Tacrolimus fails to regulate collagen expression in dermal fibroblasts

Wong, Victor W.; You, Fanglei; Januszyk, Michael; Kuang, Anna A.

doi:10.1016/j.jss.2013.04.006

Cited by 9 publications

(7 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, a subsequent genome‐wide microarray analysis, followed by quantitative PCR, showed that treating human keloid fibroblasts for 72 hours with 2 nmol/L tacrolimus in vitro did not directly block their collagen expression pathways; rather, tacrolimus acts by inhibiting NME/NM23 nucleoside diphosphate kinase 1 (a metastasis suppressor) and heterogeneous nuclear ribonucleoprotein H3‐2H9. The latter is involved in the fibrogenic epithelial‐mesenchymal interactions and the post‐transcriptional control of collagens . In terms of clinical evidence, a patient in a clinical trial for conventional topical treatment of atopic dermatitis with tacrolimus reported that he had also treated his keloid with the agent and had observed marked clearing of the keloid …”

Section: Current and Emerging Pharmaceuticals In Clinical Keloid Manamentioning

confidence: 99%

“…The latter is involved in the fibrogenic epithelial-mesenchymal interactions and the posttranscriptional control of collagens. 28 In terms of clinical evidence, a patient in a clinical trial for conventional topical treatment of atopic dermatitis with tacrolimus reported that he had also treated his keloid with the agent and had observed marked clearing of the keloid. 29 Imiquimod is a Toll-like receptor agonist.…”

Section: Immunotherapiesmentioning

confidence: 99%

See 1 more Smart Citation

Managing keloid scars: From radiation therapy to actual and potential drug deliveries

Huang

Liu

You

et al. 2019

International Wound Journal

View full text Add to dashboard Cite

The aetiology of keloids is becoming clearer, but many questions remain, including about the most optimal treatment. Current therapies include surgical excision, radiotherapy, and various pharmaceutical drugs. However, none of these drugs are keloid‐specific. Moreover, all current interventions are associated with high recurrence rates. Here, we review the pharmaceutical interventions that are currently available. All are based on the fact that keloids are an expanding solid mass with intense chronic inflammation at its advancing edges. Consequently, current pharmaceuticals aim to reduce the mass and/or symptoms of keloids, similar to surgery and radiotherapy. They include chemotherapies, immunotherapies, volume‐reducing therapies, and anti‐inflammatory therapies. We also describe new advances in keloid pharmaceuticals. They include drugs that were designed to treat systemic diseases such as hypertension or breast cancer but were found to also treat keloids. Furthermore, recent progress in genetic, epigenetic, and stem cell therapies suggests that they could become useful in the keloid field. This review of pharmaceutical advances will hopefully promote additional research and the development of effective and specific pharmaceuticals for keloids.

show abstract

Section: Current and Emerging Pharmaceuticals In Clinical Keloid Manamentioning

confidence: 99%

Section: Immunotherapiesmentioning

confidence: 99%

Managing keloid scars: From radiation therapy to actual and potential drug deliveries

Huang

Liu

You

et al. 2019

International Wound Journal

View full text Add to dashboard Cite

show abstract

“…A total of 5 sets of keloid gene expression microarray data were used for further analysis. The GEO datasets were GSE7980 ( 7 ), GSE44270 ( 13 ), and GSE145725 ( 6 ), and the ArrayExpress datasets were E-MTAB-2509 ( 14 ) and E-MTAB-4945 ( Table 1 ).…”

Section: Resultsmentioning

confidence: 99%

The Polygenic Map of Keloid Fibroblasts Reveals Fibrosis-Associated Gene Alterations in Inflammation and Immune Responses

Yang

Li²,

Qu³

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

Due to many inconsistencies in differentially expressed genes (DEGs) related to genomic expression changes during keloid formation and a lack of satisfactory prevention and treatment methods for this disease, the critical biomarkers related to inflammation and the immune response affecting keloid formation should be systematically clarified. Normal skin/keloid scar tissue-derived fibroblast genome expression data sets were obtained from the Gene Expression Omnibus (GEO) and ArrayExpress databases. Hub genes have a high degree of connectivity and gene function aggregation in the integration network. The hub DEGs were screened by gene-related protein–protein interactions (PPIs), and their biological processes and signaling pathways were annotated to identify critical biomarkers. Finally, eighty-one hub DEGs were selected for further analysis, and some noteworthy signaling pathways and genes were found to be closely related to keloid fibrosis. For example, IL17RA is involved in IL-17 signal transduction, TIMP2 and MMP14 activate extracellular matrix metalloproteinases, and TNC, ITGB2, and ITGA4 interact with cell surface integrins. Furthermore, changes in local immune cell activity in keloid tissue were detected by DEG expression, immune cell infiltration, and mass CyTOF analyses. The results showed that CD4+ T cells, CD8+ T cells and NK cells were abnormal in keloid tissue compared with normal skin tissue. These findings not only support the key roles of fibrosis-related pathways, immune cells and critical genes in the pathogenesis of keloids but also expand our understanding of targets that may be useful for the treatment of fibrotic diseases.

show abstract

“…Animal models have shown that intralesional tacrolimus injection can have a potential use in preventing keloid scar formation [38]. Nonetheless, fibroblast gene expression analysis after the use of tacrolimus demonstrated no modulation of collagens 1 or 3 expressions in human dermal fibroblasts in vitro [39]. Topical tacrolimus for penile keloids has not been used, but future studies may provide information about its benefit in keloid management.…”

Section: Discussionmentioning

confidence: 99%

Keloid formation after pediatric male genital surgeries: an uncommon and difficult problem to manage

Alyami

Ferandez

Koyle

et al. 2019

Journal of Pediatric Urology

View full text Add to dashboard Cite

Tacrolimus fails to regulate collagen expression in dermal fibroblasts

Cited by 9 publications

References 30 publications

Managing keloid scars: From radiation therapy to actual and potential drug deliveries

Managing keloid scars: From radiation therapy to actual and potential drug deliveries

The Polygenic Map of Keloid Fibroblasts Reveals Fibrosis-Associated Gene Alterations in Inflammation and Immune Responses

Keloid formation after pediatric male genital surgeries: an uncommon and difficult problem to manage

Contact Info

Product

Resources

About