Autophagy attenuates particulate matter 2.5-induced damage in HaCaT cells

Abstract

Background: Keratinocyte is a key component of the skin barrier and maintains skin homeostasis. As an environmental pathogenic factor, PM2.5 can cause epidermal cell damage, but the mechanism remains to be elucidated. The present study aimed to evaluate the effect caused by PM2.5 in HaCaT cells and investigate the underlying mechanisms.Methods: HaCaT cells were treated with PM2.5 for 12 h or 24 h, either alone or combined with UVB irradiation. A Cell Counting Kit (CCK-8) assay was carried out to detect the effect of PM2.5 on HaCaT cell viability. Flow cytometry, Western Blot, and AO staining were employed to detect the changes of apoptosis and autophagy. The changes of cytotoxicity and apoptosis in HaCaT cells were analyzed by CCK-8 and flow cytometry after pretreatment with autophagy inhibitor 3-MA. Results:The results showed that PM2.5 induced cytotoxicity by increasing cell apoptosis and activating autophagy. Apoptosis was determined to be increased significantly after autophagy inhibition. Moreover, solar radiation intensified PM2.5-induced damage in HaCaT cells, which further enhanced the autophagy.However, there was no significant difference in apoptosis after inhibition of autophagy in combined treatment.Conclusions: Our data reveals that PM2.5 induces damage in HaCaT cells, and autophagy plays a protective role to promote cell survival.

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy

“…Different from the protective effect of PM2.5-induced autophagy in this study, the study of Dai et al showed that autophagy could alleviate PM2.5-induced apoptosis [ 40 ], which seems to indicate that PM2.5-induced autophagy might have a different physiological function in HaCaT cells. To further study how autophagy induced by PM2.5 leads to apoptosis, we have further studied a special form of autophagy, mitophagy.…”

Can l‐ascorbic acid and trans‐resveratrol protect HaCaT cells from fine particulate matter toxicity?

“…The inhibitory effect of PM for the proliferation of HaCaT cells and wound healing capabilities, even at low concentrations, was previously demonstrated in in vitro skin models 46,59 . Furthermore, an in vivo study demonstrated that the skin of wounded mice exposed to total PM from cigarette smoke showed impairment of re‐epithelialization, dermal matrix, and maturation of collagen bundles compared to not treated 60 .…”

“…The inhibitory effect of PM for the proliferation of HaCaT cells and wound healing capabilities, even at low concentrations, was previously demonstrated in in vitro skin models. 46,59 Furthermore, an in vivo study demonstrated that the skin of wounded mice exposed to total PM from cigarette smoke showed impairment of re-epithelialization, dermal matrix, and maturation of collagen bundles compared to not treated. 60 In this study, we demonstrated that the presence of PM 2.5 interfered with the ability of HaCaT cells to close the wound, diminishing the velocity of wound closure by 12%-42%, and 60%-68% for nonirradiated and irradiated cells, respectively, with the highest inhibition observed for Winter and Spring particles.…”

UPLC-ESI-MS/MS-Based Analysis of Various Edible Rosa Fruits Concerning Secondary Metabolites and Evaluation of Their Antioxidant Activities

“…The CCK-8 assay was performed to determine the effects of the five fruit extracts on HaCaT keratinocyte viability at three different concentrations [ 52 ]. The results in Figure 11 A show that, at concentrations < 0.25 mg/mL, the viabilities of RRT-F and RSL-F cells were not significantly different from that of the control.…”