Modeled vascular microenvironments: immune-endothelial cell interactions in vitro

Silberman, Justin; Jha, Aakanksha; Ryan, Holly; Abbate, Talia; Moore, Erika

doi:10.1007/s13346-021-00970-1

Cited by 8 publications

(4 citation statements)

References 81 publications

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“…As the activation of endothelial cells has proved important in the regulation of metastasis formation, HUVECs were stimulated with tumor necrosis factor-alpha (TNF-α) to simulate the vascular endothelial cells in the tumor metastasis area in vitro . This method has been widely used in previous studies to mimic the tumor vascular endothelium. , The successfully activation of HUVECs was verified by high expression of VCAM-1, which is highly expressed on vascular endothelial from tumor and premetastatic niche (Figure S12). , We subsequently simulated the binding of neutrophils to vascular endothelial cells in the tumor or tumor metastasis area by coincubating them with TNF-α-treated or untreated HUVECs.…”

Section: Resultsmentioning

confidence: 99%

“…31 This method has been widely used in previous studies to mimic the tumor vascular endothelium. 32,33 The successfully activation of HUVECs was verified by high expression of VCAM-1, which is highly expressed on vascular endothelial from tumor and premetastatic niche (Figure S12). 34,35 We subsequently simulated the binding of neutrophils to vascular endothelial cells in the tumor or tumor metastasis area by coincubating them with TNF-αtreated or untreated HUVECs.…”

Section: Synthesis and Characterization Of Anem Npsmentioning

confidence: 96%

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Neutrophil Nanodecoys Inhibit Tumor Metastasis by Blocking the Interaction between Tumor Cells and Neutrophils

Zeng,

Wang,

Zhang

et al. 2024

ACS Nano

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Cancer metastasis is the main cause of cancerrelated deaths and involves the interaction between tumor cells and neutrophils. In this study, we developed activated neutrophil membrane-coated nanoparticles (aNEM NPs) as nanodecoys to block neutrophil-mediated cancer metastasis. The aNEM NPs were fabricated by cloaking poly(lactic acid) nanoparticles with membranes derived from activated neutrophils and inherited the functional proteins of activated neutrophils. We demonstrated that aNEM NPs could interfere with the recruitment of neutrophils to the primary tumor and premetastatic niches, inhibit the adhesion of neutrophils to tumor vascular endothelium and circulating tumor cells (CTCs), and disrupt the formation of CTC−neutrophil clusters in vitro and in vivo. In 4T1-bearing mice, aNEM NPs could effectively reduce breast cancer metastasis to various organs in mice. Our results suggest that aNEM NPs are a promising nanomedicine for preventing or treating cancer metastasis by acting as neutrophil nanodecoys.

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Section: Resultsmentioning

confidence: 99%

Section: Synthesis and Characterization Of Anem Npsmentioning

confidence: 96%

Neutrophil Nanodecoys Inhibit Tumor Metastasis by Blocking the Interaction between Tumor Cells and Neutrophils

Zeng,

Wang,

Zhang

et al. 2024

ACS Nano

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“…Such studies would allow inflammatory pathways common between human and murine SLE cells to be investigated without potential effects from hemodynamic differences. Many types of in vitro platforms such as microfluidics devices and transwell assays allow for the study of interactions between diseased inflammatory cells, such as T cells or monocytes, with ECs ( 66 ). For example, in one study conducted to observe changes in angiogenesis in the setting of glioblastoma, ECs displayed increased sprouting when co-cultured with tumor-associated macrophages than with unstimulated macrophages ( 67 ).…”

Section: Future Directionsmentioning

confidence: 99%

Vascular Inflammation in Mouse Models of Systemic Lupus Erythematosus

Ryan

Morel

Moore

2022

Front. Cardiovasc. Med.

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Vascular inflammation mediated by overly activated immune cells is a significant cause of morbidity and mortality in systemic lupus erythematosus (SLE). Several mouse models to study the pathogenesis of SLE are currently in use, many of which have different mechanisms of pathogenesis. The diversity of these models allows interrogation of different aspects of the disease pathogenesis. To better determine the mechanisms by which vascular inflammation occurs in SLE, and to assist future researchers in choosing the most appropriate mouse models to study cardiovascular complications in SLE, we suggest that direct comparisons of vascular inflammation should be conducted among different murine SLE models. We also propose the use of in vitro vascular assays to further investigate vascular inflammation processes prevalent among different murine SLE models.

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“…However, the exact mechanisms of endothelial-macrophage crosstalk re-quire further investigation with explicit consideration of age. To study these effects, immune cells must be in coculture with endothelial cells in vitro or ex vivo, or via an in vivo model [Irimia and Wang, 2018;Silberman et al, 2021].…”

Section: Introductionmentioning

confidence: 99%

A Biomaterial Model to Assess the Effects of Age in Vascularization

Silberman¹,

Boehlein²,

Abbate³

et al. 2022

Cells Tissues Organs

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As humans age, there is an increased risk for developing age-associated diseases. Many of these diseases, such as cardiovascular disease, involve dysfunction in the vasculature. Cardiovascular disease stems from endothelial cell dysfunction and reduction in vascularization. Macrophages, prominent innate immune cells involved in orchestrating inflammation and wound healing, have a significant influence on vascularization. While much recent work has investigated the crosstalk between endothelial cells and macrophages, it is still not well defined. The interactions between the cell types are even less understood in specific disease states such as advanced age. Understanding how age influences macrophage/endothelial cell interaction is essential for understanding cardiovascular disease development in the elderly. In the polyethylene glycol (PEG)-based hydrogel system, we model the effects of age on vascularization by encapsulating endothelial cells, pericytes, and human donor macrophages. We created a biomaterial model system in which macrophages, either from young (<35 years old) or old (>65 years old) donors, interact with the modeled vasculature, termed microvessels. Confocal image analysis of vessel density, vessel length, and branch points were used to quantify microvessel growth depending on the age of the macrophage donor. Alongside this, soluble factor secretion and gene expression were evaluated using ELISA and NanoString to showcase biological mechanisms based on the age of each donor. Endothelial cells cultured with macrophages from old donors have reduced microvessel density. There also is reduced soluble factor secretion by the macrophages from old donors, which likely influenced microvessel growth. Altogether, we establish our PEG-based hydrogel vascular model as a system to evaluate patient-specific cell function as well as proposed mechanisms for how age influences microvessels.

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Modeled vascular microenvironments: immune-endothelial cell interactions in vitro

Cited by 8 publications

References 81 publications

Neutrophil Nanodecoys Inhibit Tumor Metastasis by Blocking the Interaction between Tumor Cells and Neutrophils

Neutrophil Nanodecoys Inhibit Tumor Metastasis by Blocking the Interaction between Tumor Cells and Neutrophils

Vascular Inflammation in Mouse Models of Systemic Lupus Erythematosus

A Biomaterial Model to Assess the Effects of Age in Vascularization

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