Human antigen R helps lung cells become scar-forming cells and boosts tissue buildup

In human lung fibroblasts treated with transforming growth factor β1 (TGF-β1), there was a significant increase in the translocation of HuR from the nucleus to the cytoplasm.

• HuR is an RNA binding protein that stabilizes messenger RNA, potentially influencing protein levels involved in fibrosis.
• Knockdown of HuR led to a significant reduction in α-SMA protein and the extracellular matrix proteins COL1A1, COL3A, and FN in TGF-β-treated human lung fibroblasts.
• HuR was found to bind to mRNA for ACTA2, COL1A1, COL3A1, and FN, indicating its role in regulating these genes.
• While HuR knockdown affected the mRNA stability of ACTA2, it did not have the same effect on the ECM genes COL1A1, COL3A1, or FN.
• Mouse models of pulmonary fibrosis showed higher levels of cytoplasmic HuR in lung structural cells compared to controls.
• In human lungs affected by idiopathic pulmonary fibrosis, increased cytoplasmic HuR was also observed.

Simplified