Genes expression of metalloproteinases (MMP-1, MMP-2, MMP-9, and MMP-12) associated with psoriasis

Стародубцева, Н. Л.; Соболев, В. В.; Соболева, А. Г.; Николаев, А. А.; Брускин, С. А.

doi:10.1134/s102279541109016x

Cited by 43 publications

(35 citation statements)

References 46 publications

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“…Moreover, TMME also reproduced the expression pattern of metalloproteinases, which included four genes: mmp1 , mmp2 , mmp9, and mmp12 . In our previous study [9], we showed that this pattern was highly reproducible in lesional skin. Notably, the changes in the expression of mki67 , fosl1, and krt16 induced by the treatment of TMME with IL17 were less evident and did not differ significantly from the control (Fig.…”

Section: Resultsmentioning

confidence: 53%

“…For instance, metalloproteinases MMP1, MMP9, and MMP12 participate in the structural re-arrangement that occurs in psoriatic epidermis [9]. Their activity is crucial for the maintenance of the extracellular matrix and basal membrane, angiogenesis and cell migration within the epidermis, such as the migration of the immune cells, which infiltrate lesional psoriatic epidermis.…”

Section: Discussionmentioning

confidence: 99%

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Three-Dimensional Model of Mouse Epidermis for Experimental Studies of Psoriasis

et al. 2013

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Three-dimensional models of skin and epidermis imitate the structure of real tissues and provide accurate information about certain skin conditions, such as psoriasis. A three-dimensional model of mouse epidermis was generated from the epidermal keratinocytes of newborn mice and treated with cytokines. The aim of this study was to evaluate this model as an experimental model of psoriasis and to assess the changes occurring in its structure and gene expression after the exposure to proinflammatory cytokines. Treatment of the three-dimensional model with either interleukin 17 or a combination of tumor necrosis factor and interferon γ was shown to produce morphological changes, which were similar to acanthosis in psoriatic skin. The observed changes in gene expression of metalloproteinases and certain psoriasis biomarkers, such as mki67, krt16 and fosl1, were similar to the changes in patients’ skin. Notably, changes caused by interleukin 17 were less evident than those caused by the combination of interferon γ and tumor necrosis factor. On the contrary, HaCaT cells exhibited no significant changes in the expression of fosl1 and had decreased levels of mki67 after being treated with a combination of TNF and IFNG. Moreover, treatment with IL17 had no significant effect on krt16 and mki67 expression and even reduced the fosl1 levels. The findings suggest that artificially generated three-dimensional models of murine skin can be used to study psoriasis.

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Section: Resultsmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Three-Dimensional Model of Mouse Epidermis for Experimental Studies of Psoriasis

et al. 2013

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“…Nevertheless, thanks to the PubMed keyword search utility [38], we eventually learned about a dietary soy isoflavone as a norminsulinemic atheroprotector [106]. Human gene MMP12 contains a clinical SNP marker (rs2276109) of lower risk of many immune diseases, such as psoriasis [107], systemic scleroderma [108], and asthma [109], because of underexpression of the macrophage elastase encoded by this gene. Because MMP12 performs degradation of fibrinogen in the blood [110,111], its underexpression accelerates atherogenesis.…”

Section: Human Genes Associated With Autoimmunity-associated Diseasesmentioning

confidence: 99%

Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters Show Stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It

Пономаренко

Рассказов

Chadaeva

et al. 2020

IJMS

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(1) Background: The World Health Organization (WHO) regards atherosclerosis-related myocardial infarction and stroke as the main causes of death in humans. Susceptibility to atherogenesis-associated diseases is caused by single-nucleotide polymorphisms (SNPs). (2) Methods: Using our previously developed public web-service SNP_TATA_Comparator, we estimated statistical significance of the SNP-caused alterations in TATA-binding protein (TBP) binding affinity for 70 bp proximal promoter regions of the human genes clinically associated with diseases syntonic or dystonic with atherogenesis. Additionally, we did the same for several genes related to the maintenance of mitochondrial genome integrity, according to present-day active research aimed at retarding atherogenesis. (3) Results: In dbSNP, we found 1186 SNPs altering such affinity to the same extent as clinical SNP markers do (as estimated). Particularly, clinical SNP marker rs2276109 can prevent autoimmune diseases via reduced TBP affinity for the human MMP12 gene promoter and therefore macrophage elastase deficiency, which is a well-known physiological marker of accelerated atherogenesis that could be retarded nutritionally using dairy fermented by lactobacilli. (4) Conclusions: Our results uncovered SNPs near clinical SNP markers as the basis of neutral drift accelerating atherogenesis and SNPs of genes encoding proteins related to mitochondrial genome integrity and microRNA genes associated with instability of the atherosclerotic plaque as a basis of directional natural selection slowing atherogenesis. Their sum may be stabilizing the natural selection that sets the normal level of atherogenesis.

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“…3) and esti mated expression of certain genes that have a key role in skin metabolism. Particularly, we verified the expression of KRT1, KRT5, KRT10, KRT16, IVL, LOR, MKI67, MMP1, MMP2 and MMP9 that play a key role in pathogenesis of psoriasis [32]. Particularly, the first five genes are the biomarkers of the terminal differentiation program in the epidermal kerati nocytes.…”

Section: Discussionmentioning

confidence: 99%

Genetically predetermined limitation in HaCaT cells that affects their ability to serve as an experimental model of psoriasis

et al. 2014

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Proinflammatory cytokines TNF, IFNG, and IL17 play an important role in eruption of psoriasis. The activation of epidermal keratinocytes with the named cytokines alters their terminal differentiation pro gram and causes their hyperproliferation in the diseased skin. HaCaT cells, which are immortalized human keratinocytes, are often used as a cellular model of psoriasis. The aim of this study was to evaluate changes in gene expression and the proliferation rates in cultured HaCaT cells treated with TNF, IFNG, and IL17. We found that HaCaT cells decrease their proliferation rate in response to either IL17 or a combination TNF and IFNG. The analysis of microarray data discovered a group of 12 genes, which were downregulated in HaCaT after treatments with the named cytokines and upregulated in psoriatic lesional skin. Eight genes were impor tant for DNA replication and they also contributed to two larger networks that regulated cell progression through the cell cycle. We conclude that HaCaT cells have a sufficient limitation as a cellular model of psori asis due to their treatment with proinflammatory cytokines, namely TNF, IFNG, and IL17 does not increase their proliferation rate. Thus, the studies of psoriasis based on HaCaT cells as an experimental model shall take in account this important phenomenon.

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Genes expression of metalloproteinases (MMP-1, MMP-2, MMP-9, and MMP-12) associated with psoriasis

Cited by 43 publications

References 46 publications

Three-Dimensional Model of Mouse Epidermis for Experimental Studies of Psoriasis

Three-Dimensional Model of Mouse Epidermis for Experimental Studies of Psoriasis

Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters Show Stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It

Genetically predetermined limitation in HaCaT cells that affects their ability to serve as an experimental model of psoriasis

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