Scopus: 16 cites, Google Scholar: cites,
Expression of REG family genes in human inflammatory bowel diseases and its regulation
Tsuchida, Chikatsugu (Saiseikai Nara Hospital, Japan)
Sakuramoto-Tsuchida, Sumiyo (Department of Biochemistry, Nara Medical University)
Taked, Maiko (Department of Laboratory Medicine and Pathology, National Hospital Organization Kinki-chuo Chest Medical Center)
Itaya-Hironaka, Asako (Department of Biochemistry, Nara Medical University)
Yamauchi, Akiyo (Department of Biochemistry, Nara Medical University)
Misu, Masayasu (Department of Biochemistry, Nara Medical University)
Shobatake, Ryogo (Department of Biochemistry, Nara Medical University)
Uchiyama, Tomoko (Department of Diagnostic Pathology, Nara Medical University)
Makino, Mai (Department of Biochemistry, Nara Medical University)
Pujol-Autonell, Irma (Institut Germans Trias i Pujol)
Vives Pi, Marta (Institut Germans Trias i Pujol)
Ohbayashi, Chiho (Department of Diagnostic Pathology, Nara Medical University)
Takasawa, Shin (Department of Biochemistry, Nara Medical University)

Data: 2017
Resum: The pathophysiology of inflammatory bowel disease (IBD) reflects a balance between mucosal injury and reparative mechanisms. Some regenerating gene (Reg) family members have been reported to be expressed in Crohn's disease (CD) and ulcerative colitis (UC) and to be involved as proliferative mucosal factors in IBD. However, expression of all REG family genes in IBD is still unclear. Here, we analyzed expression of all REG family genes (REG Iα, REG Iβ, REG III, HIP/PAP, and REG IV) in biopsy specimens of UC and CD by real-time RT-PCR. REG Iα, REG Iβ, and REG IV genes were overexpressed in CD samples. REG IV gene was also overexpressed in UC samples. We further analyzed the expression mechanisms of REG Iα, REG Iβ, and REG IV genes in human colon cells. The expression of REG Iα was significantly induced by IL-6 or IL-22, and REG Iβ was induced by IL-22. Deletion analyses revealed that three regions (− 220 to − 211, − 179 to − 156, and − 146 to − 130) in REG Iα and the region (− 274 to− 260) in REG Iβ promoter were responsible for the activation by IL-22/IL-6. The promoters contain consensus transcription factor binding sequences for MZF1, RTEF1/TEAD4, and STAT3 in REG Iα, and HLTF/FOXN2F in REG Iβ, respectively. The introduction of siRNAs for MZF1, RTEF1/TEAD4, STAT3, and HLTF/FOXN2F abolished the transcription of REG Iα and REG Iβ. The gene activation mechanisms of REG Iα/REG Iβ may play a role in colon mucosal regeneration in IBD.
Drets: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, i la comunicació pública de l'obra, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. No es permet la creació d'obres derivades. Creative Commons
Llengua: Anglès
Document: article ; recerca ; publishedVersion
Matèria: CD, Crohn's disease ; CDX2, caudal-type homeobox transcription factor 2 ; FOXN2, forkhead box protein N2 ; GATA6, GATA DNA-binding protein 6 ; HLTF, helicase-like transcription factor ; IBD, inflammatory bowel disease ; IL, interleukin ; MZF1, myeloid zinc finger 1 ; REG, regenerating gene ; RTEF1, related transcriptional enhancer factor-1 ; Sirna, small interfering RNA ; SOCS3, suppressors of the cytokine signaling 3 ; STAT3, signal transducer and activator of transcription 3 ; TEAD4, TEA Domain transcription Factor 4 ; UC, ulcerative colitis ; REG family genes ; Crohn's disease ; Ulcerative colitis ; Transcription ; Celiac disease
Publicat a: Biochemistry and Biophysics Reports, Vol. 12 (october 2017) , p. 198-205, ISSN 2405-5808

DOI: 10.1016/j.bbrep.2017.10.003
PMID: 29090282

8 p, 1.1 MB

El registre apareix a les col·leccions:
Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut d'Investigació en Ciencies de la Salut Germans Trias i Pujol (IGTP)
Articles > Articles de recerca
Articles > Articles publicats

 Registre creat el 2018-02-08, darrera modificació el 2021-02-18

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