Nanostructured Organosilica Nitric Oxide Donors Intrinsically Regulate Macrophage Polarization with Antitumor Effect

Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational d...

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Published inACS nano Vol. 16; no. 7; pp. 10943 - 10957
Main Authors Theivendran, Shevanuja, Gu, Zhengying, Tang, Jie, Yang, Yannan, Song, Hao, Yang, Yang, Zhang, Min, Cheng, Dan, Yu, Chengzhong
Format Journal Article
LanguageEnglish
Published United States American Chemical Society 26.07.2022
Subjects
Humans
Macrophage Activation
Macrophages
Nanoparticles
Neoplasms
Nitric Oxide
Nitric Oxide Donors - pharmacology
Silicon Dioxide - pharmacology
macrophage
nitric oxide
organosilica
nanoparticles
immunotherapy
Online AccessGet full text
ISSN1936-0851
1936-086X
1936-086X
DOI10.1021/acsnano.2c03348

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Abstract Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational design for effective NO delivery and macrophage activation. S-Nitrosothiol (SNO) modified organosilica nanoparticles with a tetrasulfide-containing composition produced a higher level of intracellular NO than their bare silica counterparts in macrophages. Enhanced intracellular delivery of NO resulted in mitochondrial dysfunction and disruption of the tricarboxylic acid cycle, leading to macrophage activation and delayed tumor growth. This study provides insights on intracellularly delivered NO for regulating the polarization of macrophages and cancer immunotherapy.
AbstractList Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational design for effective NO delivery and macrophage activation. S-Nitrosothiol (SNO) modified organosilica nanoparticles with a tetrasulfide-containing composition produced a higher level of intracellular NO than their bare silica counterparts in macrophages. Enhanced intracellular delivery of NO resulted in mitochondrial dysfunction and disruption of the tricarboxylic acid cycle, leading to macrophage activation and delayed tumor growth. This study provides insights on intracellularly delivered NO for regulating the polarization of macrophages and cancer immunotherapy.Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational design for effective NO delivery and macrophage activation. S-Nitrosothiol (SNO) modified organosilica nanoparticles with a tetrasulfide-containing composition produced a higher level of intracellular NO than their bare silica counterparts in macrophages. Enhanced intracellular delivery of NO resulted in mitochondrial dysfunction and disruption of the tricarboxylic acid cycle, leading to macrophage activation and delayed tumor growth. This study provides insights on intracellularly delivered NO for regulating the polarization of macrophages and cancer immunotherapy.
Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational design for effective NO delivery and macrophage activation. -Nitrosothiol (SNO) modified organosilica nanoparticles with a tetrasulfide-containing composition produced a higher level of intracellular NO than their bare silica counterparts in macrophages. Enhanced intracellular delivery of NO resulted in mitochondrial dysfunction and disruption of the tricarboxylic acid cycle, leading to macrophage activation and delayed tumor growth. This study provides insights on intracellularly delivered NO for regulating the polarization of macrophages and cancer immunotherapy.
Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the activation of macrophages for cancer immunotherapy. Herein, we report the synthesis of a nanoparticle-based NO delivery platform with a rational design for effective NO delivery and macrophage activation. S-Nitrosothiol (SNO) modified organosilica nanoparticles with a tetrasulfide-containing composition produced a higher level of intracellular NO than their bare silica counterparts in macrophages. Enhanced intracellular delivery of NO resulted in mitochondrial dysfunction and disruption of the tricarboxylic acid cycle, leading to macrophage activation and delayed tumor growth. This study provides insights on intracellularly delivered NO for regulating the polarization of macrophages and cancer immunotherapy.
Author Yu, Chengzhong
Song, Hao
Theivendran, Shevanuja
Gu, Zhengying
Yang, Yannan
Cheng, Dan
Yang, Yang
Tang, Jie
Zhang, Min
AuthorAffiliation Australian Institute for Bioengineering and Nanotechnology
School of Chemistry and Molecular Engineering
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Snippet Nitric oxide (NO) has many important biological functions; however, it has been a long-standing challenge to utilize the exogenous NO donor itself in the...
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SubjectTerms Humans
Macrophage Activation
Macrophages
Nanoparticles
Neoplasms
Nitric Oxide
Nitric Oxide Donors - pharmacology
Silicon Dioxide - pharmacology
Title Nanostructured Organosilica Nitric Oxide Donors Intrinsically Regulate Macrophage Polarization with Antitumor Effect
URI http://dx.doi.org/10.1021/acsnano.2c03348
https://www.ncbi.nlm.nih.gov/pubmed/35735363
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