Scientists have discovered a protein that could be the key to a new gene therapy for skin problems, including psoriasis — a common chronic skin disease that affects more than 100 million people worldwide.
The protein is a fragment of a larger molecule called JARID2, which was previously thought to be present only in the developing embryo, where it coordinates tissue and organ formation.
However, researchers at the University of Birmingham School of Biosciences have found a truncated form of JARID2 in adult skin cells and have shown that it is responsible for promoting cell differentiation.
In the article estet-portal.com you can read in detail the results of a prospective study on gene therapy for psoriasis.
Gene correction of cell differentiation: formation of skin layers
Scientists have named the newly discovered protein ΔN-JARID2. The significance of this discovery was immediately recognized by the team that studies the regulation of gene expression under normal and pathological conditions.
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Dr. Kanere explains: “In some diseases, cells lose their ability to differentiate and multiply faster. The ability to redirect cells back to their normal life cycle could alleviate the underlying processes of disease.
For example, psoriasis is caused by the rapid differentiation of skin cells.
The excess cells in psoriasis are then pushed too quickly to the surface of the skin, resulting in accumulation, not fully maturing on the surface of the skin, leading to the appearance of red spots covered with silvery scales.
And
A study by Dr. Kanhere, published in December 2018 in the EMBO Journal, shows that ΔN-JARID2 is present in the layers of the skin, where it is responsible for ensuring that tissues maintain their normal state of differentiation, which is necessary for proper formation skin layers.
Substantiation of the possibility of gene therapy for psoriasis using the protein ΔN-JARID2
In a study, JARID2 was found to exist as a ~80 kDa low molecular weight form that consists of a C-terminal domain. This low molecular weight form (called .delta.N-JARID2) is a cleavage product of full-length JARID2, which lacks PRC2 interacting domains, and is the predominant form in many human cells, including keratinocytes.
The C-terminal portion (or .delta.N-JARID2) of JARID2 was found in keratinocytes, but its N-cleaved portion was absent. This suggests that the N-terminus is not very stable in these cells. It can be hypothesized that cleavage of the unstable N-terminus from full-length JARID2 may make its C-terminus more stable, resulting in higher levels of .Delta.N-JARID2.
The authors found that during keratinocyte differentiation, .Delta;N-JARID2 levels increase.
This is important because the identification of ?N-JARID2 and its role in the activation of differentiation genes implies that JARID2 can function in two ways. In its full-length form it acts as a transcriptional co-repressor that functions through its interaction with PRC2, while in its cleaved form it acts as an activator of PRC2 target genes.
The resulting form of .Delta.N-JARID2 directly or indirectly recruits transcriptional activators such as AP-1, resulting in upregulation of differentiation genes. However, the relationship between transcription factors AP-1 and N-JARID2 will require further study.
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Practical significance of the findings
This discovery has attracted the attention of a team of researchers at the University of Birmingham who have filed a patent application covering the use of ΔN-JARID2 in therapy targeting conditions caused by hyperproliferation of skin cells such as psoriasis.
A research team is currently investigating how ΔN-JARID2 is generated and its broader impact on disease. The team hopes this discovery will eventually lead to new treatments for skin conditions.
Thank you for staying with estet-portal.com. Read other interesting articles in the "Dermatology" section. You may be interested in Psoriasis treatment: experience with vitamin D
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