Premium
Molecular signature in asthmatic mice model lung by microarray analysis
Author(s) -
Kim Hyun Jae,
Lee Seung Ku,
Cha YunYi,
Kim Hyoun Geun,
Yun HongShik,
Kang HyunJun,
Kim Kyung Yeon,
Park Seong Gyu,
Choi JungWon,
Kim Yeon jung,
Roh Gu Seob,
Oh Berm seok,
Kwack KyuBum
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1142
Subject(s) - ovalbumin , microarray , asthma , microarray analysis techniques , immunology , pathogenesis , gene chip analysis , medicine , allergen , lung , immunoglobulin e , gene , gene expression , biology , allergy , immune system , antibody , genetics
Asthma has become substantially more prevalent in recent decades and is one of the foremost contributors to morbidity and mortality in industrialized countries. To identify novel genes implicated in the pathogenesis of asthma, we had carried out oligonucleotide microarray analysis with total RNA extracted from the whole lung of ovalbumin‐induced asthmatic model mice. We observed an increased level of total IgE in asthmatic model mice serum and histological changes in lung tissues from mice treated with the allergen over a short (acute) or long (chronic) period of time, relative to the untreated mice, which indicated that our animals effectively represented acute and chronic asthmatic model systems. Our analysis revealed that 305 genes were differentially expressed in both acute and chronic asthmatic mice in comparison to the matched control models. Among all genes, 344 genes were up‐ or down‐regulated after 4 and 24 hours of the allergen treatment, and 424 genes were affected after 4 and 6 weeks of an extended exposure to the allergen. Taken together, we attempted to diagnosis and monitoring for progress of the acute and chronic asthma with the animal model system and microarray approach. Profile of the gene expression in acute and chronic asthmatic mice model revealed that although the two clinical differences of asthmatic mice share a common pathway to develop the symptom, a distinct set of the genes may also be implicated suggesting their different pathophysiology.