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

Hong Zhu; Constantin Bona; Tracy L. McGaha

doi:10.1080/08916930310001633782

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

Hong Zhu, Constantin Bona, Tracy L. McGaha

Nephrology

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

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 language	English (US)
Pages (from-to)	51-55
Number of pages	5
Journal	Autoimmunity
Volume	37
Issue number	1
DOIs	https://doi.org/10.1080/08916930310001633782
State	Published - Feb 2004

Keywords

Polymorphisms
Promoter
Scleroderma
TGF-β1
Tight skin mice

ASJC Scopus subject areas

Immunology and Allergy
Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/08916930310001633782

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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.}",

note = "Funding Information: This work was supported by grant PO1 AI24671-14 from NIAID-NIH and the Seleroderma Foundation.",

year = "2004",

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doi = "10.1080/08916930310001633782",

language = "English (US)",

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

AU - Zhu, Hong

AU - Bona, Constantin

AU - McGaha, Tracy L.

N1 - Funding Information: This work was supported by grant PO1 AI24671-14 from NIAID-NIH and the Seleroderma Foundation.

PY - 2004/2

Y1 - 2004/2

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

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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