Apoptosis induced by the sonomechanical effects of low intensity pulsed ultrasound in a human leukemia cell line

Feril, Loreto B.; Kondo, Takashi; Cui, Zheng‐Guo; Tabuchi, Yoshiaki; Zhao, Qing; Ando, Hidetaka; Misaki, Takuro; Yoshikawa, Hiroyuki; Umemura, Shin Ichiro

doi:10.1016/j.canlet.2004.08.034

Cited by 133 publications

(104 citation statements)

References 20 publications

Supporting

Mentioning

100

Contrasting

Order By: Relevance

“…The involvement of Ca 2+ , free radicals [15], cell membrane damage [12,13] and DNA damage with p53 activation [10] have been proposed for the mechanisms of apoptosis induced by ultrasound. Some have speculated that direct destruction or disturbance of the mitochondrial membrane upon ultrasound exposure can result in apoptotic cell death [10,15].…”

Section: Resultsmentioning

confidence: 99%

“…Since the first discovery of ultrasound being capable of inducing apoptosis [5,[9][10][11][12][13][14][15][16][17][18][19], the exact mechanisms of apoptosis caused by ultrasound are unknown and only a few documentations can be found challenging this issue. The involvement of Ca 2+ , free radicals [15], cell membrane damage [12,13] and DNA damage with p53 activation [10] have been proposed for the mechanisms of apoptosis induced by ultrasound.…”

Section: Resultsmentioning

confidence: 99%

“…It has also become evident that ultrasound can cause cell death by an apoptotic mechanism as well as cell lysis or necrotic cell death both in vitro [9][10][11][12][13][14][15][16][17][18] and in vivo [5,19]. The triggers and the molecular pathway to lead each cell death mechanism are not well elucidated, and should be clarified for overall understanding of the ultrasound-induced cell death.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Activation of Bak in ultrasound-induced, JNK- and p38-independent apoptosis and its inhibition by Bcl-2

Kinoshita¹,

Eguchi²,

Hynynen³

2007

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

The molecular mechanisms underlying ultrasound-induced apoptosis remain poorly understood. We have demonstrated that in Jurkat cells, the over-expression of the anti-apoptotic protein Bcl-2 inhibited ultrasound-induced apoptosis, but not necrosis. Inhibition of caspase activity also protected the cells from apoptosis, but not from necrosis, showing the involvement of different mechanisms in ultrasound-induced apoptosis and necrosis. Bak, a pro-apoptotic member of the Bcl-2 family proteins, was activated by ultrasound and its activation was completely inhibited by Bcl-2 overexpression, but not by caspase inhibition. Antioxidant N-acetyl cysteine did not protect the cells from ultrasound-induced apoptosis or necrosis, nor did the inhibition of either c-Jun N-terminal kinase or p38, key factors in the radical oxygen species (ROS)-mediated cell stress response, suggesting that ROS do not play a crucial role in ultrasound-induced apoptosis. Our results confirm that ultrasound induces apoptosis via a pathway that involves Bak, Bcl-2, and caspases, but not ROS.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of Bak in ultrasound-induced, JNK- and p38-independent apoptosis and its inhibition by Bcl-2

Kinoshita¹,

Eguchi²,

Hynynen³

2007

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

show abstract

“…Furthermore, apoptosis (13 %) and late apoptosis (11 %) were observed after 6-h incubation. Since other study report on optimal apoptosis detected after 12-h incubation [2], it is expected to have better results with a post-treatment longer incubation.…”

Section: Resultsmentioning

confidence: 94%

“…It is known that low intensity ultrasounds induce cancer cell death, apoptosis in vitro [1,2] and in vivo [3,4] and stiffening of some cancer cells [5], while the healthy cells are more resistant than cancer cells to ultrasonic irradiation [6]. Since cancer cells with high metastatic potential are softer than healthy cells [7][8][9], cancer cell proliferation should be inhibited by low intensity ultrasounds.…”

Section: Introductionmentioning

confidence: 99%

Study of cellular response induced by low intensity ultrasound frequency sweep pattern on myelomonocytic lymphoma U937 cells

et al. 2016

View full text Add to dashboard Cite

Purpose This study will analyze the mechanical effects (immediate lysis) and biological effects (cell survival, apoptosis, cell cycle) on U937 cells subjected to different sonication conditions with increasing and decreasing frequencies and burst rate (number of burst of a repeating signal in a specific time unit), in order to determine the best conditions of sonication to produce high mortality, apoptosis and inhibition of hyperproliferation. Method Cells are been stressed by pulse wave ultrasounds with increasing and decreasing frequencies between 400 and 620 kHz, at burst rates of 0.5, 10, 50 Hz and 50 % duty cycle (percentage of one period in which a signal is active), ultrasound intensities (spatial average-temporal peak) 0.045 and 0.09 W/cm 2 . The sonication durations were 90 and 180 s. Results The decreasing mode was found to be better than the increasing mode for 10 and 50 Hz burst rates, while at 0.5 Hz the increasing mode gave better results for the time of 180 s. For 10 Hz burst rate, decreasing frequency, 180 s, 0.09 W/cm 2 , 20 % survival rate was found; after 6-h incubation, cells showed 13 % of early apoptosis and 11 % of late apoptosis. For these conditions of sonication, the hyperproliferation of cells was inhibited. Conclusion Survival rate decreases for increasing intensity and duration with each burst rate. The best performance is decreasing mode in a range between 620 and 400 kHz, duty cycle 50 %, burst rate 10 Hz. In these conditions after 180 s duration, the average survival rate is 20 %, the survived cells manifest apoptosis after 6-h incubation and hyperproliferation is prevented. The results seem to lead toward a non-invasive and effective purging of leukemic cells.Keywords Low intensity ultrasound Á Cell lysis Á Hyperproliferation apoptosis Á Cell cycle Sommario Scopo Questo studio analizzerà gli effetti meccanici (lisi valutata immediatamente dopo la sonicazione) e gli effetti biologici (sopravvivenza delle cellule, apoptosis e lisi cellulare) su cellule U937 soggette a differenti condizioni di sonicazione con frequenze crescenti e decrescenti, a burst rate (numero di impulsi di un segnale che si ripete in una specifica unità di tempo) variabili, al fine di determinare le migliori condizioni di sonicazione per produrre alta mortalità, apoptosi e inibizione dell'iperproliferazione cellulare. Metodi Le cellule sono state sollecitate con ultrasuoni ad onda pulsata con frequenze crescenti e decrescenti fra 400 e 620 kHz a burst rate di 0.5 Hz, 10 Hz, 50 Hz, con un ciclo di lavoro (frazione di tempo in cui il segnale è attivo in proporzione al tempo totale) del 50 %, intensità (picco spaziale medio-temporale) 0.045 W/cm 2 and 0.09 W/cm 2 . I tempi di sonicazione erano di 90 s e 180 s. Risultati La modalità a frequenza decrescente risultava essere migliore di quella crescente per burst rate 10 Hz e 50 Hz, mentre a 0.5 Hz la modalità a frequenza crescente risultava migliore per un tempo di 180 s. Con un burst rate di 10 Hz, a frequenza decrescente fra 620 e 400 kHz, esposizione per ...

show abstract

Nanotechnology‐Based Systems for Enhancing the Efficacy of Sonodynamic Therapy in Cancer Treatment

Wang,

Nomikou

2024

Advanced Therapeutics

View full text Add to dashboard Cite

Sonodynamic therapy (SDT) is a minimally invasive cancer therapeutic modality that utilizes low‐intensity ultrasound to activate sensitizers for the production of cytotoxic reactive oxygen species (ROS) and the site‐specific ablation of tumors. Compared to conventional cancer treatments, SDT has no adverse side effects, has been shown to radically reduce tumor volume, and has the potential to raise antitumor immune response. Ever‐increasing studies have demonstrated that nanotechnology can significantly enhance the efficacy of SDT against certain cancers and improve its therapeutic effects. Nanosystems are developed that can improve the intratumoral delivery and cellular uptake of sensitizers, can reduce intrinsic cancer defenses against ROS, can act synergistically for the production of ROS and can tackle cancer immune tolerance. In this review, the various strategies to enhance SDT performance with the assistance of nanotechnology, and the outstanding research outcomes, are discussed.

show abstract

Apoptosis induced by the sonomechanical effects of low intensity pulsed ultrasound in a human leukemia cell line

Cited by 133 publications

References 20 publications

Activation of Bak in ultrasound-induced, JNK- and p38-independent apoptosis and its inhibition by Bcl-2

Activation of Bak in ultrasound-induced, JNK- and p38-independent apoptosis and its inhibition by Bcl-2

Study of cellular response induced by low intensity ultrasound frequency sweep pattern on myelomonocytic lymphoma U937 cells

Nanotechnology‐Based Systems for Enhancing the Efficacy of Sonodynamic Therapy in Cancer Treatment

Contact Info

Product

Resources

About