Particulate matter exposure induces maternal scalp hair loss after birth in C57/B6 mouse via alteration of inflammatory and apoptotic pathways.

PM 2.5 exposure is associated with a variety of health effects, including effects on the reproductive and skin. However, the relationship between PM2.5 exposure and postpartum hair loss has not been investigated. In this study, we evaluated the effect of PM2.5 exposure on hair loss after birth in mouse model and analyzed possible associated molecular changes. Female mice were exposed to PM2.5 using nasal inhalation method. After 4 weeks, mating tests were conducted and postpartum scalp tissues from PM2.5-exposed mice and those without exposure were harvested and analyzed. Then, human immortalized keratinocyte cell line (HaCaT cells) and fibroblasts were cultured and treated with PM2.5 for 24 hours. Changes in the inflammatory, apoptotic, fibrotic, and proliferative pathways were evaluated. Postpartum scalp hair loss was evident in PM2.5 exposed mice group with significant morphological changes in scalp tissues. The expression levels of IL-6, IL-1β, TNF-α and p-NF-κB, Caspase-3, the BAX/Bcl-2 ratio, COL1A1, MMP2 and MMP9 were significantly higher in the PM2.5-exposed group than in the control group. The expressions of were elevated in PM2.5 exposed group than the controls, where the expressions of PR-B, PR-A, CD34 and K15 were significantly lower in the exposed group. Histologic analysis showed that PM2.5 exposed postpartum scalp showed thickened stratum corneum, migration of hair follicles deeper into the dermis with a decrease in the number of hair follicles. Increased collagen density in the dermis was also observed in scalp tissues from the PM2.5-exposed group. In vitro experiments showed that PM2.5 exposure significantly increased expressions of p-NF-κB/NF-κB, p-c-jun/c-jun, p-p53/p53, p27, Caspase-3 and BAX/Bcl-2, where p-ERK/ERK and VEGF expressions were significantly reduced in HaCaT cells and fibroblasts. These findings suggest that PM2.5 exposure induces postpartum hair loss via alterations of inflammatory and apoptotic pathways. PM2.5 exposure induces significant downregulation of progesterone receptors and reduces the hair follicle stem cells (HFSCs) population, which may contribute to the exacerbation of postpartum hair loss.