Low-frequency ultrasound induces apoptosis of rat aortic smooth muscle cells (A7r5) via the intrinsic apoptotic pathway

Zhang, B.; Zhou, Hongsheng; Cheng, Qian; Li, Lei; Hu, Bing

doi:10.4238/2014.april.17.10

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…LIPUS is a kind of micromechanical stress that is already clinically applied in treating several diseases including tumours and bone fracture healing. Numerous studies have also revealed the bio-effects of LIPUS such as increasing cell membrane penetrability and regulating cell apoptosis, proliferation, differentiation and migration [28][29][30][31][32]. Our previous study has found that an average intensity of 109.44 mW/cm 2 significantly promoted rat visceral preadipocyte apoptosis via elevating p-p38 [23].…”

Section: Discussionmentioning

confidence: 99%

Low-intensity pulsed ultrasound inhibits adipogenic differentiation via HDAC1 signalling in rat visceral preadipocytes

Zhao

Guo

et al. 2019

Adipocyte

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Non-drug strategy targeting adipocyte differentiation is critical for alleviating visceral obesity and its related diseases. However, whether and how low intensity pulsed ultrasound (LIPUS) could be used for inhibiting visceral adipocyte differentiation is not fully understood. In this study, we aim to investigate the effect and associated mechanism of LIPUS on primary visceral preadipocyte differentiation and explore its potential role for clinical visceral obesity management. The preadipocytes were daily exposed to LIPUS (0.5 MHz, 1.2 MPa) for 10 min. Adipogenic differentiation was estimated by the formation of lipid droplets and the levels of adipogenic transcriptional factors and representative markers. Mitogen-activated protein kinase (MAPK) member proteins and histone acetylation-related molecules were measured by western blotting. LIPUS stimulation with an average acoustic pressure of 1.2 MPa led to a prominent inhibition of adipogenic differentiation and expression of adipogenic markers. As a mechanism, LIPUS treatment increased the nuclear levels of histone deacetylase 1 (HDAC1) and decreased the acetylation of histone 3 and histone 4. Meanwhile, the inhibition of the HDAC1 could block the inhibitory effect of LIPUS on adipogenic differentiation via increasing AcH3 and AcH4 levels. Our study may provide an ultrasound-based promising strategy for clinical visceral obesity control.

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Section: Discussionmentioning

confidence: 99%

Low-intensity pulsed ultrasound inhibits adipogenic differentiation via HDAC1 signalling in rat visceral preadipocytes

Zhao

Guo

et al. 2019

Adipocyte

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“…In previous studies, ultrasound of 1 MHz or >1 MHz was usually used by a combination of microbubbles, which induced apoptosis (20,24). Ultrasound frequencies markedly <1 MHz, in particular ~45 kHz, have not been widely studied (11).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have demonstrated that ultrasound is able to induce the apoptosis of endothelial cells and several tumor cells (9,10). However, there have been few reports regarding the effect of ultrasound on VSMCs and there are limited studies on the effect of ultrasound on restenosis (11).…”

Section: Introductionmentioning

confidence: 99%

“…It is hypothesized that lower frequency ultrasound may have cavitational effects on VSMCs and affect VSMC proliferation and apoptosis, which may potentially be harnessed as a therapy for preventing restenosis of blood vessels following PTA. However, to date, there have been few studies on the effect of irradiation of low-frequency low-energy ultrasound (10-60 kHz) combined with bubble cavitation on apoptosis of VSMCs (11), and the therapeutic use of low-frequency kilohertz ultrasound for preventing restenosis of blood vessels following PTA and stenting has not been well characterized.…”

Section: Introductionmentioning

confidence: 99%

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Low-frequency low energy ultrasound combined with microbubbles induces distinct apoptosis of A7r5 cells

Zhang

Zhou

Cheng

et al. 2014

Molecular Medicine Reports

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The present study aimed to investigate whether low frequency low energy ultrasound combined with microbubbles induces apoptotic cell death of A7r5 rat aortic vascular smooth muscle cells, and to identify the possible mechanisms underlying this effect. Ultrasonic waves (45 kHz with 0.3 Wcm2 of intensity for 0, 10, 20 and 30 sec) were used together with different dosages of SonoVue™ microbubbles (0, 14, 28, 42 and 56 µl), respectively. The cell viability and apoptotic rate were determined by trypan blue staining immediately following treatment and flow cytometry 24 h thereafter. The treatment conditions resulting in the lowest amount of necrosis, highest apoptotic rate and lowest microbubble dosage was selected for the US+MB group, which was treated with ultrasound combined with microbubbles. The cell proliferation 24 h following treatment was determined and western blot analysis was applied to examine the expression of apoptosis‑associated proteins, B-cell lymphoma 2 (Bcl‑2) and Bcl-2-associated X (Bax). The harmonic acoustic pressure amplitude was measured to obtain the cavitation intensity. The combination of 20 sec ultrasound irradiation and 14 µl SonoVue™ was selected as the treatment conditions for the US+MB group. The results demonstrated that both ultrasound alone (the US group) and in combination with microbubbles significantly inhibited the proliferation of A7r5 cells compared with that of the control (P<0.01), and the suppression in the US+MB group was significantly greater (P<0.01). The apoptotic rate in A7r5 cells induced by this combination treatment (16.62±0.93%) was significantly higher than that in the control (3.93±0.39%; P<0.01) and US (6.88±1.87%; P<0.01) groups. Treatment with ultrasound combined with microbubbles increased the expression of Bax and decreased the ratio of Bcl‑2/Bax compared with those in the control and US groups. The cavitation induced by ultrasound combined with microbubble treatment was more intense than that by ultrasound alone. The results demonstrated that the cell death and apoptosis of A7r5 cells were associated with ultrasound duration and microbubble dosage. Low frequency ultrasound combined with microbubbles induced apoptosis in A7r5 cells through the upregulation of Bax and the downregulation of the Bcl‑2/Bax ratio, where the cavitation effect may have an important role.

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“…Changes of inner hair cells (IHCs) and outer hair cells (OHCs) are the most significant effect in sound-induced hearing loss due to various causes, such as aging and noise (Han et al, 2013;Sergeyenko et al, 2013;Heeringa and van Dijk, 2014). Studies have shown that after noise exposure, necrosis and apoptosis occurred simultaneously in the cochlea, and apoptosis was the main cause of the early death of hair cells (Zhang et al, 2014). In a study in which guinea pigs were subjected to a narrow band noise centred at 4 kHz with 110 dB, 115 dB or 120 dB sound pressure levels (SPL), it was suggested that the apoptotic process may be involved in intense noise-induced hair cell death (Hu et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Short-term exposure to high-intensity sound induces hearing loss and apoptosis in guinea pigs

Liu¹,

Wang²,

Liu³

et al. 2019

Acta Neurobiologiae Experimentalis

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The aim of this study was to investigate the effect and underlying mechanisms of short-term high-intensity sound exposure on guinea pigs to mimic the effects of non-lethal anti-riot weapons. A total of 92 male adult guinea pigs were exposed to high-intensity sound at 0 dB, 110 dB and 130 dB for 5 min. Basic clinical observation, repellent behaviour detection, peripheral blood routine examination, serum cortisol detection and hearing ability assessment were performed to analyse the functional changes after high intensity sound exposure. Meanwhile, routine haematoxylin and eosin staining, scanning electron microscopy and transmission electron microscopy were used to observe the structure of the cochlear tissue. To investigate the mechanisms underlying the tissue changes, the levels of apoptosis and caspase 3, 8 and 9 were detected using TUNEL staining and immunohistochemistry. After short-term exposure to high-intensity sound, the guinea pigs exhibited fear and agitation, increased repulsive behaviour, high serum cortisol and an increase in auditory threshold. The inner hair cells and outer hair cells exhibited degeneration. In addition, apoptosis was observed in the cochlear tissue. After short-term exposure to high-intensity sound, the guinea pigs exhibited not only stress reactions but also impaired hearing and signs of hair cell degeneration. Apoptosis in the cochlear tissue may play an important role in the functional and structural injuries caused by high-intensity sound.

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Low-frequency ultrasound induces apoptosis of rat aortic smooth muscle cells (A7r5) via the intrinsic apoptotic pathway

Cited by 4 publications

References 28 publications

Low-intensity pulsed ultrasound inhibits adipogenic differentiation via HDAC1 signalling in rat visceral preadipocytes

Low-intensity pulsed ultrasound inhibits adipogenic differentiation via HDAC1 signalling in rat visceral preadipocytes

Low-frequency low energy ultrasound combined with microbubbles induces distinct apoptosis of A7r5 cells

Short-term exposure to high-intensity sound induces hearing loss and apoptosis in guinea pigs

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