BACKGROUND: Connective tissue growth factor (CCN2; CTGF) is a newly identified growth factor, which is involved in the regulation of wound repair and fibrosis. Because there is variation among individuals with respect to tissue response to injury, genetic factors might be involved in the final outcome of tissue repair or scarring. For example, polymorphisms in the promoter region of genes, such as those encoding transforming growth factor beta1 (TGF-beta1), interleukin 10 (IL-10), and tumour necrosis factor alpha (TNF-alpha), influence transcriptional responses and are thought to contribute to the dysregulation of these genes in pathological conditions. AIM: To investigate whether the promoter region of the ccn2 (ctgf) gene contains polymorphic sequences that might account for differential expression. MATERIALS/ METHODS: Seventy seven human DNA samples were sequenced-45 were from healthy controls and 32 were from patients with ischaemic heart disease (IHD)-using M13 tailed sequence specific ccn2 (ctgf) primers for amplification of a 600 bp fragment upstream of the transcription start site. Amplicons were bidirectionally sequenced with a dye primer M13 forward and reverse sequencing kit. RESULTS: A C to G substitution was identified at position -132 in one of the patients with IHD. Moreover, in five of the 32 patients with IHD and in six of the 45 healthy controls, a G to C polymorphism was found at position -447. These substitutions at -132 and -447 are thought to lie within predicted binding domains for the transcription factors Pbx-1 and MZF1, respectively. In addition, insertions at position -43 (G), -47 (C), -71 (G) and a C to T substitution at position -198 were found in all DNA samples compared with the published ccn2 (ctgf) promoter sequence. These corrections do not involve sequences predicted to function as transcription factor binding sites. CONCLUSION: Sequence analysis of the ccn2 (ctgf) promoter of 77 human DNA samples has revealed corrections and polymorphic sites. The latter lie within putative regulatory elements.
BACKGROUND:Connective tissue growth factor (CCN2; CTGF) is a newly identified growth factor, which is involved in the regulation of wound repair and fibrosis. Because there is variation among individuals with respect to tissue response to injury, genetic factors might be involved in the final outcome of tissue repair or scarring. For example, polymorphisms in the promoter region of genes, such as those encoding transforming growth factor beta1 (TGF-beta1), interleukin 10 (IL-10), and tumour necrosis factor alpha (TNF-alpha), influence transcriptional responses and are thought to contribute to the dysregulation of these genes in pathological conditions. AIM: To investigate whether the promoter region of the ccn2 (ctgf) gene contains polymorphic sequences that might account for differential expression. MATERIALS/ METHODS: Seventy seven human DNA samples were sequenced-45 were from healthy controls and 32 were from patients with ischaemic heart disease (IHD)-using M13 tailed sequence specific ccn2 (ctgf) primers for amplification of a 600 bp fragment upstream of the transcription start site. Amplicons were bidirectionally sequenced with a dye primer M13 forward and reverse sequencing kit. RESULTS: A C to G substitution was identified at position -132 in one of the patients with IHD. Moreover, in five of the 32 patients with IHD and in six of the 45 healthy controls, a G to C polymorphism was found at position -447. These substitutions at -132 and -447 are thought to lie within predicted binding domains for the transcription factors Pbx-1 and MZF1, respectively. In addition, insertions at position -43 (G), -47 (C), -71 (G) and a C to T substitution at position -198 were found in all DNA samples compared with the published ccn2 (ctgf) promoter sequence. These corrections do not involve sequences predicted to function as transcription factor binding sites. CONCLUSION: Sequence analysis of the ccn2 (ctgf) promoter of 77 human DNA samples has revealed corrections and polymorphic sites. The latter lie within putative regulatory elements.
Authors: J Bidwell; L Keen; G Gallagher; R Kimberly; T Huizinga; M F McDermott; J Oksenberg; J McNicholl; F Pociot; C Hardt; S D'Alfonso Journal: Genes Immun Date: 1999-09 Impact factor: 2.676
Authors: T Mori; S Kawara; M Shinozaki; N Hayashi; T Kakinuma; A Igarashi; M Takigawa; T Nakanishi; K Takehara Journal: J Cell Physiol Date: 1999-10 Impact factor: 6.384
Authors: R Hromas; J Morris; K Cornetta; D Berebitsky; A Davidson; M Sha; G Sledge; F Rauscher Journal: Cancer Res Date: 1995-08-15 Impact factor: 12.701
Authors: V Paradis; D Dargere; M Vidaud; A C De Gouville; S Huet; V Martinez; J M Gauthier; N Ba; R Sobesky; V Ratziu; P Bedossa Journal: Hepatology Date: 1999-10 Impact factor: 17.425
Authors: A Igarashi; K Nashiro; K Kikuchi; S Sato; H Ihn; M Fujimoto; G R Grotendorst; K Takehara Journal: J Invest Dermatol Date: 1996-04 Impact factor: 8.551
Authors: Jan R Ortlepp; Jürgen Graf; Katharina Vesper; Fabian Schmitz; Vera Mevissen; Sebastian Sucigan; Alexander Kersten; Christian Weber; Uwe Janssens Journal: Inflammation Date: 2005-04 Impact factor: 4.092
Authors: Bing Wang; Rickey E Carter; Miran A Jaffa; Sashidhar Nakerakanti; Daniel Lackland; Maria Lopes-Virella; Maria Trojanowska; Louis M Luttrell; Ayad A Jaffa Journal: J Med Genet Date: 2010-06 Impact factor: 6.318
Authors: Amy Jayne McKnight; David A Savage; Chris C Patterson; Hugh R Brady; A Peter Maxwell Journal: J Hum Genet Date: 2006-02-24 Impact factor: 3.172
Authors: Antonios G Mikos; Susan W Herring; Pannee Ochareon; Jennifer Elisseeff; Helen H Lu; Rita Kandel; Frederick J Schoen; Mehmet Toner; David Mooney; Anthony Atala; Mark E Van Dyke; David Kaplan; Gordana Vunjak-Novakovic Journal: Tissue Eng Date: 2006-12
Authors: J A Arnott; X Zhang; A Sanjay; T A Owen; S L Smock; S Rehman; W G DeLong; F F Safadi; S N Popoff Journal: Bone Date: 2008-01-26 Impact factor: 4.398