NDLI: TGF-beta1 is a negative regulator of lymphatic regeneration during wound repair.

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TGF-beta1 is a negative regulator of lymphatic regeneration during wound repair.

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TGF-beta1 is a negative regulator of lymphatic regeneration during wound repair.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Clavin, Nicholas W. Avraham, Tomer Fernandez, John Daluvoy, Sanjay V. Soares, Marc A. Chaudhry, Arif Mehrara, Babak J.
Description	Country affiliation: United States Author Affiliation: Clavin NW ( Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.)
Abstract	Although clinical studies have identified scarring/fibrosis as significant risk factors for lymphedema, the mechanisms by which lymphatic repair is impaired remain unknown. Transforming growth factor -beta1 (TGF-beta1) is a critical regulator of tissue fibrosis/scarring and may therefore also play a role in the regulation of lymphatic regeneration. The purpose of this study was therefore to assess the role of TGF-beta1 on scarring/fibrosis and lymphatic regeneration in a mouse tail model. Acute lymphedema was induced in mouse tails by full-thickness skin excision and lymphatic ligation. TGF-beta1 expression and scarring were modulated by repairing the wounds with or without a topical collagen gel. Lymphatic function and histological analyses were performed at various time points. Finally, the effects of TGF-beta1 on lymphatic endothelial cells (LECs) in vitro were evaluated. As a result, the wound repair with collagen gel significantly reduced the expression of TGF-beta1, decreased scarring/fibrosis, and significantly accelerated lymphatic regeneration. The addition of recombinant TGF-beta1 to the collagen gel negated these effects. The improved lymphatic regeneration secondary to TGF-beta1 inhibition was associated with increased infiltration and proliferation of LECs and macrophages. TGF-beta1 caused a dose-dependent significant decrease in cellular proliferation and tubule formation of isolated LECs without changes in the expression of VEGF-C/D. Finally, the increased expression of TGF-beta1 during wound repair resulted in lymphatic fibrosis and the coexpression of alpha-smooth muscle actin and lymphatic vessel endothelial receptor-1 in regenerated lymphatics. In conclusion, the inhibition of TGF-beta1 expression significantly accelerates lymphatic regeneration during wound healing. An increased TGF-beta1 expression inhibits LEC proliferation and function and promotes lymphatic fibrosis. These findings imply that the clinical interventions that diminish TGF-beta1 expression may be useful in promoting more rapid lymphatic regeneration.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
Journal	AJP: Heart and Circulatory Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Lymphangiogenesis Lymphatic Vessels Physiopathology Lymphedema Skin Transforming Growth Factor Beta1 Metabolism Wound Healing Administration, Cutaneous Animals Cell Movement Cell Proliferation Cicatrix Collagen Administration & Dosage Dermatologic Surgical Procedures Endothelium, Lymphatic Fibroblasts Fibrosis Gels Ligation Drug Effects Pathology Surgery Prevention & Control Macrophages Mice Mice, Inbred C57bl Recombinant Proteins Tail Time Factors Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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