Expression of pro‐angiogenic genes in mesenchymal stem cells derived from dermis of patients with psoriasis

Niu, Xuping; Chang, Wenjuan; Liu, Ruifeng; Hou, Ruixia; Li, Junqin; Wang, Chunfang; Li, Xinhua; Zhang, Kaiming

doi:10.1111/ijd.13197

Cited by 17 publications

(12 citation statements)

References 22 publications

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“…Unexpectedly, our results demonstrated a disability of psoriatic fibroblasts to induce COX-2 and generate PGE 2 under inflammatory conditions. Even constitutive COX-1 was less expressed in psoriatic than in healthy fibroblasts, in accordance with Niu et al (42), who described a significant decrease in COX-1 expression by mesenchymal stem cells derived from dermis of psoriatic lesions compared to healthy controls. Interestingly, a similar behavior has been described in other diseases such as idiopathic pulmonary fibrosis and chronic asthma, where the inability of lung fibroblasts to upregulate PGE 2 in response to a cytokine stimulus seems to contribute to the evolution of airway fibrosis (27, 28, 43).…”

Section: Discussionsupporting

confidence: 89%

Defective Induction of COX-2 Expression by Psoriatic Fibroblasts Promotes Pro-inflammatory Activation of Macrophages

et al. 2019

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Fibroblasts play an important role as members of the innate immune system through the secretion of COX-2-derived inflammatory mediators such as prostaglandin E 2 (PGE 2 ). However, it has been described that dermal fibroblasts behave like mesenchymal stem cells reducing lymphocyte recruitment and dendritic cell activation through PGE 2 release. As the role of fibroblasts in psoriasis remains poorly characterized, in the present study we have evaluated the possible influence of PGE 2 derived from dermal fibroblasts as modulator of the immune response in psoriatic skin. Our results indicate that under inflammatory conditions, psoriatic fibroblasts showed defective induction of COX-2, which resulted in diminished production of PGE 2 , in contrast to healthy fibroblasts. This phenotype correlated with deficient c-Jun N-terminal kinase (JNK) activation, in accordance with the hypothesis that alterations in members of the JNK pathway are associated with psoriasis. Furthermore, conditioned medium from psoriatic fibroblasts promoted the polarization of monocytic cells toward a pro-inflammatory profile, effect that was mimicked in healthy fibroblasts after pre-incubation with indomethacin. These results are consistent with a prominent role of dermal fibroblasts in the regulation of inflammatory response through the participation of COX-derived metabolites. This resolutive behavior seems to be defective in psoriatic fibroblasts, offering a possible explanation for the chronification of the disease and for the exacerbation triggered by nonsteroidal anti-inflammatory drugs (NSAIDS) such as indomethacin.

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Section: Discussionsupporting

confidence: 89%

Defective Induction of COX-2 Expression by Psoriatic Fibroblasts Promotes Pro-inflammatory Activation of Macrophages

et al. 2019

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“…This is supported in transcriptomics by the involvement of proangiogenetic genes which are already expressed in non-lesional psoriatic skin [174]. Dermal mesenchymal stem cells are discussed as potential contributors in regulating angiogenesis in the skin [175][176][177][178]. In addition, anti-TNFα treatment led to the upregulation of VEGF negative regulating pathways [179].…”

Section: Dcsmentioning

confidence: 93%

Review—Current Concepts in Inflammatory Skin Diseases Evolved by Transcriptome Analysis: In-Depth Analysis of Atopic Dermatitis and Psoriasis

Schwingen

Kaplan

Kurschus

2020

IJMS

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During the last decades, high-throughput assessment of gene expression in patient tissues using microarray technology or RNA-Seq took center stage in clinical research. Insights into the diversity and frequency of transcripts in healthy and diseased conditions provide valuable information on the cellular status in the respective tissues. Growing with the technique, the bioinformatic analysis toolkit reveals biologically relevant pathways which assist in understanding basic pathophysiological mechanisms. Conventional classification systems of inflammatory skin diseases rely on descriptive assessments by pathologists. In contrast to this, molecular profiling may uncover previously unknown disease classifying features. Thereby, treatments and prognostics of patients may be improved. Furthermore, disease models in basic research in comparison to the human disease can be directly validated. The aim of this article is not only to provide the reader with information on the opportunities of these techniques, but to outline potential pitfalls and technical limitations as well. Major published findings are briefly discussed to provide a broad overview on the current findings in transcriptomics in inflammatory skin diseases.

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“…According to the authors, low expression of PECAM1 and MCAM may be interpreted as a method of inflammation modulation by dental matrix components (DMCs). However, their ability to differentiate in vitro into adipocytes and osteoblasts is preserved [ 37 ].…”

Section: Pathogenesis Of Psoriasis and Dermal Stem Cellsmentioning

confidence: 99%

Stem Cells as Potential Candidates for Psoriasis Cell-Replacement Therapy

Owczarczyk‐Saczonek

Krajewska–Włodarczyk

Kruszewska

et al. 2017

IJMS

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Recent years have seen considerable progress in explaining the mechanisms of the pathogenesis of psoriasis, with a significant role played in it by the hyper-reactivity of Th1 and Th17 cells, Treg function disorder, as well as complex relationships between immune cells, keratinocytes, and vascular endothelium. The effect of stem cells in the epidermis and stem cells on T cells has been identified and the dysfunction of various types of stem cells may be a prime cause of dysregulation of the inflammatory response in psoriasis. However, exploring these mechanisms in detail could provide a chance to develop new therapeutic strategies. In this paper, the authors reviewed data on the role played by stem cells in the pathogenesis of psoriasis and initial attempts at using them in treatment.

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Expression of pro‐angiogenic genes in mesenchymal stem cells derived from dermis of patients with psoriasis

Cited by 17 publications

References 22 publications

Defective Induction of COX-2 Expression by Psoriatic Fibroblasts Promotes Pro-inflammatory Activation of Macrophages

Defective Induction of COX-2 Expression by Psoriatic Fibroblasts Promotes Pro-inflammatory Activation of Macrophages

Review—Current Concepts in Inflammatory Skin Diseases Evolved by Transcriptome Analysis: In-Depth Analysis of Atopic Dermatitis and Psoriasis

Stem Cells as Potential Candidates for Psoriasis Cell-Replacement Therapy

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