Neuronal ERK signaling in response to graphene oxide in nematode <i>Caenorhabditis elegans</i>

<p>ERK signaling is one of the important mitogen-activated protein kinases (MAPKs). However, the role of ERK signaling in the regulation of response to engineered nanomaterial exposure is still largely unclear. In this study, using <i>in vivo</i> assay system of <i>Caenorhabditis elegans</i>, we investigated the function of ERK signaling in response to graphene oxide (GO) exposure and the underlying molecular mechanism. GO exposure increased the expression of MEK-2/MEK and MPK-1/ERK in the ERK signaling pathway. Mutation of <i>mek-2</i> or <i>mpk-1</i> resulted in a susceptibility to GO toxicity. Both the MEK-2 and the MPK-1 acted in neurons to regulate the response to GO exposure, and the neuronal expression of MEK-2 or MPK-1 caused a resistance to GO toxicity. In the neurons, SKN-1b/Nrf acted downstream of the MPK-1, and AEX-3, a guanine exchange factor for GTPase, further acted downstream of the SKN-1b to regulate the response to GO exposure. Therefore, a signaling cascade of MEK-2-MPK-1-SKN-1b/-AEX-3 was identified in the neurons required for the regulation of response to GO exposure. Moreover, genetic interaction assay demonstrated that the neuronal ERK signaling-mediated signaling pathway and the intestinal p38 MAPK-mediated signaling pathway functioned synergistically in the regulation of response to GO exposure. Our results highlight the crucial function of the neuronal ERK signaling in the regulation of response to nanomaterial exposure in organisms.</p

Association and stratification analysis between rs6688832 and risk of PCOS.

<p>OR, odds ratio; CI, confidence interval. Bold values indicate significant findings (<i>P</i> < 0.05).</p><p>^<b>a</b>Adjusted for age and BMI, where it was appropriate.</p><p>Association and stratification analysis between rs6688832 and risk of PCOS.</p

Classification result by OPLS-DA model.

<p>A. training set; B. validation set.</p

PCA score plot for training set.

<p>PCA score plot for training set.</p

Additional file 2: of Carbon black suppresses the osteogenesis of mesenchymal stem cells: the role of mitochondria

Figure S1. Characterization of Printex 90. (a) Summarization of the size and zeta potential of CB dispersed in PBS, H2O and the complete culture medium. (b) Particle-size distribution of CB prepared in PBS, H2O and the culture medium. (JPEG 2194 kb

supplementary_fig_S1_and_table_S1 – Supplemental material for Cortisol, cortisone, and 4-methoxyphenylacetic acid as potential plasma biomarkers for early detection of non-small cell lung cancer

<p>Supplemental material, supplementary_fig_S1_and_table_S1 for Cortisol, cortisone, and 4-methoxyphenylacetic acid as potential plasma biomarkers for early detection of non-small cell lung cancer by Chengcheng Xiang, Shidai Jin, Juan Zhang, Minjian Chen, Yankai Xia, Yongqian Shu and Renhua Guo in The International Journal of Biological Markers</p

OPLS-DA score plot for training set.

<p>A. Generated with metabolomic profiling data; B. Generated with quality parameter of seminal plasma data.</p

Additional file 3: of Carbon black suppresses the osteogenesis of mesenchymal stem cells: the role of mitochondria

Figure S2. Absorbance of the supernatant of the CCK-8 reagent diluted with the cultured medium containing 0 to 30 μg / mL Printex 90 at 450 nm. After two hr. incubation at 37 °C, the solution was centrifuged by 1500 g for 2 min, and the absorbance of supernatant was measured immediately by Infinite M200 Pro (TECAN, Switzerland) at 450 nm, four repeats at each dosage have been calculated. (TIFF 12726 kb

Result from pathway analysis.

<p>Result from pathway analysis.</p

Additional file 4: of Carbon black suppresses the osteogenesis of mesenchymal stem cells: the role of mitochondria

Figure S3. The protein content of oxygen consumption rate (OCR) (a), and OCR values of different dose groups normalized by the protein content at Day 1 (b), and the protein content of oxygen consumption rate (OCR) (c), and OCR values of different dose groups normalized by the protein content at 3 d (d). Decreased proton leak was showed by XF-96 Flux Analyzer after 1 d osteo-induction (a), whereas other parameters including basal oxygen consumption rate (OCR), ATP-linked respiration, proton leak, the maximal OCR as well as non-mitochondrial respiration were inhibited after 3 d osteo-induction (c). No significant shifts for the values normalized by the protein content were found when compared to the values calculated without protein normalization (also see Fig. 6b-c). (JPEG 5670 kb