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Cellular stress modulates severity of the inflammatory response in lungs via cell surface BiP

ABSTRACT: As BiP is involved in the ARDS mechanism of disease, we analyzed the proteomic profile of lung tissue challenged with LPS and/or treated with 4-PBA to identify pathways and components that link BiP and cellular stress with the hyperinflammatory response.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Lung

SUBMITTER: Ivan Duran

LAB HEAD: Duran Lab

PROVIDER: PXD037978 | Pride | 2023-03-11

REPOSITORIES: Pride

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			Action	DRS
	211025-10_LPS.raw	Raw
	211025-11_LPS.raw	Raw
	211025-12_LPS4PBA.raw	Raw
	211025-13_LPS4PBA.raw	Raw
	211025-14_LPS4PBA.raw	Raw

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Publications

Cellular stress modulates severity of the inflammatory response in lungs <i>via</i> cell surface BiP.

Rico-Llanos Gustavo G Porras-Perales Óscar Ó Escalante Sandra S Vázquez-Calero Daniel B DB Valiente Lucía L Castillo María I MI Pérez-Tejeiro José Miguel JM Baglietto-Vargas David D Becerra José J Reguera José María JM Duran Ivan I Csukasi Fabiana F

Frontiers in immunology 20221118

Inflammation is a central pathogenic feature of the acute respiratory distress syndrome (ARDS) in COVID-19. Previous pathologies such as diabetes, autoimmune or cardiovascular diseases become risk factors for the severe hyperinflammatory syndrome. A common feature among these risk factors is the subclinical presence of cellular stress, a finding that has gained attention after the discovery that BiP (GRP78), a master regulator of stress, participates in the SARS-CoV-2 recognition. Here, we show ...[more]

PMID: 36466830

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