Fli-1 inhibits collagen type I production in dermal fibroblasts via a Sp1- dependent pathway Running title: Fli-1 inhibits COL1A2 transcription

نویسندگان

  • Joanna Czuwara-Ladykowska
  • Fumiaki Shirasaki
  • Pascale Jackers
  • Dennis K. Watson
  • Maria Trojanowska
چکیده

Joanna Czuwara-Ladykowska‡, Fumiaki Shirasaki‡¶, Pascale Jackers§, Dennis K. Watson§, and Maria Trojanowska‡ Both authors contributed equally to this work. ‡Department of Medicine, Division of Rheumatology and Immunology, §Center for Molecular and Structural Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, and ¶Department of Dermatology, Kanazawa University, Japan. Corresponding author, mailing address: Division of Rheumatology and Immunology Medical University of South Carolina 96 Jonathan Lucas St, Suite 912 Charleston SC 29401 Tel: 843-792-7921 Fax: 843-792-7121 e-mail: [email protected]

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Marinobufagenin induces increases in procollagen expression in a process involving protein kinase C and Fli-1: implications for uremic cardiomyopathy.

The cardiotonic steroid marinobufagenin (MBG) has been implicated in the pathogenesis of experimental uremic cardiomyopathy, which is characterized by progressive cardiac fibrosis. We examined whether the transcription factor Friend leukemia integration-1 (Fli-1) might be involved in this process. Fli-1-knockdown mice demonstrated greater cardiac collagen-1 expression and fibrosis compared with...

متن کامل

Transcriptional regulation of matrix metalloproteinase-1 and collagen 1A2 explains the anti-fibrotic effect exerted by proteasome inhibition in human dermal fibroblasts

INTRODUCTION Extracellular matrix (ECM) turnover is controlled by the synthetic rate of matrix proteins, including type I collagen, and their enzymatic degradation by matrix metalloproteinases (MMPs). Fibrosis is characterized by an unbalanced accumulation of ECM leading to organ dysfunction as observed in systemic sclerosis. We previously reported that proteasome inhibition (PI) in vitro decre...

متن کامل

Human collagen Krox up-regulates type I collagen expression in normal and scleroderma fibroblasts through interaction with Sp1 and Sp3 transcription factors.

Despite several investigations, the transcriptional mechanisms that regulate the expression of both type I collagen genes (COL1A1 and COL1A2) in either physiological or pathological situations, such as scleroderma, are not completely known. We have investigated the role of hc-Krox transcription factor on type I collagen expression by human dermal fibroblasts. hc-Krox exerted a stimulating effec...

متن کامل

Constitutively phosphorylated Smad3 interacts with Sp1 and p300 in scleroderma fibroblasts.

OBJECTIVE To elucidate the role of transforming growth factor-beta (TGF-beta)/Smad signalling in the increased expression of the collagen gene in systemic sclerosis (SSc) fibroblasts. METHODS Dermal fibroblasts from seven patients with diffuse SSc of recent onset and from seven healthy individuals were studied. The expression levels of Smad2, Smad3 and Smad4 proteins were determined by immuno...

متن کامل

Interferon- Interferes with Transforming Growth Factor- Signaling through Direct Interaction of YB-1 with Smad3*

Transforming growth factor(TGF) and interferon(IFN) exert antagonistic effects on collagen synthesis in human dermal fibroblasts. We have recently shown that Y box-binding protein YB-1 mediates the inhibitory effects of IFNon 2(I) procollagen gene (COL1A2) transcription through the IFNresponse element located between 161 and 150. Here we report that YB-1 counter-represses TGF-stimulated COL1A2 ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2001