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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE232586 | GEO | 2024/03/20

REPOSITORIES: GEO

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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

Project description:When treated with FGF8+10, LM makers were upregulated and the expression levels were higher than that of the Mock cells.

2024-03-20 | GSE232584 | GEO

Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

Project description:Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

Project description:Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

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PCSK9 is not secreted from mature differentiated intestinal cells.

Project description:Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes lysosomal degradation of the LDL receptor and is a key regulator of cholesterol metabolism. After the liver, the small intestine is the second organ that highly expresses PCSK9. However, the small intestine's ability to secrete PCSK9 remains a matter of debate. While liver-specific PCSK9-deficient mice present no PCSK9 in systemic blood, human intestinal Caco-2 cells can actively secrete PCSK9. This raises the possibility for active intestinal secretion via the portal blood. Here, we aimed to determine whether enterocytes can secrete PCSK9 using in vitro, ex vivo, and in vivo approaches. We first observed that PCSK9 secretion from Caco-2 cells was biphasic and dependent on Caco-2 maturation status. Transcriptional analysis suggested that this transient reduction in PCSK9 secretion might be due to loss of SREBP2-mediated transcription of PCSK9. Consistently, PCSK9 secretion was not detected ex vivo in human or mouse intestinal biopsies mounted in Ussing chambers. Finally, direct comparison of systemic versus portal blood PCSK9 concentrations in WT or liver-specific PCSK9-deficient mice confirmed the inability of the small intestine to secrete PCSK9 into the portal compartment. Altogether, our data demonstrate that mature enterocytes do not secrete PCSK9 and reinforce the central role of the liver in the regulation of the concentration of circulating PCSK9 and consequently of cellular LDL receptors.

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Direct reprogramming of terminally differentiated mature B lymphocytes to pluripotency.

Project description:Pluripotent cells can be derived from fibroblasts by ectopic expression of defined transcription factors. A fundamental unresolved question is whether terminally differentiated cells can be reprogrammed to pluripotency. We utilized transgenic and inducible expression of four transcription factors (Oct4, Sox2, Klf4, and c-Myc) to reprogram mouse B lymphocytes. These factors were sufficient to convert nonterminally differentiated B cells to a pluripotent state. However, reprogramming of mature B cells required additional interruption with the transcriptional state maintaining B cell identity by either ectopic expression of the myeloid transcription factor CCAAT/enhancer-binding-protein-alpha (C/EBPalpha) or specific knockdown of the B cell transcription factor Pax5. Multiple iPS lines were clonally derived from both nonfully and fully differentiated B lymphocytes, which gave rise to adult chimeras with germline contribution, and to late-term embryos when injected into tetraploid blastocysts. Our study provides definite proof for the direct nuclear reprogramming of terminally differentiated adult cells to pluripotency.

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Gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos [scRNA-seq]

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Mature miRNAs form secondary structure, which suggests their function beyond RISC.

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Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice.

Project description:During neurogenesis, the progression from a progenitor cell to a differentiated neuron is believed to be unidirectional and irreversible. The Rb family of proteins (Rb, p107, and p130) regulates cell-cycle exit and differentiation during retinogenesis. Rb and p130 are redundantly expressed in the neurons of the inner nuclear layer (INL) of the retina. We have found that in the adult Rb;p130-deficient retinae p107 compensation prevents ectopic proliferation of INL neurons. However, p107 is haploinsufficient in this process. Differentiated Rb(-/-);p107(+/-);p130(-/-) horizontal interneurons re-entered the cell cycle, clonally expanded, and formed metastatic retinoblastoma. Horizontal cells were not affected in Rb(+/-);p107(-/-);p130(-/-) or Rb(-/-);p107(-/-);p130(+/-), retinae suggesting that one copy of Rb or p130 was sufficient to prevent horizontal proliferation. We hereby report that differentiated neurons can proliferate and form cancer while maintaining their differentiated state including neurites and synaptic connections.

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The Ubiquitination of PINK1 Is Restricted to Its Mature 52-kDa Form.

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