ArticlePloS one2012
A possible contribution of altered cathepsin B expression to the development of skin sclerosis and vasculopathy in systemic sclerosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 38 citations in OpenAlex.
- Fli1 represses transcription of the human α2(I) collagen gene by recruitment of the HDAC1/p300 complex.PloS one · 2013Trial
- A cysteine proteinase inhibitor ALLN alleviates bleomycin-induced skin and lung fibrosis.Arthritis research & therapy · 2023Article
- Fli1 and Tissue Fibrosis in Various Diseases.International journal of molecular sciences · 2023Review
- Fli1 deficiency suppresses RALDH1 activity of dermal dendritic cells and related induction of regulatory T cells: a possible role in scleroderma.Arthritis research & therapy · 2021Article
- FLI1 and ERG protein degradation is regulated via Cathepsin B lysosomal pathway in human dermal microvascular endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Visfatin and chemerin levels correspond with inflammation and might reflect the bridge between metabolism, inflammation and fibrosis in patients with systemic sclerosis.Postepy dermatologii i alergologii · 2019Article
- Cyclophosphamide Pulse Therapy Normalizes Vascular Abnormalities in a Mouse Model of Systemic Sclerosis Vasculopathy.The Journal of investigative dermatology · 2019Article
- Epithelial Fli1 deficiency drives systemic autoimmunity and fibrosis: Possible roles in scleroderma.The Journal of experimental medicine · 2017Article
- Vasculopathy in scleroderma.Seminars in immunopathology · 2015Review
- Endothelin receptor blockade ameliorates vascular fragility in endothelial cell-specific Fli-1-knockout mice by increasing Fli-1 DNA binding ability.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Fibrosis, vascular activation, and immune abnormalities resembling systemic sclerosis in bleomycin-treated Fli-1-haploinsufficient mice.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Animal models of scleroderma: current state and recent development.Current rheumatology reports · 2013Review
- Expression of Cathepsin B and Cystatin A in Oral Lichen Planus.Journal of International Society of Preventive & Community DentistryArticle
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cathepsin B (CTSB) is a proteolytic enzyme potentially modulating angiogenic processes and extracellular matrix remodeling. While matrix metalloproteinases are shown to be implicated in tissue fibrosis and vasculopathy associated with systemic sclerosis (SSc), the role of cathepsins in this disease has not been well studied. The aim of this study is to evaluate the roles of CTSB in SSc. Serum pro-CTSB levels were determined by enzyme-linked immunosorbent assay in 55 SSc patients and 19 normal controls. Since the deficiency of transcription factor Fli1 in endothelial cells is potentially associated with the development of SSc vasculopathy, cutaneous CTSB expression was evaluated by immunostaining in Fli1(+/-) and wild type mice as well as in SSc and control subjects. The effects of Fli1 gene silencing and transforming growth factor-β (TGF-β) on CTSB expression were determined by real-time PCR in human dermal microvascular endothelial cells (HDMECs) and dermal fibroblasts, respectively. Serum pro-CTSB levels were significantly higher in limited cutaneous SSc (lcSSc) and late-stage diffuse cutaneous SSc (dcSSc) patients than in healthy controls. In dcSSc, patients with increased serum pro-CTSB levels showed a significantly higher frequency of digital ulcers than those with normal levels. CTSB expression in dermal blood vessels was increased in Fli1(+/-) mice compared with wild type mice and in SSc patients compared with healthy controls. Consistently, Fli1 gene silencing increased CTSB expression in HDMECs. In cultured dermal fibroblasts from early dcSSc, CTSB expression was decreased compared with normal fibroblasts and significantly reversed by TGF-β1 antisense oligonucleotide. In conclusion, up-regulation of endothelial CTSB due to Fli1 deficiency may contribute to the development of SSc vasculopathy, especially digital ulcers, while reduced expression of CTSB in lesional dermal fibroblasts is likely to be associated with skin sclerosis in early dcSSc.
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