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Biology subjects

Liu, H.-l.

Publications and source records attributed to Liu, H.-l..

2 recordsLinked to original sources

Autophagy-associated Production of Antimicrobial Peptides hBD1 and LL37 Exhibits Anti-Bacillus Calmette-Guerin Effects in Lung Epithelial Cells.

Antimicrobial peptides (AMPs) constitute important groups of bactericidal polypeptides against various microorganisms that exhibit their anti-bacteria activity through cleavage of precursor peptides into the active form of 50-100 amino acids in length. Various AMP cleavage mechanisms have been reported in different cell types; however, those in Mycobacterium tuberculosis (MTB)-infected lung epithelial cells remain unknown. In the present study, we found that MTB-infected lung epithelial cells expressed high level of the AMPs hBD1 and LL37 to kill intracellular MTB as the first-line immune barrier against MTB infection. Notably, their production in the lung epithelial cells was closely related to the function of autophagosomes and lysosomes. Experimental induction of autophagy in lung epithelial cells could enhance the expression of active hBD1 and LL37 at the post-transcriptional level, whereas silencing of these two active AMPs could decrease the bactericidal effect of autophagy. These findings indicated that cleavage of peptide precursors to form active AMPs might constitute a previously unrecognized antibacterial mechanism of autophagy. Author summaryLM and RW conceived and designed the experiments; RW performed the experiments and analyzed the data; QW analyzed the data and contributed reagents/materials/analysis tools; HL performed the experiments; XZ, JY, YL and ZH analyzed the data. LM and RW drafted the manuscript.

immunology

eIF5a reduction via decreased Klf5 leads to cell senescence by mitochondrial fission in VSMCs

Though dysregulation of mitochondrial dynamics has been linked to cellular senescence, which contributes to advanced age-related disorders, it is unclear how Klf5, an essential transcriptional factor of cardiovascular remodeling, mediates the link between mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence. Here we show that Klf5 downregulation in VSMCs is correlated with rupture of abdominal aortic aneurysm (AAA), an age-related vascular disease. Mice lacking Klf5 in VSMCs exacerbate vascular senescence and progression of Ang II-induced AAA by facilitating ROS formation. Klf5 knockdown enhances, while Klf5 overexpression suppresses mitochondrial fission. Mechanistically, Klf5 activates eIF5a transcription through binding to the promoter of eIF5a, which in turn preserves mitochondrial integrity by interacting with Mfn1. Accordingly, decreased expression of eIF5a elicited by Klf5 downregulation leads to mitochondrial fission and excessive ROS production. Inhibition of mitochondrial fission decreases ROS production and VSMC senescence. Our studies provide a potential therapeutic target for age-related vascular disorders.

biochemistry