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Transcription profiling of human pulmonary epithelial cells cultured in plasma from sickle cell disease acute chest syndrome and steady-state patients

ABSTRACT: Clinical variability in sickle cell disease (SCD) suggests a role for extra-erythrocytic factors in the pathogenesis of vasoocclusion. We hypothesized that one potential factor, endothelial dysfunction, results from induction of phenotypic changes by circulating factors in SCD patients. The database reports gene expression in cultured human pulmonary artery endothelial cells (HPAEC) exposed to plasma from: a) sickle acute chest syndrome (ACS) patients (samples ; b) SCD patients at steady-state and c) normal volunteers using microarrays (U133A-B GeneChip Affymetrix).

ORGANISM(S): Homo sapiens

DISEASE(S): normal

SUBMITTER: Paola Sebastiani

PROVIDER: E-GEOD-1849 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Differential gene expression in pulmonary artery endothelial cells exposed to sickle cell plasma.

Klings Elizabeth S ES Safaya Surinder S Adewoye Adeboye H AH Odhiambo Adam A Frampton Garrett G Lenburg Marc M Gerry Norman N Sebastiani Paola P Steinberg Martin H MH Farber Harrison W HW

Physiological genomics 20050301 3

Clinical variability in sickle cell disease (SCD) suggests a role for extra-erythrocytic factors in the pathogenesis of vasoocclusion. We hypothesized that endothelial cell (EC) dysfunction, one possible modifier of disease variability, results from induction of phenotypic changes by circulating factors. Accordingly, we analyzed gene expression in cultured human pulmonary artery ECs (HPAEC) exposed to plasma from 1) sickle acute chest syndrome (ACS) patients, 2) SCD patients at steady state, 3) ...[more]

PMID: 15741505

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Differential Gene Expression in Pulmonary Artery Endothelial Cells Exposed to Sickle Cell Plasma

Project description:Clinical variability in sickle cell disease (SCD) suggests a role for extra-erythrocytic factors in the pathogenesis of vasoocclusion. We hypothesized that one potential factor, endothelial dysfunction, results from induction of phenotypic changes by circulating factors in SCD patients. The database reports gene expression in cultured human pulmonary artery endothelial cells (HPAEC) exposed to plasma from: a) sickle acute chest syndrome (ACS) patients (samples ; b) SCD patients at steady-state and c) normal volunteers using microarrays (U133A-B GeneChip Affymetrix). Keywords: other

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