Linked Life Data

19155472

Source:http://linkedlifedata.com/resource/pubmed/id/19155472

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-1-21
pubmed:abstractText
Lymphangioleiomyomatosis (LAM) is characterized by cystic lung destruction caused by LAM cells (smooth-muscle-like cells) that have mutations in the tumor suppressor genes tuberous sclerosis complex (TSC) 1 or 2 and have the capacity to metastasize. Since chemokines and their receptors function in chemotaxis of metastatic cells, we hypothesized that LAM cells may be recruited by chemokine(s) in the lung. Quantification of 25 chemokines in bronchoalveolar lavage fluid from LAM patients and healthy volunteers revealed that concentrations of CCL2, CXCL1, and CXCL5 were significantly higher in samples from LAM patients than those from healthy volunteers. In vitro, CCL2 or MCP-1 induced selective migration of cells, showing loss of heterozygosity of TSC2 from a heterogeneous population of cells grown from explanted LAM lungs. Additionally, the frequencies of single-nucleotide polymorphisms in the CCL2 gene promoter region differed significantly in LAM patients and healthy volunteers (p = 0.018), and one polymorphism was associated significantly more frequently with the decline of lung function. The presence (i.e., potential functionality) of chemokine receptors was evaluated using immunohistochemistry in lung sections from 30 LAM patients. Expression of chemokines and these receptors varied among LAM patients and differed from that seen in some cancers (e.g., breast cancer and melanoma cells). These observations are consistent with the notion that chemokines such as CCL2 may serve to determine mobility and specify the site of metastasis of the LAM cell.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
182
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1270-7
pubmed:dateRevised
2010-10-4
pubmed:meshHeading
pubmed-meshheading:19155472-Adult, pubmed-meshheading:19155472-Case-Control Studies, pubmed-meshheading:19155472-Cell Line, pubmed-meshheading:19155472-Cell Line, Tumor, pubmed-meshheading:19155472-Chemokine CCL2, pubmed-meshheading:19155472-Chemokine CCL27, pubmed-meshheading:19155472-Chemokines, pubmed-meshheading:19155472-Chemokines, CC, pubmed-meshheading:19155472-Chemotaxis, Leukocyte, pubmed-meshheading:19155472-Female, pubmed-meshheading:19155472-Gene Expression Profiling, pubmed-meshheading:19155472-Genes, Tumor Suppressor, pubmed-meshheading:19155472-Humans, pubmed-meshheading:19155472-Lung, pubmed-meshheading:19155472-Lymphangioleiomyomatosis, pubmed-meshheading:19155472-Middle Aged, pubmed-meshheading:19155472-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:19155472-Polymorphism, Genetic, pubmed-meshheading:19155472-Tumor Suppressor Proteins
pubmed:year
2009
pubmed:articleTitle
Chemokine-enhanced chemotaxis of lymphangioleiomyomatosis cells with mutations in the tumor suppressor TSC2 gene.
pubmed:affiliation
Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural