Dataset Information

LPC 18:1 protein interaction (OPC)

ABSTRACT: Oligodendrocyte progenitor cells (OPC) were cultured in the presence of LPC 18:1-Cy5. Proteins interacting with LPC 18:1-Cy5 were UV crossed linked and cell lysates were separated via isoelectric focusing gel electrophoresis. Band was cut out from gel and processed for mass spectrometry. OPC lysates were also incubated with LPC 18:1-micelles and allowed to interact with OPC proteins. Samples were separated using sucrose gradient (Liposome floatation assay), top fraction was collected and processed for mass spectrometry.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Oligodendrocyte Precursor Cell, Cell Culture

SUBMITTER: Sanjoy Bhattacharya

LAB HEAD: Sanjoy Bhattacharya

PROVIDER: PXD025175 | Pride | 2022-02-17

REPOSITORIES: Pride

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Publications

Lyso-Lipid-Induced Oligodendrocyte Maturation Underlies Restoration of Optic Nerve Function.

Valdivia Anddre Osmar AO Bhattacharya Sanjoy K SK

eNeuro 20220126 1

Protein hyperdeimination and deficiency of lyso-phospholipids (LPC 18:1) has been associated with the pathology of demyelinating disease in both humans and mice. We uncovered interesting biology of LPC 18:1, in which LPC 18:1 induced optic nerve function restoration through oligodendrocyte maturation and remyelination in mouse model systems. Our <i>in vitro</i> studies show LPC 18:1 protection against neuron-ectopic hyperdeimination and stimulation of oligodendrocyte maturation, while <i>in vivo ...[more]

PMID: 35027445

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Project description:We previously showed that severe liver diseases are characterized by expansion of liver progenitor cells (LPC), which correlates with disease severity. However, the origin and role of LPC in liver physiology and in the hepatic response to injury remains a contentious topic. We have now used genetic lineage tracing of Hnf1Î²-expressing biliary duct cells to assess their contribution to LPC expansion and hepatocyte generation during normal liver homeostasis, and following different types of liver injury. We found that ductular reaction cells in human cirrhotic livers express HNF1Î². However, HNF1Î² expression was not present in newly generated EpCAM-positive hepatocytes. Using a tamoxifen-inducible Hnf1Î²CreER/R26RYFP/LacZ mouse, we show that there is no contribution of the biliary epithelium to hepatocyte turnover during liver homeostasis in healthy mice. Moreover, after loss of liver mass, Hnf1Î²+ LPC did not contribute to hepatocyte regeneration. We also assessed the contribution of Hnf1Î²+ cells following acute and repeated liver injury. All animal models showed expansion of LPC, as assessed by immunostaining and gene expression profile of sorted YFP-positive cells. A contribution of Hnf1Î²+ LPC to hepatocyte generation was not detected in animal models of liver injury with preserved hepatocyte regenerative potential such as acute acetaminophen, carbon tetrachloride injury, or chronic diethoxycarbonyl-1,4-dihydro-collidin (DDC)-diet. However, in mice fed with choline-deficient ethionine-supplemented (CDE)-diet, which causes profound hepatocyte damage and arrest, a small number of hepatocytes were derived from Hnf1Î²+ cells. Conclusion: Hnf1Î²+ cells do not participate in hepatocyte turnover in the healthy liver or during liver regeneration after partial hepatectomy. After liver injury, LPC arise from the biliary duct epithelium, which gives rise to a limited number of hepatocytes only when hepatocyte regeneration is compromised. Transcriptomic profile using MoGeneST-2.0 chip from 3 samples of YFP+ CDE, 3 samples of YFP+ DDC, 2 samples of YFP+ UTR and 3 samples YFP-

			Action	DRS
	18_0_LFA_T.mzML	Mzml
	18_0_LFA_T.mzid.gz	Mzid
	18_0_LFA_T.raw	Raw
	Band.mzML	Mzml
	Band.mzid.gz	Mzid