Pregled bibliografske jedinice broj: 338610
Cytokine regulation of the TFF binding protein GKN2(GDDR/TFIZ1/blottin) in human GI epithelial cells
Cytokine regulation of the TFF binding protein GKN2(GDDR/TFIZ1/blottin) in human GI epithelial cells // Fifth International Conference on Trefoil Factors, Book of Abstracts
Kopenhagen, Danska, 2007. (predavanje, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 338610 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Cytokine regulation of the TFF binding protein GKN2(GDDR/TFIZ1/blottin) in human GI epithelial cells
Autori
Baus Lončar, Mirela ; Lubka, M ; Otto W.R ; Poulsom R ; Pusch C.M ; Blin N.
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Fifth International Conference on Trefoil Factors, Book of Abstracts
/ - , 2007
Skup
Fifth International Conference on Trefoil Factors
Mjesto i datum
Kopenhagen, Danska, 30.05.2007. - 01.06.2007
Vrsta sudjelovanja
Predavanje
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
TFF proteins; blottin; GDDR; TFIZ1; gastrointestinal epithelial cells
Sažetak
INTRODUCTION: Trefoil factor family (TFF) peptides are major secretory products of mucous epithelia and play a multifunctional role in cytoprotection, apoptosis, and immune response. Recently, a TFF2-binding protein was discovered in mice and named blottin. It is down-regulated in gastric cancer (GDDR), abundant in human gastric surface (TFIZ1) and its similarity to gastrokine-1 led to the gene’ s name gastrokine 2 (GKN2). The aim of our study was to see how the GKN2 gene is regulated by different cytokines. METHOD: GKN2 gene promoter (position – 1906 to -20) was cloned into luciferase reporter gene plasmid (pGL3 basic vector) and introduced into gastrointestinal cell lines (HT-29, KATO III, AGS). The expression of reporter gene controlled by GKN2 promoter was monitored (Dual Luciferase Assay system) upon treatment with various pro-inflammatory (TNF-α , IL1-β , IL-6, INF-γ ) and anti-inflammatory (TGF-β ) cytokines. To assess direct role of transcription factors in regulating GKN2 (NF-κ B, p65, HNF-3β , hGATA6) we performed transient co-expression of their expression plasmids and the reporter gene vector. Statistical analysis was performed by using one way ANOVA (*p < 0.05, **p < 0.01). CONCLUSION: Statistically significant down-regulation of GKN2 transcription was observed by TNF-α , IL1-β and IL-6 (Fig 1a, b). Transcription factor NF-κ B also inhibits transcription of GKN2 gene (Fig 2). TGF-β and transcription factors hGATA6 and HNF3-β caused an up-regulation of the GKN2 gene (Fig 1a and 3). Various cytokines regulate GKN2 gene expression, suggesting the crosstalk of GKN2 as an TFF interacting protein with immune response.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Projekti:
219-0982914-2179 - Uloga malih zaštitinih TFF proteina u zdravlju i bolesti (Belovari, Tatjana, MZOS ) ( CroRIS)
Ustanove:
Medicinski fakultet, Osijek
Profili:
Mirela Baus Lončar
(autor)
