| Project/Area Number |
23591148
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 間質性肺炎 / マイクロアレイ / バイオマーカー / 分子標的治療薬 / 国際情報交換 / KL-6 / SP-A / SP-D |
|---|
| Research Abstract |
Idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP) are subtypes of idiopathic interstitial pneumonia (IIP), which is characterized by alveolar epithelial damage, activation of fibroblast proliferation, and loss of normal pulmonary architecture and function. Clinical differentiation between IPF and NSIP is difficult, and the molecular basis for IIP remains unclear. The study included 12 patients with IIP (IPF, n = 7; NSIP, n = 5). RNA extracted from lung specimens was profiled using Illumina Human WG-6 v3 BeadChips, and an Ingenuity Pathway Analysis was performed to identify altered functional and canonical signaling pathways. Genes and pathways related to cancer, cell death and survival, and cellular growth and proliferation were differentially expressed in IIP patients. These data provide valuable information on the possible mechanisms underlying pulmonary fibrosis, and reveal several potential biomarkers for IIP diagnosis and therapeutic targeting.
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