Back to Search
Start Over
Cyclosporine A inhibits TGF-β2-induced myofibroblasts of primary cultured human pterygium fibroblasts
- Source :
- Biochemical and Biophysical Research Communications. 482:1148-1153
- Publication Year :
- 2017
- Publisher :
- Elsevier BV, 2017.
-
Abstract
- Cyclosporine A (CsA), an immunomodulatory drug, and is increasingly used to treat moderate dry eye syndrome and ocular surface inflammation. However, any inhibitory effect on differentiation of fibroblasts to myofibroblasts remains unclear. Here, we show that the inhibitory effect of CsA on transforming growth factor-beta2 (TGF-β2)-induced myofibroblasts in primary cultured human pterygium fibroblasts. CsA significantly decreased mRNA and protein expression of myofibroblast-related markers including α-SMA, laminin, and fibronectin. These findings were supported by the results from immunofluorescence staining. Taken together, these results indicate the therapeutic potential of CsA against pterygium progression. Further studies are necessary to elucidate the precise intracellular signal mechanism responsible for CsA-induced downregulation of myofibroblast markers in pterygium fibroblasts.
- Subjects :
- Male
0301 basic medicine
Oligonucleotides
Biophysics
Inflammation
Pterygium
Biochemistry
Transforming Growth Factor beta2
03 medical and health sciences
0302 clinical medicine
Downregulation and upregulation
Laminin
Humans
Medicine
Myofibroblasts
Molecular Biology
Cells, Cultured
Messenger RNA
biology
business.industry
Cell Differentiation
Muscle, Smooth
Cell Biology
Fibroblasts
Actins
eye diseases
Fibronectins
Fibronectin
030104 developmental biology
Microscopy, Fluorescence
Immunology
Cyclosporine
030221 ophthalmology & optometry
Cancer research
biology.protein
Female
sense organs
medicine.symptom
business
Myofibroblast
Immunosuppressive Agents
Software
Intracellular
Signal Transduction
Transforming growth factor
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 482
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....006dc1bcfc53ccda7404cb6901ee2599