LncRNA SAL-RNA1 Knockdown Suppressed Pink1-Mediated Mitophagy Protects Against CS-Induced Alveolar Cells Senescence Through Regulation of Sirt1

Background LncRNAs pays an important roles in the regulation of alveolar cells in cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD). However, the role of lncRNA SAL-RNA1 in promoting mitophagy and reduces senescence of alveolar cells in COPD is unknow. Methods This study is aims to elucidate the underlying mechanism of LncRNA SAL-RNA1 and phosphatase and tensin homolog (PTEN)-induced putative protein kinase 1 (PINK1) expression were upregulated in alveolar of emphysema mice and CS treated alveolar epithelial cells. LncRNA SAL-RNA1 knockdown suppressed mitophagy and induced senescence of alveolar cells while overexpressing lncRNA SAL-RNA1 promoted mitophagy and reduced the senescence of alveolar cells. In addition, lncRNA SAL-RNA1 interacted with Sirt1 and regulated the upgradation of Sirt1. Results We further found lncRNA SAL-RNA1 regulated Pink1 expression through Sirt1. Mechanistically, lncRNA SAL-RNA1 regulated PinK1-mediated mitophagy and senescence of alveolar cells through regulation Sirt1. Conclusion Finally, overexpression lncRNA SAL-RNA1 promote mitophagy and relieved emphysema.

Phosphorylation of Zona Occludens-2 by Protein Kinase Cε Regulates Its Nuclear Exportation

Here, we have analyzed the subcellular destiny of newly synthesized tight junction protein zona occludens (ZO)-2. After transfection in sparse cells, 74% of cells exhibit ZO-2 at the nucleus, and after 18 h the value decreases to 17%. The mutation S369A located within the nuclear exportation signal 1 of ZO-2 impairs the nuclear export of the protein. Because Ser369 represents a putative protein kinase C (PKC) phosphorylation site, we tested the effect of PKC inhibition and stimulation on the nuclear export of ZO-2. Our results strongly suggest that the departure of ZO-2 from the nucleus is regulated by phosphorylation at Ser369 by novel PKCε. To test the route taken by ZO-2 from synthesis to the plasma membrane, we devised a novel nuclear microinjection assay in which the nucleus served as a reservoir for anti-ZO-2 antibody. Through this assay, we demonstrate that a significant amount of newly synthesized ZO-2 goes into the nucleus and is later relocated to the plasma membrane. These results constitute novel information for understanding the mechanisms that regulate the intracellular fate of ZO-2.