What is it about?

Gasdermin (GSDM) B is is a protein that may be involved in the cell pyroptosis process. It is reported to be associated with inflammatory diseases. However, the correlation between GSDMB and psoriasis vulgaris is not clear. In our study, the level of GSDMB protein in the skin lesions of patients with psoriasis vulgaris was detected. We establish a cell model with low GSDMB gene expression through interfering sequence siRNA, and measured the mRNA and protein expression levels of the GSDMB before and after gene silencing. The cell viability and cell apoptosis was also detected. We found the lower level of GSDMB protein in the skin lesions of patients with psoriasis vulgaris than that in normal skin tissues, the lower mRNA and protein expression levels in GSDMB silencing group, and the decreased proliferation and increased apoptosis of HaCaT cells in the cell model. As is reported that overdevelopment of keratinocytes toward differentiation inhibits their own proliferation, we believe that down-regulation of GSDMB expression can inhibit cell proliferation and promote cell apoptosis. We speculate that GSDMB may play a role in the pathogenesis of psoriasis by affecting the differentiation of keratinocytes.

Featured Image

Why is it important?

Our findings show that down-regulation of GSDMB expression can inhibit cell proliferation and promote cell apoptosis. Thus we speculate that GSDMB may play a role in the pathogenesis of psoriasis by affecting the differentiation of keratinocytes.

Perspectives

I hope this article makes people understand psoriasis in another perspective. Though, GSDMB may not be the main pathogenic factor of psoriasis, it is still involved in the pathogenesis of psoriasis through some unknown way. Maybe GSDMB is of being indispensable in the occurrence of the psoriasis lesion just like an unremarkable individual in human society.

Longnian Li
Gannan Medical University

Read the Original

This page is a summary of: The study of GSDMB in pathogenesis of psoriasis vulgaris, PLoS ONE, January 2023, PLOS,
DOI: 10.1371/journal.pone.0279908.
You can read the full text:

Read
Open access logo

Contributors

The following have contributed to this page