TGase-mediated cell membrane modification and targeted cell delivery to inflammatory endothelium

Cui, Qi; Jin, Yuqi; Chen, Yuyang; Li, Wenjing; Li, Yaqian; Liang, Kai; Li, Yan; Zhang, Yonghui; Du, Yanan

doi:10.1016/j.biomaterials.2020.120276

Cited by 9 publications

(7 citation statements)

References 41 publications

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“…Through membrane modification of fpp, a liver‐targeting peptide, we have previously promoted MSCs to target to and stay in livers in a liver injury model. [ 23 ] Likewise, we modified fpp to the membrane of dLSECs (dLSEC‐fpp) and nLSECs (nLSEC‐fpp), and found that dLSECs could be effectively modified by incubating cells with 1 m m fpp for 30 min (Figure 6H ; Figure S25 , Supporting Information). dLSEC‐fpp showed high ECM degradation ability comparable to the unmodified dLSECs (Figure S26 , Supporting Information).…”

Section: Resultsmentioning

confidence: 99%

“…For one‐dose dLSEC or dHUVEC therapy, 4 × 10 5 LSECs (dLSECs or nLSECs) and HUVECs (dHUVECs or nHUVECs) in 100 µL PBS were intrasplenically injected into mice with established fibrosis using a syringe pump as described previously. [ 23 ] Cell distribution in mice was imaged on day 1, 3, and 5 post‐injection. The mice were sacrificed and the livers were harvested on day 5 of post‐treatment.…”

Section: Methodsmentioning

confidence: 99%

“…Liver‐targeting peptides (fpps, GQLKHLEQQEG) [ 23 ] were dissolved in DMEM medium containing 1% PS, 1× GlutaMax (Thermo Fisher, 35 050 061), and 0.5 mg mL −1 albumin (oryzogen, HYC002M01). To optimize the conditions of peptide modification, fpps with different concentrations (0.01 m m , 0.1 m m , 1 m m , 5 m m , and 10 m m ) were incubated with cells for different modification time (5 min, 10 min, 20 min, 30 min, 40 min, 50 min, and 60 min).…”

Section: Methodsmentioning

confidence: 99%

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Scar‐Degrading Endothelial Cells as a Treatment for Advanced Liver Fibrosis

et al. 2022

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matrix (ECM) in the liver is an important feature of liver cirrhosis. Recovery from liver cirrhosis is physiologically challenging, partially due to the ECM in scar tissue showing resistance to cell-mediated degradation by secreted matrix metalloproteinases (MMPs). Here, a cell-mediated ECM-degradation screening system (CEDSS) in vitro is constructed for high-throughput searching for cells with tremendous degradation ability. ECM-degrading liver sinusoidal endothelial cells (dLSECs) are screened using CEDSS, which exhibit 17 times the ability to degrade collagen when compared to other cells. The degradation ability of dLSECs is mediated by the upregulation of MMP9. In particular, mRNA expression of MMP9 shows an 833-fold increase in dLSECs compared to normal endothelial cells (nLSECs), and MMP9 is regulated by transcription factor c-Fos. In vivo, single intrasplenic injection of dLSECs alleviates advanced liver fibrosis in mice, while intraperitoneal administration of liver-targeting peptide-modified dLSECs shows enhanced fibrosis-targeting effects. Degradative human umbilical vein endothelial cells (dHUVECs) prove their enhanced potential of clinical translation. Together, these results highlight the potential of ECM-degrading endothelial cells in alleviating advanced liver fibrosis, thus providing remarkable insights in the development of ECM-targeting therapeutics.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Scar‐Degrading Endothelial Cells as a Treatment for Advanced Liver Fibrosis

et al. 2022

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“…Gene delivery agents targeting E-selectin have been developed using LNPs and polymer NPs conjugated to antibodies, − thioaptamers, and the E-selectin binding molecule Sialyl Lewis A . Additional proteins that have been used to target the inflamed endothelium include integrins, cell adhesion molecules VCAM-1 and ICAM-1, transglutaminase, and von Willebrand factor …”

Section: The Vascular Endothelium As a Therapeutic Targetmentioning

confidence: 99%

Nucleic Acid Delivery to the Vascular Endothelium

et al. 2022

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This Review examines the state-of-the-art in the delivery of nucleic acid therapies that are directed to the vascular endothelium. First, we review the most important homeostatic functions and properties of the vascular endothelium and summarize the nucleic acid tools that are currently available for gene therapy and nucleic acid delivery. Second, we consider the opportunities available with the endothelium as a therapeutic target and the experimental models that exist to evaluate the potential of those opportunities. Finally, we review the progress to date from investigations that are directly targeting the vascular endothelium: for vascular disease, for peri-transplant therapy, for angiogenic therapies, for pulmonary endothelial disease, and for the blood− brain barrier, ending with a summary of the future outlook in this field.

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“…Among them, covalent conjugation is the most forthright method by harnessing the naturally existed functional groups on cell surface. Concisely, functional peptides were bestowed onto the MSCs, inflammatory endothelial cells (ECs) or immune cells whose membrane expresses Transglutaminase 2 via enzyme-catalyzed crosslinking with the surface lysine residue, thus enhancing the cell targeting efficiency to injured tissues [7] . Meanwhile, electrostatic interactions between the negatively charged plasma membrane surfaces with cationic/anionic polymers is extensively employed to shield the cells from shears and immune responses.…”

Section: Cell Engineering Strategies As Cell Formulation Technologies...mentioning

confidence: 99%

Cell engineering techniques improve pharmacology of cellular therapeutics

Liang

2021

Biomaterials and Biosystems

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TGase-mediated cell membrane modification and targeted cell delivery to inflammatory endothelium

Cited by 9 publications

References 41 publications

Scar‐Degrading Endothelial Cells as a Treatment for Advanced Liver Fibrosis

Scar‐Degrading Endothelial Cells as a Treatment for Advanced Liver Fibrosis

Nucleic Acid Delivery to the Vascular Endothelium

Cell engineering techniques improve pharmacology of cellular therapeutics

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