Lipopolysaccharide triggers nuclear import of Lpcat1 to regulate inducible gene expression in lung epithelia

• 作者: Bryon Ellis Courtney Snavely Leah Kaercher
• 来源期刊: 世界生物化学杂志：英文版（电子版）
• 学科: 医学
• 关键词: LIPOPOLYSACCHARIDE Nuclear import LYSOPHOSPHATIDYLCHOLINE ACYLTRANSFERASE 1 Gene expression LUNG EPITHELIA Epigenetic code Quantitative reverse transcription polymerase chain reaction HAEMOPHILUS influenza Escherichia coli
• 年，卷（期）: 2012,（7）
• 页码范围: 159-166
• 页数: 8页
• 分类号: R378

摘要

AIM:To report that Lpcat1 plays an important role in regulating lipopolysaccharide (LPS) inducible gene tran-scription. METHODS:Gene expression in Murine Lung Epithelial MLE-12 cells with LPS treatment or Haemophilus influenza and Escherichia coli infection was analyzed by employing quantitative Reverse Transcription Polymerase Chain Reaction techniques. Nucleofection was used to deliver Lenti-viral system to express or knock down Lpcat1 in MLE cells. Subcellular protein fractionation and Western blotting were utilized to study Lpcat1 nuclear relocation. RESULTS:Lpcat1 translocates into the nucleus from thecytoplasm in murine lung epithelia (MLE) after LPS treatment. Haemophilus influenza and Escherichia coli , two LPS-containing pathogens that cause pneumonia, triggered Lpcat1 nuclear translocation from the cytoplasm. The LPS inducible gene expression profile was determined by quantitative reverse transcription polymerase chain reaction after silencing Lpcat1 or overexpression of the enzyme in MLE cells. We detected that 17 out of a total 38 screened genes were upregulated, 14 genes were suppressed, and 7 genes remained unchanged in LPS treated cells in comparison to controls. Knockdown of Lpcat1 by shRNA dramatically changed the spectrum of the LPS inducible gene transcription, as 18 genes out of 38 genes were upregulated, of which 20 genes were suppressed or unchanged. Notably, in Lpcat1 overex-pressed cells, 25 genes out of 38 genes were reduced in the setting of LPS treatment.CONCLUSION:These observations suggest that Lpcat1 relocates into the nucleus in response to bacterial infection to differentially regulate gene transcriptional repression.