scholarly journals Myofibroblasts in Murine Cutaneous Fibrosis Originate From Adiponectin-Positive Intradermal Progenitors

2015 ◽  
Vol 67 (4) ◽  
pp. 1062-1073 ◽  
Author(s):  
Roberta Goncalves Marangoni ◽  
Benjamin D. Korman ◽  
Jun Wei ◽  
Tammara A. Wood ◽  
Lauren V. Graham ◽  
...  
Keyword(s):  
Cutaneous Fibrosis

scholarly journals An acute bleomycin inflammatory and fibrotic mouse model of morphea is dependent upon CXCL9 and CXCR3

2019 ◽  
Author(s):  
Jillian M. Richmond ◽  
Dhrumil Patel ◽  
Tomoya Watanabe ◽  
Colton J. Garelli ◽  
Madhuri Garg ◽  
...  
Keyword(s):  
Mouse Model ◽  
Localized Scleroderma ◽  
Lesional Skin ◽  
Chemokine Expression ◽  
Inflammatory Phase ◽  
Deficient Mice ◽  
Over Time ◽  
Cutaneous Fibrosis

AbstractMorphea, or localized scleroderma, is characterized by an inflammatory phase followed by cutaneous fibrosis, which may lead to disfigurement and/or disability. Previous work from our group showed that the CXCR3 ligands CXCL9 and CXCL10 are highly upregulated in lesional skin of morphea patients. Here, we used an acute inflammatory and fibrotic bleomycin mouse model of morphea to examine the role of the CXCR3 chemokine axis in pathogenesis. We first characterized which cells produce the CXCR3 ligands in the skin using the Reporter of Expression of CXCR3 ligands mouse (REX3). We found that fibroblasts contribute the bulk of CXCL9 and CXCL10, whereas endothelial cells are key dual chemokine producers. Macrophages, which have high MFI of chemokine expression, upregulated CXCL9 production over time, fibroblasts CXCL10 production, and T cells dual chemokine expression. To determine whether bleomycin treatment could directly induce expression of these chemokines, we treated cultured REX3 mouse dermis monolayers in vitro with bleomycin or IFNγ with TNF and found that bleomycin could induce low amounts of CXCL9 directly in fibroblasts, whereas the cytokines were required for optimal CXCL9 and CXCL10 production. To determine whether these chemokines are mechanistically involved in pathogenesis, we induced fibrosis in CXCL9, CXCL10, or CXCR3 deficient mice and found that fibrosis is dependent on CXCL9 and CXCR3. Addition of recombinant CXCL9, but not CXCL10, to cultured mouse fibroblasts induces collagen 1a1 mRNA expression, indicating the chemokine itself can contribute to fibrosis. Taken together, our studies provide evidence that acute intradermal bleomycin administration in mice can model inflammatory morphea, and that CXCL9 and its receptor CXCR3 are mechanistically involved in pathogenesis.One Sentence SummaryCXCL9 drives acute morphea pathogenesis in mice.

Extensive cutaneous fibrosis and ulceration caused by methadone injection

2005 ◽  
Vol 30 (1) ◽  
pp. 87-88 ◽  
Author(s):  
P. Farrant ◽  
D. Creamer ◽  
C. Fuller
Keyword(s):  
Cutaneous Fibrosis

Decreased IL-20 expression in scleroderma skin contributes to cutaneous fibrosis

2016 ◽  
Vol 84 (1) ◽  
pp. e10
Author(s):  
Hideo Kudo ◽  
Masatoshi Jinnin ◽  
Hironobu Ihn
Keyword(s):  
Cutaneous Fibrosis

Cutaneous Fibrosis and Normal Wound Healing

2017 ◽  
pp. 577-600
Author(s):  
Emily Hamburg-Shields ◽  
Peggy Myung ◽  
Shawn E. Cowper
Keyword(s):  
Wound Healing ◽  
Normal Wound Healing ◽  
Cutaneous Fibrosis

scholarly journals Increased KGF Expression Promotes Fibroblast Activation in a Double Paracrine Manner Resulting in Cutaneous Fibrosis

2013 ◽  
Vol 133 (3) ◽  
pp. 647-657 ◽  
Author(s):  
Johanna Canady ◽  
Stephanie Arndt ◽  
Sigrid Karrer ◽  
Anja K. Bosserhoff
Keyword(s):  
Fibroblast Activation ◽  
Cutaneous Fibrosis

Bosentan therapy for cutaneous fibrosis in systemic sclerosis

2007 ◽  
Vol 23 (sup2) ◽  
pp. S89-S96 ◽  
Author(s):  
J. J. Alegre-Sancho ◽  
J. A. Roman-Ivorra ◽  
C. Chalmeta-Verdejo ◽  
C. Fernandez-Carballido ◽  
N. Fernández-Llanio ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Cutaneous Fibrosis
Sign in / Sign up

Export Citation Format

Share Document