Formulation and In Vitro Characterization of PLGA/PLGA-PEG Nanoparticles Loaded with Murine Granulocyte-Macrophage Colony-Stimulating Factor

Mihalik, Nicole E; Wen, Sijin; Driesschaert, Benoît; Eubank, Timothy D.

doi:10.1208/s12249-021-02049-z

Cited by 6 publications

(2 citation statements)

References 73 publications

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“…The effectiveness of GM-CSF can potentially be increased by use on a polymer scaffold. The slow release of the drug from the implant does not cause cytotoxicity and ensures longlasting drug action [104]. Additionally, several findings showed defects in the upregulation of GM-CSF contributing to diseases of the circulatory system such as AAA.…”

Section: Chymase and Tryptasementioning

confidence: 99%

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Domagała,

Data,

Szyller

et al. 2024

Cells

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A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes.

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Section: Chymase and Tryptasementioning

confidence: 99%

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Domagała,

Data,

Szyller

et al. 2024

Cells

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“…For example, in alignment with the anti-angiogenesis field in the mid-2000s, we reported the vessel remodeling ability of intratumor injections of GM-CSF resulting in sequestration of tumor VEGF through TAM-derived sVEGFR-1 leading to increased hypoxia [ 156 , 157 , 158 , 159 , 160 ]. In recent works, we are testing intratumor delivery of GM-CSF using systemic PLGA/PEG-PLGA nanoparticles [ 161 ] as a method to remove excessive tumor VEGF that promotes vessel leakiness and aberrant sprouting, which in turn perpetuate tumor hypoxia leading to increased treatment resistance. While macrophages have been more thoroughly explored for their role in vascular remodeling in pancreatic cancer, additional studies are needed to understand how macrophages interact with other cells in the TME to influence this phenomenon.…”

Section: Sequelae Of Macrophages and Neutrophils In Pdacmentioning

confidence: 99%

Macrophage and Neutrophil Interactions in the Pancreatic Tumor Microenvironment Drive the Pathogenesis of Pancreatic Cancer

Pratt

Steinberger

Mihalik

et al. 2021

Cancers

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Despite modest improvements in survival in recent years, pancreatic adenocarcinoma remains a deadly disease with a 5-year survival rate of only 9%. These poor outcomes are driven by failure of early detection, treatment resistance, and propensity for early metastatic spread. Uncovering innovative therapeutic modalities to target the resistance mechanisms that make pancreatic cancer largely incurable are urgently needed. In this review, we discuss the immune composition of pancreatic tumors, including the counterintuitive fact that there is a significant inflammatory immune infiltrate in pancreatic cancer yet anti-tumor mechanisms are subverted and immune behaviors are suppressed. Here, we emphasize how immune cell interactions generate tumor progression and treatment resistance. We narrow in on tumor macrophage (TAM) spatial arrangement, polarity/function, recruitment, and origin to introduce a concept where interactions with tumor neutrophils (TAN) perpetuate the microenvironment. The sequelae of macrophage and neutrophil activities contributes to tumor remodeling, fibrosis, hypoxia, and progression. We also discuss immune mechanisms driving resistance to standard of care modalities. Finally, we describe a cadre of treatment targets, including those intended to overcome TAM and TAN recruitment and function, to circumvent barriers presented by immune infiltration in pancreatic adenocarcinoma.

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Inhibitory effects of surface-grafted polylactide-co-glycolide nanoparticles on the pro-inflammatory polarization of macrophages

Choi¹,

Seon²,

Vo³

et al. 2022

kjdm

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Formulation and In Vitro Characterization of PLGA/PLGA-PEG Nanoparticles Loaded with Murine Granulocyte-Macrophage Colony-Stimulating Factor

Cited by 6 publications

References 73 publications

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology

Macrophage and Neutrophil Interactions in the Pancreatic Tumor Microenvironment Drive the Pathogenesis of Pancreatic Cancer

Inhibitory effects of surface-grafted polylactide-co-glycolide nanoparticles on the pro-inflammatory polarization of macrophages

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