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Inflammatory disease progression shapes nanoparticle biomolecular corona-mediated immune activation profiles

ABSTRACT: Polymeric nanoparticles (NPs) have emerged as promising tools for immunomodulation in various disease contexts. The interactions between the NP surface and plasma-resident biomolecules result in the formation of a biomolecular corona (BC), which varies patient-to-patient and as a function of disease state, resulting in the concept of the personalized NP-BC. This study investigates how the progression of systemic inflammatory disease influences the NP-BC composition and its corresponding effects on innate immune cell interactions and activation profiles. Employing a murine model of systemic inflammation, the dynamic changes in plasma biomolecule composition and their corresponding NP-BC fingerprints were elucidated. An integrated multi-omics approach was developed to reveal disease state-specific alterations in innate immune cell phenotypes and modulated signaling pathways to identify and confirm key circulating biomolecules that contribute to the dynamic immunostimulatory capabilities of BCs.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Mehari Weldemariam

LAB HEAD: Maureen Kane

PROVIDER: PXD050918 | Pride | 2025-01-17

REPOSITORIES: Pride

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			Action	DRS
	20221224_RyanLab_nanoparticle_mouse_serum_01.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_02.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_03.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_04.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_05.raw	Raw

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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.

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Inflammatory disease progression shapes nanoparticle biomolecular corona-mediated immune activation profiles

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