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Abstract: Cholesterol is a major component of skin lipids and acts as a regulator of vesicular trafficking and signal transduction. However, the function of cholesterol on matrix metalloproteinases (MMPs) expression of human skin is not fully understood. Here, we investigated the effects of cholesterol on MMP-9 expression in normal human keratinocytes (NHK) and HaCaT cells. Basal level of MMP-9 expression was decreased by cholesterol in NHK. On the other hand, MMP-9 expression was increased by the cholesterol depletion agent, methyl-β-cyclodextrin (MβCD), while it was inhibited by cholesterol repletion in HaCaT cells. MβCD induced ERK and JNK phosphorylation were prevented by cholesterol repletion. The inhibition of ERK and JNK decreased MβCD-induced MMP-9 expression. Therefore, our results suggest that cholesterol regulates MMP-9 expression through ERK and JNK-dependent pathways. [Copyright &y& Elsevier]

In this work, a flexible perovskite photodetector is demonstrated with a transferable TiO2 nanorod (NR) as an electron transport layer (ETL). The TiO2 NRs are grown by the hydrothermal method on Ni metal buffer layer/Si (100) substrates. During the growth process of TiO2 NRs in solution, the Ni sacrificial buffer layer is removed by hydrochloric acid in the initial stage. The resulting suspended seed layer can then sustain the growth of TiO2 NRs in both the top and bottom directions. The successfully grown TiO2 NRs are now transferred onto an ITO‐coated PET substrate as an ETL for the flexible Cs2AgBiBr6 perovskite photodetectors. The fabricated photodetector operates under a wavelength of 405 nm, and at an external bias voltage of −0.3 V, it exhibits an outstanding performance with an on/off ratio of 1.23 × 104, photoresponsivity (R) of 0.666 A W−1, and a detectivity (D*) of 9.29 × 1012 Jones. In terms of flexibility, the optoelectronic performance of each device is well kept within 5% after 300 bending test cycles with a radius of 1 cm. The suggested transferable TiO2 NRs can improve the efficiency of flexible optoelectronic devices that require synergistic electron transfer effects by using heterostructures with TiO2 nanostructures. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Activation of toll-like receptors 2, 3 or 5 induces matrix metalloproteinase-1 and -9 expression with the involvement of MAPKs and NF-κB in human epidermal keratinocytes. Experimental Dermatology 2010; 19: e44-e49. Abstract: Toll-like receptors (TLRs) on epidermal keratinocytes are the first line of defense against microbe invasion, and matrix metalloproteases (MMPs) regulate inflammation, cell migration and wound healing. In this study, we demonstrate that the mRNA and protein expressions of MMP-1 and MMP-9 in human epidermal keratinocytes are induced by ligands for TLR2, TLR3 and TLR5 [Pam3CSK4, Poly(I:C) and flagellin, respectively] in a dose-dependent manner. We also found that the ligands for TLR2, TLR3 and TLR5 activate the MAP kinases, JNK and p38 MAPK, but not ERK1/2. Furthermore, treatment with the ligands for TLR2, TLR3 and TLR5 also induced the degradation of IκB-α and activated the nuclear translocation of NF-κB. MMP-1 induction by the ligands for TLR2, TLR3 and TLR5 was inhibited by pretreatment with BAY11-7082 (NF-κB inhibitor) or SP600125 (JNK inhibitor), whereas MMP-9 expression was inhibited by pretreatment with BAY11-7082, SP600125 or SB203580. These findings demonstrate that the activation of TLR2, TLR3 or TLR5 induces the expression of MMP-1 and MMP-9 in human epidermal keratinocytes. In addition, NF-κB or JNK mediated the MMP-1 expression induced by TLR2, TLR3 and TLR5, whereas NF-κB, JNK or p38 MAPK mediated the MMP-9 expression induced by TLR2, TLR3 and TLR5. [ABSTRACT FROM AUTHOR]

Melatonin suppresses tumor development. However, the exact relationship between melatonin and cancer stem cells (CSCs) is poorly understood. This study found that melatonin inhibits colon CSCs by regulating the PrPC‐Oct4 axis. In specimens from patients with colorectal cancer, the expressions of cellular prion protein (PrPC) and Oct4 were significantly correlated with metastasis and tumor stages. Co‐treatment with 5‐fluorouracil (5‐FU) and melatonin inhibited the stem cell markers Oct4, Nanog, Sox2, and ALDH1A1 by downregulating PrPC. In this way, tumor growth, proliferation, and tumor‐mediated angiogenesis were suppressed. In colorectal CSCs, PRNP overexpression protects Oct4 against inhibition by 5‐FU and melatonin. In contrast, Nanog, Sox2, and ALDH1A1 have no such protection. These results indicate that PrPC directly regulates Oct4, whereas it indirectly regulates Nanog, Sox2, and ALDH1A1. Taken together, our findings suggest that co‐treatment with anticancer drug and melatonin is a potential therapy for colorectal cancer. Furthermore, PrPC maintains cancer stemness during tumor progression. Therefore, targeting the PrPC‐Oct4 axis may prove instrumental in colorectal cancer therapy. [ABSTRACT FROM AUTHOR]