Reconstruction after skin sparing mastectomy

Arumugam, Eswaran; Pereira, Jerome; Gilbert, PM

doi:10.1308/147870805x42545

Cited by 1 publication

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“…These data collectively indicate that primary HBAE cells support influenza virus replication. In addition, to verify that HBAE cells could be labeled, we analyzed only heavy-labeled cells using LC–MS/MS and ProteinPilot. − Using the data from ProteinPilot, we determined that 91% of all peptides contained the “C13-label” modification (Supplementary Figure 1). In addition, H:L ratios were reported for each peptide.…”

Section: Resultsmentioning

confidence: 99%

Response of Primary Human Airway Epithelial Cells to Influenza Infection: A Quantitative Proteomic Study

et al. 2012

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Influenza A virus exerts a large health burden during both yearly epidemics and global pandemics. However, designing effective vaccine and treatment options has proven difficult since the virus evolves rapidly. Therefore, it may be beneficial to identify host proteins associated with viral infection and replication to establish potential new antiviral targets. We have previously measured host protein responses in continuously cultured A549 cells infected with mouse-adapted virus strain A/PR/8/34(H1N1; PR8). We here identify and measure host proteins differentially regulated in more relevant primary human bronchial airway epithelial (HBAE) cells. A total of 3740 cytosolic HBAE proteins were identified by 2D LC–MS/MS, of which 52 were up-regulated ≥2-fold and 41 were down-regulated ≥2-fold after PR8 infection. Up-regulated HBAE proteins clustered primarily into interferon signaling, other host defense processes, and molecular transport, whereas down-regulated proteins were associated with cell death signaling pathways, cell adhesion and motility, and lipid metabolism. Comparison to influenza-infected A549 cells indicated some common influenza-induced host cell alterations, including defense response, molecular transport proteins, and cell adhesion. However, HBAE-specific alterations consisted of interferon and cell death signaling. These data point to important differences between influenza replication in continuous and primary cell lines and/or alveolar and bronchial epithelial cells.

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Section: Resultsmentioning

confidence: 99%