Mouse Model of Experimental Dermal Fibrosis: The Bleomycin-Induced Dermal Fibrosis

2014 ◽  
pp. 91-98 ◽  
Author(s):  
Jérôme Avouac
Keyword(s):  
Mouse Model ◽  
Dermal Fibrosis

scholarly journals Amelioration of dermal fibrosis by genetic deletion or pharmacologic antagonism of lysophosphatidic acid receptor 1 in a mouse model of scleroderma

2011 ◽  
Vol 63 (5) ◽  
pp. 1405-1415 ◽  
Author(s):  
Flavia V. Castelino ◽  
Jon Seiders ◽  
Gretchen Bain ◽  
Sarah F. Brooks ◽  
Christopher D. King ◽  
...  
Keyword(s):  
Mouse Model ◽  
Lysophosphatidic Acid ◽  
Acid Receptor ◽  
Lysophosphatidic Acid Receptor ◽  
Dermal Fibrosis ◽  
Genetic Deletion

scholarly journals Adipose tissue-derived stem cells ameliorates dermal fibrosis in a mouse model of scleroderma

2017 ◽  
Vol 10 (1) ◽  
pp. 52-56 ◽  
Author(s):  
Wei Chen ◽  
Zhi-Kuan Xia ◽  
Man-Hui Zhang ◽  
Gui-Chun Ding ◽  
Xiao-Yan Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Mouse Model ◽  
Dermal Fibrosis

The Antifibrotic Effect of A2B Adenosine Receptor Antagonism in a Mouse Model of Dermal Fibrosis

2018 ◽  
Vol 70 (10) ◽  
pp. 1673-1684 ◽  
Author(s):  
Harry Karmouty-Quintana ◽  
Jose G. Molina ◽  
Kemly Philip ◽  
Chiara Bellocchi ◽  
Brent Gudenkauf ◽  
...  
Keyword(s):  
Mouse Model ◽  
Adenosine Receptor ◽  
Receptor Antagonism ◽  
Antifibrotic Effect ◽  
A2b Adenosine Receptor ◽  
Dermal Fibrosis

Loss of LPA1 Signaling Protects Against Dermal Fibrosis in a Mouse Model of Systemic Sclerosis

2010 ◽  
Vol 135 ◽  
pp. S56
Author(s):  
Flavia Castelino ◽  
Sarah Brooks ◽  
Manuela Funke ◽  
Jerold Chun ◽  
Andrew Luster ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Mouse Model ◽  
Dermal Fibrosis

scholarly journals Mouse model of dermal fibrosis induced by one-time injection of bleomycin-poly(L-lactic acid) microspheres

Rheumatology ◽  
2007 ◽  
Vol 47 (4) ◽  
pp. 454-457 ◽  
Author(s):  
Y. Shibusawa ◽  
I. Negishi ◽  
Y. Tabata ◽  
O. Ishikawa
Keyword(s):  
Lactic Acid ◽  
Mouse Model ◽  
Dermal Fibrosis ◽  
Time Injection

scholarly journals The cannabinoid WIN55, 212-2 abrogates dermal fibrosis in scleroderma bleomycin model

2010 ◽  
Vol 70 (4) ◽  
pp. 695-699 ◽  
Author(s):  
Epifania Balistreri ◽  
Estrella Garcia-Gonzalez ◽  
Enrico Selvi ◽  
Alfiya Akhmetshina ◽  
Katrin Palumbo ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Transforming Growth Factor ◽  
Tissue Growth ◽  
Synthetic Cannabinoid ◽  
Skin Fibrosis ◽  
Control Group ◽  
Skin Thickness ◽  
Dermal Fibrosis ◽  
Dermal Thickness

ObjectivesThere is increasing evidence that the endocannabinoid system may be involved in pathological fibrosis, and that its modulation might limit fibrotic responses. The aim of this study was to examine the capacity of a synthetic cannabinoid receptor agonist to modify skin fibrosis in the bleomycin mouse model of scleroderma.MethodsSkin fibrosis was induced by local injections of bleomycin in two groups of DBA/2J mice. One group was cotreated with the synthetic cannabinoid WIN55,212-2 at 1 mg/kg/day. Skin fibrosis was evaluated by histology and skin thickness and hydroxyproline content were quantified. Markers of fibroblast activation, including α smooth muscle actin and the profibrotic cytokines transforming growth factor (TGF)β, connective tissue growth factor (CTGF) and platelet-derived growth factor (PDGF)-BB, were examined. Levels of PSMAD2/3, which are crucial in extracellular matrix overproduction, were analysed.ResultsBleomycin treatment induced typical skin fibrosis. Upon WIN55,212-2 treatment dermal fibrosis was completely prevented. Subcutaneous inflammatory cell infiltration, dermal thickness and collagen content resulted similar to those of the control group. The synthetic cannabinoid prevented fibroblasts activation induced by bleomycin, paralleled by a strong inhibition of TGFβ, CTGF and PDGF-BB expression. Phosphorylation of SMAD2/3 was significantly downregulated after WIN55,212-2 exposure.ConclusionsTaken together, the results indicate that the synthetic cannabinoid WIN55,212-2 is capable of preventing skin fibrosis in a mouse model of scleroderma.

scholarly journals Angiotensin II induces skin fibrosis: a novel mouse model of dermal fibrosis

2012 ◽  
Vol 14 (4) ◽  
pp. R194 ◽  
Author(s):  
Lukasz Stawski ◽  
Rong Han ◽  
Andreea M Bujor ◽  
Maria Trojanowska
Keyword(s):  
Angiotensin Ii ◽  
Mouse Model ◽  
Skin Fibrosis ◽  
Dermal Fibrosis

scholarly journals Scleroderma-like Impairment in the Network of Telocytes/CD34+ Stromal Cells in the Experimental Mouse Model of Bleomycin-Induced Dermal Fibrosis

2021 ◽  
Vol 22 (22) ◽  
pp. 12407
Author(s):  
Irene Rosa ◽  
Eloisa Romano ◽  
Bianca Saveria Fioretto ◽  
Daniele Guasti ◽  
Lidia Ibba-Manneschi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Stromal Cells ◽  
Skin Lesions ◽  
Disease Stage ◽  
Dermal Fibrosis ◽  
Transmission Electron ◽  
Experimental Mouse Model ◽  
Severe Impairment ◽  
Experimental Mouse ◽  
Early Disease Stage

Considerable evidence accumulated over the past decade supports that telocytes (TCs)/CD34+ stromal cells represent an exclusive type of interstitial cells identifiable by transmission electron microscopy (TEM) or immunohistochemistry in various organs of the human body, including the skin. By means of their characteristic cellular extensions (telopodes), dermal TCs are arranged in networks intermingled with a multitude of neighboring cells and, hence, they are thought to contribute to skin homeostasis through both intercellular contacts and releasing extracellular vesicles. In this context, fibrotic skin lesions from patients with systemic sclerosis (SSc, scleroderma) appear to be characterized by a disruption of the dermal network of TCs, which has been ascribed to either cell degenerative processes or possible transformation into profibrotic myofibroblasts. In the present study, we utilized the well-established mouse model of bleomycin-induced scleroderma to gain further insights into the TC alterations found in cutaneous fibrosis. CD34 immunofluorescence revealed a severe impairment in the dermal network of TCs/CD34+ stromal cells in bleomycin-treated mice. CD31/CD34 double immunofluorescence confirmed that CD31−/CD34+ TC counts were greatly reduced in the skin of bleomycin-treated mice compared with control mice. Ultrastructural signs of TC injury were detected in the skin of bleomycin-treated mice by TEM. The analyses of skin samples from mice treated with bleomycin for different times by either TEM or double immunostaining and immunoblotting for the CD34/α-SMA antigens collectively suggested that, although a few TCs may transition to α-SMA+ myofibroblasts in the early disease stage, most of these cells rather undergo degeneration, and then are lost. Taken together, our data demonstrate that TC changes in the skin of bleomycin-treated mice mimic very closely those observed in human SSc skin, which makes this experimental model a suitable tool to (i) unravel the pathological mechanisms underlying TC damage and (ii) clarify the possible contribution of the TC loss to the development/progression of dermal fibrosis. In perspective, these findings may have important implications in the field of skin regenerative medicine.

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