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Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
Published on: November 8, 2015
Tacrolimus fails to regulate collagen expression in dermal fibroblasts
Victor W Wong1, Fanglei You, Michael Januszyk
1Division of Plastic and Reconstructive Surgery, Department of Surgery, Oregon Health and Science University, Portland, Oregon 97239, USA.
The Journal of Surgical Research
|May 8, 2013
Summary
Tacrolimus does not affect collagen production in skin fibroblasts from normal, hypertrophic scar, or keloid tissue. However, it does impact gene expression in scar-related fibroblasts, suggesting alternative therapeutic targets for fibrotic conditions.
Area of Science:
- Dermatology
- Molecular Biology
- Pharmacology
Background:
- Fibrosis, including hypertrophic scars (HTS) and keloids, involves excessive collagen deposition.
- Tacrolimus, an immunosuppressant, is known to reduce fibrosis in organ transplant patients.
- The effect of tacrolimus on fibroblast collagen production in scar tissue is not well understood.
Purpose of the Study:
- To investigate the impact of tacrolimus on collagen expression in human dermal fibroblasts from normal skin, HTS, and keloids.
- To identify potential molecular targets of tacrolimus in fibrotic skin conditions.
Main Methods:
- Genomewide microarray analysis of human dermal fibroblasts treated with tacrolimus.
- Principal component analysis and hierarchical clustering to identify tacrolimus-regulated genes.
- Quantitative polymerase chain reaction (qPCR) to validate collagen 1 and 3 expression.
Main Results:
- Tacrolimus did not significantly alter collagen 1 or 3 expression in any fibroblast type.
- Microarray analysis revealed significant regulation of 62, 136, and 185 gene probes in normal, HTS, and keloid fibroblasts, respectively.
- Tacrolimus downregulated NME/NM23 nucleoside diphosphate kinase 1 and heterogeneous nuclear ribonucleoprotein H3-2H9 in HTS and keloid fibroblasts, but not normal fibroblasts.
Conclusions:
- Tacrolimus does not directly inhibit collagen synthesis in human dermal fibroblasts.
- NME/NM23 nucleoside diphosphate kinase 1 and heterogeneous nuclear ribonucleoprotein H3-2H9 may be novel targets in keloid and HTS pathogenesis.
- Future anti-fibrotic therapies targeting tacrolimus may need to focus on non-fibroblast cells like inflammatory cells and keratinocytes.
