Pancreatic cancer is characterized by a high frequency of cachexia, pain and neural invasion (N-inv). Neural damage is occurred by N-inv and modulates pain and muscle atrophy via the activation of astrocyte in the connected spine. The activated astrocyte by N-inv, thus, may affect cachexia in pancreatic cancer. Clinical studies in patients and autopsy cases with pancreatic cancer have revealed that N-inv is related to cachexia and astrocytic activation. We established a novel murine model of cancer cachexia using N-inv of human pancreatic cancer cells. Mice with N-inv showed a loss of body weight, skeletal muscle, and fat mass without appetite loss, which are compatible with an animal model of cancer cachexia. Activation of astrocytes in the spinal cord connected with N-inv was observed in our model. Experimental cachexia was suppressed by disrupting neural routes or inhibiting the activation of astrocytes. These data provide the first evidence that N-inv induces cachexia via astrocytic activation of neural route in pancreatic cancer.
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Sex, Age, Specimen part
View SamplesSegregated nucleus atypical monocyte (SatM) is novel monocyte cell type. Complehensive Gene expression pattern was examined not only in SatM but also its related cell type.
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Sex, Age, Specimen part
View SamplesThe B1 SOX transcription factors SOX1/2/3/19 have been implicated in various processes of early embryogenesis. However, their regulatory functions in stages from the blastula to early neurula remain largely unknown, primarily because loss-of-function studies have not been informative to date. In our present study, we systematically knocked down the B1 sox genes in zebrafish. Only the quadruple knockdown of the four B1 sox genes sox2/3/19a/19b, which are active in the early embryo, resulted in very severe developmental abnormalities, confirming that the B1 sox genes are functionally redundant. We characterized the sox2/3/19a/19b quadruple knockdown embryos in detail by examining the changes in gene expression through microarray analysis as well as in situ hybridization.
B1 SOX coordinate cell specification with patterning and morphogenesis in the early zebrafish embryo.
Specimen part
View SamplesWe identified RNA targets of Matrin3 using SH-SY5Y by PAR-CLIP analysis. Because Matrin3 mainly bound to intron of pre-mRNA, in order to find the effect of Matrin3 on splicing pattern and expression, we knocked down Matrin3 using SH-SY5Y cells by electroporation and extracted total RNAs from those cells. The total RNAs were subjected to whole transcripts microarray GeneChip Affymetrix Human Transcriptome array 2.0.
Matrin3 binds directly to intronic pyrimidine-rich sequences and controls alternative splicing.
Cell line, Treatment
View SamplesWe previously isolated a subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated insulin secretion in response to glucose, glybenclamide, and KCl, even after prolonged culture. To investigate the molecular mechanisms responsible for preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP (parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number), C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and C4-HP cells as responder cells. In a DNA microarray analysis, we identified a group of genes with high expression in responder cells (responder genes), but extremely low expression in the Pr-HP cells.
Microarray analysis of novel candidate genes responsible for glucose-stimulated insulin secretion in mouse pancreatic β cell line MIN6.
Cell line
View SamplesAnalysis of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells. Results indicate regulatory T cell (Treg) ontogenesis requires two independent processes, expression of the transcription factor Foxp3 and establishment of Treg epigenetic programs induced by T cell receptor (TCR) stimulation.
T cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development.
Specimen part
View SamplesThe purpose of this experiment was to compare the gene expression pattern between wild-type and Trib1-deficient macrophages in response to LPS.
Enhanced TLR-mediated NF-IL6 dependent gene expression by Trib1 deficiency.
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View SamplesNlrc5 is encoding a Nod-like receptor protein NLRC5/NOD27. To check the involvement of Nlrc5 in antiviral response, we examined gene expression profile in wild-type and Nlrc5 knockout GM-CSF bone marrow macrophage with using microarrays.
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Specimen part, Time
View SamplesWe induced chondrogenic cells from adult mouse dermal fibroblast culture by transduction of c-Myc, Klf4, and SOX9 using retroviral vectors. We selected chondrogenic cells for promoter / enhancer activities of the Col11a2 gene, and established cell lines.
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Sex, Age, Specimen part, Cell line
View SamplesTrib1 is critical for some myeloid cell differentiation.
Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages.
Specimen part
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