A new sensitizer DVDMS combined with multiple focused ultrasound treatments: an effective antitumor strategy

Xiong, Wenli; Wang, Pan; Hu, Jianmin; Jia, Yali; Wu, Linquan; Chen, Xiyang; Liu, Quanhong; Wang, Xiaobing

doi:10.1038/srep17485

Cited by 53 publications

(42 citation statements)

References 37 publications

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“…8 SDT induces the generation of reactive oxygen species (ROS) and apoptosis in tumor cells, and has been shown to greatly improve the outcome of cancer patient by promoting tumor shrinkage while reducing metastases of tumor cells. 9, 10, 11, 12, 13 We previously revealed that SDT could effectively induce apoptosis of macrophage and macrophage foam cell via mitochondrial-caspase dependent pathway 14, 15 and rapidly stabilize atherosclerotic plaques. 16 Meanwhile, SDT possesses high repeatability owing to its relative security and accessibility.…”

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confidence: 99%

Hypericin-mediated sonodynamic therapy induces autophagy and decreases lipids in THP-1 macrophage by promoting ROS-dependent nuclear translocation of TFEB

Zhang

Zheng

et al. 2016

Cell Death Dis

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Lipid catabolism disorder is the primary cause of atherosclerosis. Transcription factor EB (TFEB) prevents atherosclerosis by activating macrophage autophagy to promote lipid degradation. Hypericin-mediated sonodynamic therapy (HY-SDT) has been proved non-invasively inducing THP-1-derived macrophage apoptosis; however, it is unknown whether macrophage autophagy could be triggered by HY-SDT to influence cellular lipid catabolism via regulating TFEB. Here, we report that HY-SDT resulted in the time-dependent THP-1-derived macrophage autophagy activation through AMPK/AKT/mTOR pathway. Besides, TFEB nuclear translocation in macrophage was triggered by HY-SDT to promote autophagy activation and lysosome regeneration which enhanced lipid degradation in response to atherogenic lipid stressors. Moreover, following HY-SDT, the ABCA1 expression level was increased to promote lipid efflux in macrophage, and the expression levels of CD36 and SR-A were decreased to inhibit lipid uptake, both of which were prevented by TFEB knockdown. These results indicated that TFEB nuclear translocation activated by HY-SDT was not only the key regulator of autophagy activation and lysosome regeneration in macrophage to promote lipolysis, but also had a crucial role in reverse cholesterol transporters to decrease lipid uptake and increase lipid efflux. Reactive oxygen species (ROS) were adequately generated in macrophage by HY-SDT. Further, ROS scavenger N-acetyl-l-cysteine abolished HY-SDT-induced TFEB nuclear translocation and autophagy activation, implying that ROS were the primary upstream factors responsible for these effects during HY-SDT. In summary, our data indicate that HY-SDT decreases lipid content in macrophage by promoting ROS-dependent nuclear translocation of TFEB to influence consequent autophagy activation and cholesterol transporters. Thus, HY-SDT may be beneficial for atherosclerosis via TFEB regulation to ameliorate lipid overload in atherosclerotic plaques.

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confidence: 99%

Hypericin-mediated sonodynamic therapy induces autophagy and decreases lipids in THP-1 macrophage by promoting ROS-dependent nuclear translocation of TFEB

Zhang

Zheng

et al. 2016

Cell Death Dis

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“…All SDT studies are focused primarily on cancer treatment [19][20][21]. Previous studies demonstrated the sonodynamic effect of ALA on macrophages that are responsible for the progression of atherosclerosis [13,14].…”

Section: Discussionmentioning

confidence: 99%

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Guo

Dong²,

Shi³

et al. 2016

Cell Physiol Biochem

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Key Words SDT • Cardiac fibroblast • TGF-β1 • GSK3β • AKT Abstract Background/Aims: Sonodynamic therapy (SDT) is a localized ultrasound-activated therapy for atherosclerosis when combined with a sonosensitizer, 5-aminolevulinic acid (ALA), but whether it can prevent cardiac fibrosis has not been studied. In the present study, we evaluated the effects SDT on fibrogenesis in rat cardiac fibroblasts. Methods: The primary cardiac fibroblasts were isolated from rats, and induced to fibrogenesis with TGF-β1. With this in vitro model, we tested the preventive effects of SDT on fibrogenesis and further the underlying mechanism. Results: TGF-β1 stimulation up-regulated α-SMA and COLI/III protein levels in cardiac fibroblasts, and enhanced the progression of cells from the G0/G1 phase to the S phase. SDT inhibited the TGF-β1 mediated cell proliferation and decreased the levels of α-SMA and COLI/III by activating AKT/GSK3β pathway and blocking TGF-β1/SMAD3 signaling. Conclusion: Our studies demonstrate an antifibrotic effect of SDT in rat cardiac fibroblasts, suggesting that SDT may intervene cardiac fibrogenesis by regulating myocardial fibrotic remodeling.

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“…[14, 17] Yet, RB4 is not a photosensitive molecule. The photon theory of sonodynamic therapy might not be applicable in RB4.…”

Section: Resultsmentioning

confidence: 99%

“…Most of the reported sonosensitizers are also photosensitizers or derived from photosensitizers; therefore, the accepted mechanism of action of SDT is similar to that of PDT. [14, 17] Conversely, a few non-photosensitive sonosensitizers have also been identified. [18–20] These sonosensitizers cannot be excited by light; but under insonation, reactive oxygen species (ROS) were generated, triggering apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Tumor ablation using low-intensity ultrasound and sound excitable drug

Tung

Han

Kim

et al. 2017

Journal of Controlled Release

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The cell membrane is a semi-fluid container that defines the boundary of cells, and provides an enclosed environment for vital biological processes. A sound excitable drug (SED) that is non-cytotoxic to cells is developed to disrupt the plasma membrane under gentle ultrasound insonation, 1 MHz, 1 W/cm2. The frequency and power density of insonation are within the physical therapy and medical imaging windows; thus the applied ultrasound is safe and not harmful to tissues. The insertion of SEDs into the plasma membrane is not toxic to cells; however, the intruding SEDs weaken the membrane’s integrity. Under insonation, the ultrasound energy destabilized the SED disrupted membranes, resulting in membrane rupture and eventual cell death. In a xenograft breast tumor model, the SED alone or the ultrasound alone caused little adverse effects to tumor tissue, while the combined treatment triggered necrosis with a brief local insonation of 3 minutes. The described sono-membrane rupture therapy could be a safe alternative to the currently used high-energy tissue ablation technology, which uses X-rays, gamma rays, electron beams, protons, or high- intensity focused ultrasound.

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A new sensitizer DVDMS combined with multiple focused ultrasound treatments: an effective antitumor strategy

Cited by 53 publications

References 37 publications

Hypericin-mediated sonodynamic therapy induces autophagy and decreases lipids in THP-1 macrophage by promoting ROS-dependent nuclear translocation of TFEB

Hypericin-mediated sonodynamic therapy induces autophagy and decreases lipids in THP-1 macrophage by promoting ROS-dependent nuclear translocation of TFEB

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Tumor ablation using low-intensity ultrasound and sound excitable drug

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