Dataset Information

The heparin-binding proteome in nomal pancreas and murine experimental acute pancreatitis, C4PR_LIV

ABSTRACT: Acute pancreatitis (AP) is an acute inflammation of the pancreas, mainly caused by gallstones and alcohol, and driven by changes in communication between cells. Heparin-binding proteins (HBPs) of the plasma membrane and extracellular matrix play a central role in cell communication. Therefore, we used heparin affinity proteomics to identify the extracellular HBPs in mouse normal pancreas (NP) and in a caerulein mouse model of AP. Many new HBPs (460) were discovered more than doubling their total number to 883. A number of the new HBPs are proteins with well-characterised intracellular functions, e.g. NDUFS4, NDUFS6, but which also have a documented extracellular presence with potential ‘moonlighting’ roles. The HBPs form highly interconnected protein-protein interaction networks in both NP and AP, as well as globally. Thus, HBPs may represent the most interconnected set of extracellular proteins and so those with the greatest regulatory potential. HBPs in NP are associated with biological functions such as molecular transport, cellular movement and tissue architecture that underlie pancreatic homeostasis. However, in AP HBPs are additionally associated with processes such as acute phase response signalling, complement system and mitochondrial dysfunction. By virtue of their extracellular location and heparin binding property, HBPs are easily accessible and are potential biomarkers and drug targets in AP.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Pancreas

DISEASE(S): Pancreatitis

SUBMITTER: Philip Brownridge

LAB HEAD: David G Fernig

PROVIDER: PXD001950 | Pride | 2018-12-11

REPOSITORIES: Pride

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Publications

The heparin-binding proteome in normal pancreas and murine experimental acute pancreatitis.

Nunes Quentin M QM Su Dunhao D Brownridge Philip J PJ Simpson Deborah M DM Sun Changye C Li Yong Y Bui Thao P TP Zhang Xiaoying X Huang Wei W Rigden Daniel J DJ Beynon Robert J RJ Sutton Robert R Fernig David G DG

PloS one 20190618 6

Acute pancreatitis (AP) is acute inflammation of the pancreas, mainly caused by gallstones and alcohol, driven by changes in communication between cells. Heparin-binding proteins (HBPs) play a central role in health and diseases. Therefore, we used heparin affinity proteomics to identify extracellular HBPs in pancreas and plasma of normal mice and in a caerulein mouse model of AP. Many new extracellular HBPs (360) were discovered in the pancreas, taking the total number of HBPs known to 786. Ext ...[more]

PMID: 31211768

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Project description:Background: Negative-pressure wound therapy has become widely available in modern chronic wound cares. Accelerated keratinocyte (HaCaT cell) movements and decreased E-cadherin expressions induced by the applied negative pressure gradient of 125 mmHg (NP) have been reported in previous studies. However, the molecular mechanism for E-cadherin regulations under NP remains unexplored. We highlighted the signal transduction involved in NP-induced E-cadherin regulation for keratinocytes in the study. Results: Microarray results showed that catenin 1 (CTNND1) gene, the gene encoding the p120-catenin (p120ctn) in cell-cell junctions, was significantly (p = 0.0005) upregulated in HaCaT cells under NP for 12 hours in comparison with those at ambient pressure (AP). Cell fractionations and immunoblotting data showed that NP increased p120ctn phosphorylation, and resulted in p120ctn translocation from the plasma membrane to the cytoplasm. Fluorescent stains suggested that NP diminished the co-localization of p120ctn and E-cadherin on the plasma membrane. Similar phenomenon was also observed in the cells with overexpressed p120ctn at NP. Interestingly, overexpression of dN- p120ctn, a deletion mutant of p120ctn without the N-terminal phosphorylation sites, restored the adherens junctions (AJ) at NP. Knockdown of p120ctn with lentiviral small hairpin RNA not only diminished E-cadherin expressions but also accelerated cell movement at AP. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process. HaCaT cells under negative pressure (NP) gradient of 125 mmHg for 12 hours in comparison with those at ambient pressure (AP) were tested for RNA extraction and hybridization on Affymetrix microarrays. The experiments have been biological replicated three times. The differential expression gene between NP and AP were selected and validated with qPCR method.

Dataset Information

The heparin-binding proteome in nomal pancreas and murine experimental acute pancreatitis, C4PR_LIV

Publications

The heparin-binding proteome in normal pancreas and murine experimental acute pancreatitis.

Similar Datasets

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