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Condition: Scleroderma

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Total 44 results found since Jan 2013.

Long non‐coding RNA TSIX is up‐regulated in scleroderma dermal fibroblasts and controls collagen mRNA stabilization
This article is protected by copyright. All rights reserved.
Source: Experimental Dermatology - November 14, 2015 Category: Dermatology Authors: Zhongzhi Wang, Masatoshi Jinnin, Kayo Nakamura, Miho Harada, Hideo Kudo, Wakana Nakayama, Kuniko Inoue, Taiji Nakashima, Noritoshi Honda, Satoshi Fukushima, Hironobu Ihn Tags: Regular Article Source Type: research

Fli1 deficiency contributes to the downregulation of endothelial protein C receptor in systemic sclerosis: a possible role in pro-thrombotic condition.
CONCLUSIONS: Endothelial EPCR down-regulation due to Fli1 deficiency may contribute to hyper-coagulation status leading to tissue fibrosis and impaired peripheral circulation in SSc. This article is protected by copyright. All rights reserved. PMID: 26399195 [PubMed - as supplied by publisher]
Source: The British Journal of Dermatology - September 24, 2015 Category: Dermatology Authors: Saigusa R, Asano Y, Yamashita T, Taniguchi T, Takahashi T, Ichimura Y, Toyama T, Yoshizaki A, Miyagaki T, Sugaya M, Sato S Tags: Br J Dermatol Source Type: research

Increased Expression of NAPDH Oxidase 4 in Systemic Sclerosis Dermal Fibroblasts: Regulation by Transforming Growth Factor β
ConclusionNOX‐4 expression and production were found to be constitutively elevated in SSc skin and cultured SSc dermal fibroblasts. TGFβ1 stimulated NOX‐4 expression in normal and SSc fibroblasts through PKCδ and Smad2/3 signaling pathways. A small‐molecule NOX‐4 inhibitor decreased collagen and fibronectin production by normal and SSc fibroblasts, and NOX‐4 siRNA knockdown reduced ROS and collagen production by SSc fibroblasts. These results demonstrate the involvement of NOX‐4 in SSc‐associated fibrosis and indicate NOX‐4 inhibitors as novel therapeutic approaches for SSc.
Source: Arthritis and Rheumatism - September 23, 2015 Category: Rheumatology Authors: Sonsoles Piera‐Velazquez, Alma Makul, Sergio A. Jiménez Tags: Systemic Sclerosis Source Type: research

S100A4 amplifies TGF-{beta}-induced fibroblast activation in systemic sclerosis
Conclusions We characterised S100A4 as a downstream mediator of the stimulatory effects of TGF-β on fibroblasts in SSc. TGF-β induces the expression of S100A4 to stimulate the release of collagen in SSc fibroblasts and induce fibrosis. Since S100A4 is essentially required for the pro-fibrotic effects of TGF-β and neutralising antibodies against S100A4 are currently evaluated, S100A4 might be a candidate for novel antifibrotic therapies.
Source: Annals of the Rheumatic Diseases - August 10, 2015 Category: Rheumatology Authors: Tomcik, M., Palumbo-Zerr, K., Zerr, P., Avouac, J., Dees, C., Sumova, B., Distler, A., Beyer, C., Cerezo, L. A., Becvar, R., Distler, O., Grigorian, M., Schett, G., Senolt, L., Distler, J. H. W. Tags: Immunology (including allergy), Connective tissue disease Basic and translational research Source Type: research

Dermal delivery of HSP47 siRNA with NOX4-modulating mesoporous silica-based nanoparticles for treating fibrosis.
Abstract Fibrotic diseases such as scleroderma have been linked to increased oxidative stress and upregulation of pro-fibrotic genes. Recent work suggests a role of NADPH oxidase 4 (NOX4) and heat shock protein 47 (HSP47) in inducing excessive collagen synthesis, leading to fibrotic diseases. Herein, we elucidate the relationship between NOX4 and HSP47 in fibrogenesis and propose to modulate them altogether as a new strategy to treat fibrosis. We developed a nanoparticle platform consisting of polyethylenimine (PEI) and polyethylene glycol (PEG) coating on a 50-nm mesoporous silica nanoparticle (MSNP) core. The na...
Source: Biomaterials - July 10, 2015 Category: Materials Science Authors: Morry J, Ngamcherdtrakul W, Gu S, Goodyear SM, Castro DJ, Reda MM, Sangvanich T, Yantasee W Tags: Biomaterials Source Type: research

Increased Expression of NAPDH Oxidase 4 (NOX4) in Systemic Sclerosis Dermal Fibroblasts: Regulation by Transforming Growth Factor ß
Conclusion: NOX4 expression and production are constitutively elevated in SSc skin and cultured SSc dermal fibroblasts. TGF‐ß1 stimulates NOX4 expression in normal and SSc fibroblasts through PKC‐δ and Smad2/3 signaling pathways. A small molecule NOX4 inhibitor decreased fibroblast collagen and fibronectin production and NOX4 siRNA knockdown reduced SSc fibroblast ROS and collagen production. These results demonstrate NOX4 involvement in SSc‐associated fibrosis and suggest NOX4 inhibitors as novel therapeutic approaches for SSc. This article is protected by copyright. All rights reserved.
Source: Arthritis and Rheumatism - June 19, 2015 Category: Rheumatology Authors: Sonsoles Piera‐Velazquez, Alma Makul, Sergio A. Jimenez Tags: Full Length Source Type: research

Global DNA hypomethylation and hypoxia‐induced expression of the ten eleven translocation (TET) family, TET1, in scleroderma fibroblasts
This article is protected by copyright. All rights reserved.
Source: Experimental Dermatology - May 25, 2015 Category: Dermatology Authors: Mai Hattori, Yoko Yokoyama, Tomoyasu Hattori, Sei‐ichiro Motegi, Hiroo Amano, Izuho Hatada, Osamu Ishikawa Tags: Regular Article Source Type: research

Vitamin D receptor regulates TGF-{beta} signalling in systemic sclerosis
Conclusions We characterise VDR as a negative regulator of TGF-β/Smad signalling. Impaired VDR signalling with reduced expression of VDR and decreased levels of its ligand may thus contribute to hyperactive TGF-β signalling and aberrant fibroblast activation in SSc.
Source: Annals of the Rheumatic Diseases - February 5, 2015 Category: Rheumatology Authors: Zerr, P., Vollath, S., Palumbo-Zerr, K., Tomcik, M., Huang, J., Distler, A., Beyer, C., Dees, C., Gela, K., Distler, O., Schett, G., Distler, J. H. W. Tags: Connective tissue disease Basic and translational research Source Type: research

Attenuation of fibrosis with selective inhibition of c-Abl by siRNA in systemic sclerosis dermal fibroblasts
In conclusion, specific c-Abl gene silencing using siRNA effectively reduced fibrosis-related gene expression. Inhibition of c-Abl by siRNA may be a potential therapeutic approach for fibrotic diseases such as systemic sclerosis.
Source: Archives of Dermatological Research - December 20, 2014 Category: Dermatology Source Type: research

The nuclear receptor CAR / NR1I3 enhances the pro‐fibrotic effects of TGF‐β and contributes to the development of experimental dermal fibrosis
Conclusion: CAR is upregulated in SSc and regulates TGF‐β signaling. Activation of CAR increases the profibrotic effects of TGF‐β in cultured fibroblasts and in different preclinical models of SSc. Thus, inactivation of CAR might be a novel approach to target aberrant TGF‐β signaling in SSc and in other fibrotic diseases. © 2014 American College of Rheumatology.
Source: Arthritis and Rheumatism - August 22, 2014 Category: Rheumatology Authors: Jérôme Avouac, Katrin Palumbo‐Zerr, Nadira Ruzehaji, Michal Tomcik, Pawel Zerr, Clara Dees, Alfiya Distler, Christian Beyer, Holm Schneider, Oliver Distler, Georg Schett, Yannick Allanore, Jörg H.W. Distler Tags: Full Length Source Type: research

Decreased cathepsin V expression due to Fli1 deficiency contributes to the development of dermal fibrosis and proliferative vasculopathy in systemic sclerosis
Conclusion. Loss of CTSV expression may contribute to the development of fibrosis, vasculopathy and the altered phenotype of keratinocytes in SSc.
Source: Rheumatology - April 19, 2013 Category: Rheumatology Authors: Noda, S., Asano, Y., Takahashi, T., Akamata, K., Aozasa, N., Taniguchi, T., Ichimura, Y., Toyama, T., Sumida, H., Kuwano, Y., Yanaba, K., Tada, Y., Sugaya, M., Kadono, T., Sato, S. Tags: Systemic Sclerosis BASIC SCIENCE Source Type: research

Sp sites contribute to basal and inducible expression of the human TNFα-Inducible Protein 3-Interacting Protein 1 (TNIP1) promoter.
Abstract TNFα-induced protein 3-interacting protein 1 (TNIP1) is a corepressor of RAR and PPAR. Additionally, it can reduce signaling stemming from cell membrane receptors such as those for TNFα and EGF. Consequently, it influences a variety of receptor-mediated events as diverse as transcription, programmed cell death, and cell cycling. Thus, changes in TNIP1 expression levels are likely to impact multiple important biological endpoints. TNIP1 expression level changes have been linked to psoriasis and systemic sclerosis. As such, it is crucial to determine what controls its expression levels starting with const...
Source: The Biochemical Journal - March 7, 2013 Category: Biochemistry Authors: Encarnacao PC, Ramirez VP, Zhang C, Aneskievich BJ Tags: Biochem J Source Type: research

Sp sites contribute to basal and inducible expression of the human TNF{alpha}-Inducible Protein 3-Interacting Protein 1 (TNIP1) promoter
TNFα-induced protein 3-interacting protein 1 (TNIP1) is a corepressor of RAR and PPAR. Additionally, it can reduce signaling stemming from cell membrane receptors such as those for TNFα and EGF. Consequently, it influences a variety of receptor-mediated events as diverse as transcription, programmed cell death, and cell cycling. Thus, changes in TNIP1 expression levels are likely to impact multiple important biological endpoints. TNIP1 expression level changes have been linked to psoriasis and systemic sclerosis. As such, it is crucial to determine what controls its expression levels starting with constitutiv...
Source: BJ Cell - March 7, 2013 Category: Biochemistry Authors: P C Encarnacao, V P Ramirez, C Zhang, B J Aneskievich Tags: BJ Gene Source Type: research

Inhibition of H3K27 histone trimethylation activates fibroblasts and induces fibrosis
Conclusions These data demonstrate a novel role of H3 Lys27 histone methylation in fibrosis. In contrast to other epigenetic modifications such as DNA methylation and histone acetylation, H3 Lys27 histone methylation acts as a negative regulator of fibroblast activation in vitro and in vivo by repressing the expression of fra-2.
Source: Annals of the Rheumatic Diseases - February 25, 2013 Category: Rheumatology Authors: Kramer, M., Dees, C., Huang, J., Schlottmann, I., Palumbo-Zerr, K., Zerr, P., Gelse, K., Beyer, C., Distler, A., Marquez, V. E., Distler, O., Schett, G., Distler, J. H. W. Tags: Immunology (including allergy), Connective tissue disease Basic and translational research Source Type: research