Sensitive skin-related CLDN5 decreases inflammatory reaction in keratinocytes
10.3760/cma.j.issn.1671-0290.2024.05.008
- VernacularTitle:敏感性皮肤紧密连接蛋白5减少对角质形成细胞炎症的影响
- Author:
Yumei JIN
1
;
Li HE
;
Wenjuan WU
Author Information
1. 昆明医科大学第一附属医院云南省皮肤病医院，昆明 650000
- Keywords:
Skin;
Sensitive skin;
CLDN5;
Keratinocytes;
Inflammation
- From:
Chinese Journal of Medical Aesthetics and Cosmetology
2024;30(5):456-460
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To clarify whether CLDN5 is involved in the pathogenesis of sensitive skin (SS) through inflammation.Methods:From January 2018 to March 2020, in the Dermatology Laboratory of the First Affiliated Hospital of Kunming Medical University, facial tissues were collected from 5 patients diagnosed with sensitive skin and 5 cases of normal facial skin. The organizational experiment was divided into two groups: SS group and normal skin (NS) group. The cell experiment was divided into two groups: sh-CLDN5 group in which CLDN5 was knocked down and sh-NC group with normal expression of CLDN5. After paraffin embedding and sectioning, immunohistochemical staining was performed to determine the expression of claudin-5 in sensitive skin and normal skin. In cell experiments, lentivirus shRNA was transfected into HaCaT cells. Three cases in sh-CLDN5 group and three cases in sh-NC group were collected for transcriptome sequencing, and differentially expressed pro-inflammatory factor mRNA was screened from the sequencing results. Western blot or ELISA was used to verify the protein level expression of differentially expressed pro-inflammatory cytokines mRNA in HaCaT cells, and Western blot was used to detect the expression of key proteins in MAPK pathway and NF-κB in the sh-CLDN5 group and sh-NC group.Results:Immunohistochemical staining showed that claudin-5 was localized in the interstitial cells of the normal skin granular layer. Patients with sensitive skin had thinner epidermis than normal skin and significantly reduced claudin-5 expression. In HaCaT cells, the expression of pro-inflammatory cytokine IL-23A was increased, and IL-8 was elevated in the sh-CLDN5 group [(272.91±30.25) pg/ml, n=3] compared with sh-NC group [(55.58±7.07) pg/ml, n=3] ( P<0.01). There was no statistically significant difference in secretion volume between sh-NC group [(8.04±1.34) pg/ml, n=3] and sh-CLDN5 group [(12.15±3.07) pg/ml, n=3]. The expression of P-JNK, p-ERK, and P-p38 in the MAPK pathway was significantly increased ( P<0.01). Conclusions:CLDN5 is an important gene involved in the pathogenesis of SS. CLDN5 upregulates IL-23A and IL-8 in HaCaT and activates the MAPK pathway, which is involved in the process of early SS inflammation.
