Lipidomics demonstrates the association of sex hormones with sebum.

BACKGROUND: The regulation of sebocytes by hormones has been unanimously certified by scholars. But how sebocytes are affected has not been fully demonstrated by the regulation of multiple hormones. AIMS: The regulation effect of sex hormone on sebocytes was further discussed. PATIENTS/METHODS: Based on our previous studies, the changes of skin surface liposomes in different sex hormone levels were analyzed by comprehensive statistics. RESULTS: We found that androgen can induce sebocytes to synthesis and secrete more fatty acids (FAs) and triglycerides (TGs) through comprehensive analysis of sebum content and composition, which is inhibited by estrogen. CONCLUSIONS: We further confirmed the regulatory effect of hormones on sebocytes from a molecular point of view using lipidomics and found that sex hormones may dominate.

Study on the skin status of mid-pregnancy women based on lipidomics.

BACKGROUND: Pregnancy is a complex physiological state and its unique changes in skin state have been discussed. Skin surface lipid (SSL) is an important molecular basis for this skin condition, and it affects skin condition in a number of ways, but there are no complete research data on it. OBJECTIVES: To analyze the lipidome profiles of SSL in pregnancies and controls in order to understand SSL changes in pregnancy. It will provide theoretical data of SSL on skin care and prevention of skin diseases during pregnancy. METHODS: Ultra-high performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) and multivariate statistics were used to investigate the changes of SSL in pregnancy. RESULTS: Results showed that there were significant differences (P < .05) in the lipidome between pregnancies and controls. Multivariate data analysis indicated that there were 20 important individual lipid species identified, and triglycerides (TGs) were the majority of differentiating lipid species. CONCLUSIONS: The increase of estrogen level in pregnancies antagonizes and inhibits the regulation of androgen on sebaceous gland, resulting in the decrease of sebum secretion and the weakening of skin barrier function. Besides, the decrease of saturated fatty acid content may be the main factor of the decrease of skin barrier function during pregnancy. Additionally, skin cells perform their self-regulation function to reduce or counteract abnormal state of the skin during pregnancy through the synthesis and secretion of more glycerophospholipids and ceramides.

Sub-lethal ultraviolet B irradiation and Poly I:C treatment synergistically induced apoptosis of HaCaT cells through NF-κB pathway.

Ultraviolet B (UVB) irradiation exerts multiple effects on skin cells, inducing apoptosis, senescence and carcinogenesis. Toll-like receptor 3, a member of pattern recognition receptors, is reported to initiate inflammation by recognizing double-strand RNA (dsRNA) released from UVB-irradiated cells. It has not been studied, however, whether apoptosis induction in UVB irradiation is attributed to TLR3 activation. Here, we report on the pro-apoptotic role of TLR3 in UVB-irradiated epidermal cells. Poly I:C, an analogue of dsRNA that activates TLR3, was used in combination with sub-lethal UVB (4.8 mJ/cm2) irradiation for investigating the effects of TLR3 activation on human immortalized keratinocyte HaCaT cells. Although sub-lethal dose of either Poly I:C or UVB alone did not induce cell death, UVB-Poly I:C co-treatment synergistically induced cell death by activation of caspase-3 and cleavages of ICAD and PARP, with apoptotic features when stained with Annexin V/PI or Hoechst 33342. Treatment with pan-caspase inhibitor, Z-VAD, attenuated UVB-Poly I:C-induced cell death. Silencing TLR3 by siRNA rescued HaCaT cells from UVB-Poly I:C-induced apoptosis. NF-κB, a major downstream component of TLR3 pathway, that usually negatively regulates the classical TLR3 apoptotic pathway, was analyzed by western blotting and immunofluorescence confocal microscopy. The results indicate to our surprise that NF-κB is translocated to nucleus in the cells co-treated with UVB-Poly I:C. The nuclear translocation of NF-κB is attenuated by TLR3 silencing. Treatment with BAY, an inhibitor of NF-κB pathway, blocked UVB-Poly I:C-induced apoptosis. Therefore, we conclude that NF-κB pathway plays a cytotoxic role in UVB-Poly I:C-treated HaCaT cells, mediating TLR3-related apoptosis.