Skip to main content
padlock icon - secure page this page is secure

Effect of the abrogation of TGF-β1 by antisense oligonucleotides on the expression of TGF-β-isoforms and their receptors I and II in isolated fibroblasts from keloid scars

Buy Article:

$42.00 + tax (Refund Policy)

Disequilibrium of dermal wound repair can result in continued accumulation of ECM and excessive scar formation. In susceptible genetically predisposed individuals, keloid formation can be observed. Keloid disease represents a benign dermal fibroproliferative tumor that is unique to humans. TGF-β is known to play a key role in the pathogenesis of this disease which is still not fully understood. The isoforms TGF-β1 and TGF-β2 have profibrotic properties, whereas TGF-β3 may have antifibrotic functions. TGF-β exerts its influence by binding to type I and type II TGF-β receptors, thereby forming a complex and activating specific downstream effector molecules. The aim of this study was to investigate the effect of TGF-β1 targeting by antisense oligonucleotides on the RNA synthesis and protein expression of TGF-β isoforms and their receptors in keloid-derived fibroblasts. In tissue samples with normal fibroblasts (NFs) serving as control samples, expression of TGF-β1 and -β2 was decreased when compared to keloid fibroblasts (KFs), while expression of TGF-β3 and of TGF-βRII was significantly higher in NFs. In the ELISA assay, abrogation of TGF-β1 led to a significant decrease in TGF-β1 and -β2 (p<0.05). Expression of TGF-β2 mRNA was reduced. Expression of TGF-β3 mRNA revealed contrary patterns in KFs from different patients while expression of TGF-βRI was found to be equal during the measurement period. TGF-βRII mRNA expression was increased after 48 and 72 h respectively. There is growing evidence for a regulatory mechanism between TGF-β1 and its receptors. Our findings support this theory by suggesting interrelations between the different TGF-β isoforms and their receptors. Abnormal response of KFs to TGF-βmight reflect a modification in the regulatory pathway that occurs at the receptor level or during intracellular trans-duction. Improving the understanding of TGF-β in keloid disease could lead to the development of clinically useful therapeutic modalities for treatment of keloid disease or even allow identification of preventive strategies.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Research Article

Affiliations: Department of Otolaryngology, Head and Neck Surgery, University Hospital of Mannheim, D-68167 Mannheim, Germany., Email: [email protected]

Publication date: June 1, 2010

More about this publication?
  • The International Journal of Molecular Medicine is a monthly, peer-reviewed journal devoted to the publication of high quality studies related to the molecular mechanisms of human disease. The journal welcomes research on all aspects of molecular and clinical research, ranging from biochemistry to immunology, pathology, genetics, human genomics, microbiology, molecular pathogenesis, molecular cardiology, molecular surgery and molecular psychology.

    The International Journal of Molecular Medicine aims to provide an insight for researchers within the community in regard to developing molecular tools and identifying molecular targets for the diagnosis and treatment of a diverse number of human diseases.
  • Editorial Board
  • Information for Authors
  • Submit a Paper
  • Subscribe to this Title
  • Information for Advertisers
  • Terms & Conditions
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more