HSP105 inhibition downregulates store-operated calcium entry and promotes acute UVB-induced tight junction disruption.

ABSTRACT:

Background

Tight junction abnormalities are a common feature of inflammatory skin diseases such as psoriasis and atopic dermatitis and contribute to systemic immune responses. Evidence provided to date suggests that Heat shock protein 105 kDa (HSP105) exhibits significant protective effects in response to destructive external stimuli. However, its role in UV-induced skin tight junction remains to be fully understood.

Objective

To investigate the role and underlying mechanisms of HSP105 in acute UVB-induced tight junction damage.

Methods

By utilizing bioinformatics analysis, together with an in vitro UVB-induced tight junction injury model in HaCaT cells, we investigated the expression and localization of HSP105 and the tight junction proteins CLDN1, CLDN4, and OCLN. T

SUBMITTER: Zhou K 

PROVIDER: S-EPMC11620698 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature