title: Gene expression profiling and pathway analysis of human bronchial epithelial cells exposed to airborne particulate matter collected from Saudi Arabia.
abstract: Epidemiological studies have established a positive correlation between human mortality and increased concentration of airborne particulate matters (PM). However, the mechanisms underlying PM related human diseases, as well as the molecules and pathways mediating the cellular response to PM, are not fully understood. This study aims to investigate the global gene expression changes in human cells exposed to PM(10) and to identify genes and pathways that may contribute to PM related adverse health effects. Human bronchial epithelial cells were exposed to PM(10) collected from Saudi Arabia for 1 or 4 days, and whole transcript expression was profiled using the GeneChip human gene 1.0 ST array. A total of 140 and 230 genes were identified that significantly changed more than 1.5 fold after PM(10) exposure for 1 or 4 days, respectively. Ingenuity Pathway Analysis revealed that different exposure durations triggered distinct pathways. Genes involved in NRF2-mediated response to oxidative stress were up-regulated after 1 day exposure. In contrast, cells exposed for 4 days exhibited significant changes in genes related to cholesterol and lipid synthesis pathways. These observed changes in cellular oxidative stress and lipid synthesis might contribute to PM related respiratory and cardiovascular disease.
authors.affiliation: Department of Environmental Medicine, NYU School of Medicine, Tuxedo, NY 10987, USA.
authors.forename: Hong
authors.initials: H
authors.lastname: Sun
authors.forename: Magdy
authors.initials: M
authors.lastname: Shamy
authors.forename: Thomas
authors.initials: T
authors.lastname: Kluz
authors.forename: Alexandra B
authors.initials: AB
authors.lastname: Muñoz
authors.forename: Mianhua
authors.initials: M
authors.lastname: Zhong
authors.forename: Freda
authors.initials: F
authors.lastname: Laulicht
authors.forename: Mansour A
authors.initials: MA
authors.lastname: Alghamdi
authors.forename: Mamdouh I
authors.initials: MI
authors.lastname: Khoder
authors.forename: Lung-Chi
authors.initials: LC
authors.lastname: Chen
authors.forename: Max
authors.initials: M
authors.lastname: Costa
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D001980:Bronchi / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D001982:Bronchial Diseases / Q000139:chemically induced / Q000235:genetics / Q000473:pathology; D002460:Cell Line; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D025341:Principal Component Analysis; D012313:RNA / Q000737:chemistry / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D012529:Saudi Arabia
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D012313:RNA