Injectable Nanocomposite Implants Reduce ROS Accumulation and Improve Heart Function after Infarction

Shilo, Malka; Oved, Hadas; Wertheim, Lior; Gal, Idan; Noor, Nadav; Green, Ori; Baruch, Ester-Sapir; Shabat, Doron; Shapira, Assaf

doi:10.1002/advs.202102919

Cited by 40 publications

(38 citation statements)

References 69 publications

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“…Our group has recently shown the ability of gold nanowires and nanospheres to improve cardiac electrical signal throughout macroporous scaffolds, electrospun fibers and hydrogels [ 13 , 15 – 17 ]. Here, we sought to evaluate the potential of the nanorods to improve the transfer of the signal in the scaffolds made of chondroitin sulfate.…”

Section: Resultsmentioning

confidence: 99%

Chondroitin sulfate-AuNRs electroactive scaffolds for on-demand release of biofactors

Malki

Shapira

2022

J Nanobiotechnol

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Controlled release systems are often integrated into polymeric scaffolds to supply essential biofactors to trigger physiological processes in engineered tissues. Here, we report the modification of chondroitin sulfate (CS) electroactive polymer with gold nanorods (AuNRs) to create hybrid macroporous scaffolds for enhanced on-demand release of growth factors and cytokines. The mechanical properties, porosity and degradation of the hybrid scaffolds were evaluated, and the viability and functionality of seeded cardiac cells were assessed. Following, the ability to control the release of the enzyme lysozyme, and the cytokine, stromal cell-derived factor 1 (SDF-1) by applying electrical stimulation, was demonstrated. The AuNRs were able to increase the current through the scaffolds, providing an efficient on–off release profile of SDF-1, which resulted in higher migration of cells expressing CXCR4 receptor. Finally, the engineered scaffolds were transplanted in rats and SDF-1 was released daily by electrical stimulation, promoting blood vessel-forming cell infiltration and vascularization. We envision that gold nanoparticles and other conducting nanomaterials can be incorporated into different electroactive materials to improve their capabilities not only for tissue engineering applications, but for a variety of biomedical applications, where enhanced electrical stimulation is needed. Graphical Abstract

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Section: Resultsmentioning

confidence: 99%

Chondroitin sulfate-AuNRs electroactive scaffolds for on-demand release of biofactors

Malki

Shapira

2022

J Nanobiotechnol

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“…Increased oxidative stress has been shown to contribute to post-infarction injury ( Shilo et al, 2021 ). During lipid peroxidation, highly reactive dicarbonyl compounds are formed, including 4-oxononenal (4-ONE), 4-hydroxynonenal (4-HNE) malondialdehyde (MDA), and isoelemic acid lipids (IsoLGs).…”

Section: Discussionmentioning

confidence: 99%

Isolevuglandins Scavenger Ameliorates Myocardial Ischemic Injury by Suppressing Oxidative Stress, Apoptosis, and Inflammation

Guo

et al. 2022

Front. Cell Dev. Biol.

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Augmented levels of reactive isolevuglandins (IsoLGs) are responsible for cardiovascular diseases. The role of IsoLGs in myocardial infarction (MI) remains elusive. Here we explored the effect of IsoLGs scavenger 2-hydroxybenzylamine (2-HOBA) in post-infarction cardiac repair. We observed that infarcted cardiac tissues expressed high IsoLGs in mice. Following MI injury, 2-HOBA treated mice displayed decreased infarction area and improved heart function compared with the saline-treated group. Moreover, 2-HOBA effectively attenuated MI-induced cardiac remodeling, oxidative stress, apoptosis, and inflammation. 4-hydroxybenzylamine (4-HOBA), a less reactive isomer of 2-HOBA, barely antagonized the MI-induced injury. These findings suggest that IsoLGs elimination may be helpful in MI therapy.

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“…In addition to pathologically increased NO, the overproduction of ROS, which normally occurs during ischemia and is further exacerbated by reperfusion, also plays a key role in the development of oxidative stress during cardiac ischemia ( Shilo et al, 2021 ). The increased ROS, together with NO, increases the production of pro-inflammatory cytokines and causes oxido-nitrosative stress, which leads to oxidative stress and cardiac dysfunction ( Rawdin et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Indole-3-Carbinol (I3C) Protects the Heart From Ischemia/Reperfusion Injury by Inhibiting Oxidative Stress, Inflammation, and Cellular Apoptosis in Mice

Xia²,

Wu³

et al. 2022

Front. Pharmacol.

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Strategies for treating myocardial ischemia in the clinic usually include re-canalization of the coronary arteries to restore blood supply to the myocardium. However, myocardial reperfusion insult often leads to oxidative stress and inflammation, which in turn leads to apoptosis and necrosis of myocardial cells, for which there are no standard treatment methods. The aim of this study was to determine the pharmacological effect of indole-3-carbinol (I3C), a phytochemical found in most cruciferous vegetables, in a mouse model of myocardial ischemia/reperfusion injury (MIRI). Our results showed that I3C pretreatment (100 mg/kg, once daily, i. p.) prevented the MIRI-induced increase in infarct size and serum creatine kinase (CK) and lactate dehydrogenase (LDH) in mice. I3C pretreatment also suppressed cardiac apoptosis in MIRI mice by increasing the expression levels of the anti-apoptotic protein Bcl-2 and decreasing the expression levels of several apoptotic proteins, including Bax, caspase-3, and caspase-9. In addition, I3C pretreatment was found to reduce the levels of parameters reflecting oxidative stress, such as dihydroethidium (DHE), malondialdehyde (MDA), reactive oxygen species (ROS), and nitric oxide (NO), while increasing the levels of parameters reflecting anti-oxidation, such as total antioxidant capacity (T-AOC) and glutathione (GSH), in MIRI-induced ischemic heart tissue. I3C pretreatment was also able to remarkably decrease the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) mRNA in ischemic heart tissue. These results demonstrate that administration of I3C protects the heart from MIRI through its anti-apoptotic, antioxidant, and anti-inflammatory effects.

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Injectable Nanocomposite Implants Reduce ROS Accumulation and Improve Heart Function after Infarction

Cited by 40 publications

References 69 publications

Chondroitin sulfate-AuNRs electroactive scaffolds for on-demand release of biofactors

Chondroitin sulfate-AuNRs electroactive scaffolds for on-demand release of biofactors

Isolevuglandins Scavenger Ameliorates Myocardial Ischemic Injury by Suppressing Oxidative Stress, Apoptosis, and Inflammation

Indole-3-Carbinol (I3C) Protects the Heart From Ischemia/Reperfusion Injury by Inhibiting Oxidative Stress, Inflammation, and Cellular Apoptosis in Mice

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