Polymorphisms of the TGF-β1 promoter in tight skin (TSK) mice

Hong Zhu, Constantin Bona, Tracy L. McGaha

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

TGF-β1 plays a major role in fibrotic diseases including scleroderma. Human fibroblasts from sclerotic lesions display an increased sensitivity to TGF-β1. Similarly, fibroblasts from TSK mice which develop a scleroderma-like syndrome are hyperresponsive to TGF-β. The aim of the present study was to investigate whether the TGF-β hypersensitivity demonstrated by TSK/+ fibroblasts is associated with polymorphisms of the TGF-β1 promoter. Sequence analysis revealed one polymorphism (a G → T at - 1133 bp) unique to the TSK/+ mouse. Transfection of fibroblasts with a 1.8 kb fragment of the TGF-β1 promoter containing the - 1133 polymorphism exhibited increased basal TGF-β1 promoter activity which was enhanced upon incubation with TGF-β1. This may be related to the loss of a negative regulatory site in the TSK/+ TGF-β1 promoter.

Original languageEnglish (US)
Pages (from-to)51-55
Number of pages5
JournalAutoimmunity
Volume37
Issue number1
DOIs
StatePublished - Feb 1 2004

Fingerprint

Fibroblasts
Skin
Transfection
Sequence Analysis
Hypersensitivity

Keywords

  • Polymorphisms
  • Promoter
  • Scleroderma
  • TGF-β1
  • Tight skin mice

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Polymorphisms of the TGF-β1 promoter in tight skin (TSK) mice. / Zhu, Hong; Bona, Constantin; McGaha, Tracy L.

In: Autoimmunity, Vol. 37, No. 1, 01.02.2004, p. 51-55.

Research output: Contribution to journalArticle

Zhu, Hong ; Bona, Constantin ; McGaha, Tracy L. / Polymorphisms of the TGF-β1 promoter in tight skin (TSK) mice. In: Autoimmunity. 2004 ; Vol. 37, No. 1. pp. 51-55.
@article{8ef526b5e4b34d5585d887819a8198b8,
title = "Polymorphisms of the TGF-β1 promoter in tight skin (TSK) mice",
abstract = "TGF-β1 plays a major role in fibrotic diseases including scleroderma. Human fibroblasts from sclerotic lesions display an increased sensitivity to TGF-β1. Similarly, fibroblasts from TSK mice which develop a scleroderma-like syndrome are hyperresponsive to TGF-β. The aim of the present study was to investigate whether the TGF-β hypersensitivity demonstrated by TSK/+ fibroblasts is associated with polymorphisms of the TGF-β1 promoter. Sequence analysis revealed one polymorphism (a G → T at - 1133 bp) unique to the TSK/+ mouse. Transfection of fibroblasts with a 1.8 kb fragment of the TGF-β1 promoter containing the - 1133 polymorphism exhibited increased basal TGF-β1 promoter activity which was enhanced upon incubation with TGF-β1. This may be related to the loss of a negative regulatory site in the TSK/+ TGF-β1 promoter.",
keywords = "Polymorphisms, Promoter, Scleroderma, TGF-β1, Tight skin mice",
author = "Hong Zhu and Constantin Bona and McGaha, {Tracy L.}",
year = "2004",
month = "2",
day = "1",
doi = "10.1080/08916930310001633782",
language = "English (US)",
volume = "37",
pages = "51--55",
journal = "Autoimmunity",
issn = "0891-6934",
publisher = "Informa Healthcare",
number = "1",

}

TY - JOUR

T1 - Polymorphisms of the TGF-β1 promoter in tight skin (TSK) mice

AU - Zhu, Hong

AU - Bona, Constantin

AU - McGaha, Tracy L.

PY - 2004/2/1

Y1 - 2004/2/1

N2 - TGF-β1 plays a major role in fibrotic diseases including scleroderma. Human fibroblasts from sclerotic lesions display an increased sensitivity to TGF-β1. Similarly, fibroblasts from TSK mice which develop a scleroderma-like syndrome are hyperresponsive to TGF-β. The aim of the present study was to investigate whether the TGF-β hypersensitivity demonstrated by TSK/+ fibroblasts is associated with polymorphisms of the TGF-β1 promoter. Sequence analysis revealed one polymorphism (a G → T at - 1133 bp) unique to the TSK/+ mouse. Transfection of fibroblasts with a 1.8 kb fragment of the TGF-β1 promoter containing the - 1133 polymorphism exhibited increased basal TGF-β1 promoter activity which was enhanced upon incubation with TGF-β1. This may be related to the loss of a negative regulatory site in the TSK/+ TGF-β1 promoter.

AB - TGF-β1 plays a major role in fibrotic diseases including scleroderma. Human fibroblasts from sclerotic lesions display an increased sensitivity to TGF-β1. Similarly, fibroblasts from TSK mice which develop a scleroderma-like syndrome are hyperresponsive to TGF-β. The aim of the present study was to investigate whether the TGF-β hypersensitivity demonstrated by TSK/+ fibroblasts is associated with polymorphisms of the TGF-β1 promoter. Sequence analysis revealed one polymorphism (a G → T at - 1133 bp) unique to the TSK/+ mouse. Transfection of fibroblasts with a 1.8 kb fragment of the TGF-β1 promoter containing the - 1133 polymorphism exhibited increased basal TGF-β1 promoter activity which was enhanced upon incubation with TGF-β1. This may be related to the loss of a negative regulatory site in the TSK/+ TGF-β1 promoter.

KW - Polymorphisms

KW - Promoter

KW - Scleroderma

KW - TGF-β1

KW - Tight skin mice

UR - http://www.scopus.com/inward/record.url?scp=0442279151&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0442279151&partnerID=8YFLogxK

U2 - 10.1080/08916930310001633782

DO - 10.1080/08916930310001633782

M3 - Article

C2 - 15115312

AN - SCOPUS:0442279151

VL - 37

SP - 51

EP - 55

JO - Autoimmunity

JF - Autoimmunity

SN - 0891-6934

IS - 1

ER -