR ACT plasmid induced increases in cell proliferation, migration, and viability. In addition, the ERS inhibitor salubrinal and the autophagy inhibitor 3-methyladenine inhibited the increased migration of L929 cells transfected with the
PPP1R13B
CRISPR ACT plasmid. These results suggest that
PPP1R13B
regulated by circ-012091 promotes the proliferation and migration of lung fibroblasts through ERS and autophagy, and plays a crucial role in the development of pulmonary fibrosis in
silicosis
.
...
PMID:CircRNA-012091/PPP1R13B-mediated Lung Fibrotic Response in Silicosis via Endoplasmic Reticulum Stress and Autophagy. 3090 29
