Linked Life Data

9870917

Source:http://linkedlifedata.com/resource/pubmed/id/9870917

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-2-4
pubmed:abstractText
Pulmonary fibrosis begins with alveolitis, which progresses to destruction of lung tissue and excess collagen deposition. This process could be the result of DNA damage and a form of apoptosis. Therefore, we hypothesized that Fas ligand (FasL), which induces apoptosis in cells expressing Fas antigen (Fas), is associated with pulmonary fibrosis. We examined frozen lung tissues from seven patients with idiopathic pulmonary fibrosis (IPF), and bronchoalveolar lavage fluid (BALF) cells from 19 patients with IPF and from 17 patients with interstitial pneumonia associated with collagen vascular diseases (CVD-IP). We used five frozen lungs with normal lung parenchyma and BALF cells from 10 patients with solitary pulmonary nodule as controls. Reverse transcription-polymerase chain reaction (RT-PCR) showed that FasL messenger RNA (mRNA) was expressed in BALF cells from all patients with IPF and from 15 of 16 patients with CVD-IP. FasL mRNA was not detected in BALF cells except in one of 10 controls. RT in situ PCR detected FasL mRNA in inflammatory cells in BALF from patients with IPF. Immunohistochemistry detected FasL protein in infiltrating lymphocytes and granulocytes in all of seven frozen lung tissues of IPF, but in none of five control lung tissues. Additionally, the expression of Fas appeared to be upregulated in bronchiolar and alveolar epithelial cells in IPF compared with normal lung parenchyma by immunohistochemistry. We conclude that Fas and FasL were upregulated in fibrosing lung diseases and may associate with DNA damage or apoptosis of bronchiolar and alveolar epithelial cells in this disorder.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9870917-Adult, pubmed-meshheading:9870917-Aged, pubmed-meshheading:9870917-Aged, 80 and over, pubmed-meshheading:9870917-Antigens, CD15, pubmed-meshheading:9870917-Antigens, CD4, pubmed-meshheading:9870917-Antigens, CD8, pubmed-meshheading:9870917-Antigens, CD95, pubmed-meshheading:9870917-Apoptosis, pubmed-meshheading:9870917-Bronchoalveolar Lavage Fluid, pubmed-meshheading:9870917-Collagen, pubmed-meshheading:9870917-Cryopreservation, pubmed-meshheading:9870917-Fas Ligand Protein, pubmed-meshheading:9870917-Female, pubmed-meshheading:9870917-Humans, pubmed-meshheading:9870917-Immunohistochemistry, pubmed-meshheading:9870917-Lung Diseases, Interstitial, pubmed-meshheading:9870917-Male, pubmed-meshheading:9870917-Membrane Glycoproteins, pubmed-meshheading:9870917-Middle Aged, pubmed-meshheading:9870917-Pulmonary Fibrosis, pubmed-meshheading:9870917-RNA, Messenger, pubmed-meshheading:9870917-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
1999
pubmed:articleTitle
The involvement of Fas-Fas ligand pathway in fibrosing lung diseases.
pubmed:affiliation
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan. kkuwano@kokyu.med.kyushu-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't