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Detection of elafin as a candidate biomarker for ulcerative colitis by whole-genome microarray screening.

Artikel i vetenskaplig tidskrift
Författare Carl-Fredrik Flach
Anders Eriksson
Eva Jennische
Stefan Lange
Charina Gunnerek
Ivar Lönnroth
Publicerad i Inflammatory bowel diseases
Volym 12
Nummer/häfte 9
Sidor 837-42
ISSN 1078-0998
Publiceringsår 2006
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för medicin, avdelningen för invärtesmedicin
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 837-42
Språk en
Länkar dx.doi.org/10.1097/01.mib.000023246...
Ämnesord Adult, Biological Markers, analysis, Biopsy, Colitis, Ulcerative, genetics, metabolism, pathology, Elafin, biosynthesis, genetics, Female, Fructose-Bisphosphate Aldolase, biosynthesis, genetics, Gene Expression, Humans, Immunohistochemistry, Male, Middle Aged, Oligonucleotide Array Sequence Analysis, methods, Rectum, metabolism, pathology, Reverse Transcriptase Polymerase Chain Reaction
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

The cause of ulcerative colitis (UC) is largely unknown. Microarray studies are an efficient way of investigating the various genes involved. Here, we have used whole-genome microarrays to clarify the clinical picture and to identify new biomarkers for improved diagnosis. Rectal biopsies were taken from five UC patients and five matched controls, and RNA transcripts were prepared. After labeling, each sample was individually applied to the microarray chips. All transcripts that were more than 10-fold up-regulated in all five patients were analyzed further in seven additional patients and seven controls using quantitative polymerase chain reaction. Of 47,000 transcripts examined, 4 were highly up-regulated in all patients: those encoding elafin, a secreted protease inhibitor, the ion and amino acid transporter B (SLC6A14), and the metabolic enzyme aldolase B, as well as a recently identified transcript named similar to numb-interacting homolog. The up-regulation of these transcripts appears to follow the progression of the disease because elevated expression was detected in the proximal part of the colon in patients with total colitis but not in patients with left-sided colitis. Immunohistologic examination showed very distinct differences in the expression of elafin. Extensive expression was detected in enterocytes and goblet cells of the affected mucosa, whereas there was no detectable expression in unaffected mucosa and in healthy controls. The results implicate four transcripts and proteins of special interest as possible targets for pharmacologic interference and as biomarkers in UC. Of these, elafin may be of special interest because it is a secreted protein that may be measured in body fluids.

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