Severe, short-duration (0–3 min) heat shocks (50–52°C) inhibit the repair of DNA damage

Roti, Joseph L. Roti; Pandita, Raj K.; Mueller, Jason D; Novák, Péter; Moros, Eduardo G.; Laszlo, Andrei

doi:10.3109/02656730903417947

Cited by 15 publications

(5 citation statements)

References 35 publications

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“…2c) are shown. The γH2AX foci and the γH2AX uorescence intensity increased under all procedures in the thermal controls showing that heating the HeLa cells by 5 ºC induces DSBs and inhibits their repair, which is consistent with previous reports 14,15 .…”

supporting

confidence: 92%

Non-thermal effect of terahertz wave radiation on DNA damage repair in living cells

Harata¹,

Ueno²,

Yamazaki

et al. 2023

Preprint

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DNA damage, which is constantly caused by exogenous and endogenous factors, is subject to immediate repair processes; delays in these repair processes cause diseases. Here, we demonstrated that terahertz irradiation enhances the repair processes of DNA double-strand break by a non-thermal effect. The modulation of DNA damage repair by terahertz irradiation provides a non-invasive method with potential medical applications, such as prevention and suppression of diseases caused by DNA instability.

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supporting

confidence: 92%

Non-thermal effect of terahertz wave radiation on DNA damage repair in living cells

Harata¹,

Ueno²,

Yamazaki

et al. 2023

Preprint

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“…Further, heat-induced HSP70 expression varies significantly with cell types [60,61,62,63,64]. Heat shocks (45 °C) for a brief period (10 -30 min) were reported to cause cell death [7,17]. However, when the cells were allowed to recover at 37 °C, the cells experienced more senescence than the loss of cell viability [7,65].…”

Section: Hyperthermia Causes G1 Arrest and Triggers Both Senescence Amentioning

confidence: 99%

“…Though human body temperature limits within 40 °C during heat stroke or fever, most of the studies reported the cellular effects of hyperthermia at 42 to 47 °C [7,17] Importantly, the human body is subjected to prolonged heat during summers and adverse working conditions; therefore, the cellular effects of the prolonged hyperthermia at a physiologically relevant temperature (40 °C) need to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Hyperthermia induced disruption of mechanical balance leads to G1 arrest and senescence in cells

Mundhara

Majumder

Panda

2021

Biochemical Journal

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Human body temperature limits below 40°C during heat stroke or fever. The implications of prolonged exposure to the physiologically relevant temperature (40°C) on cellular mechanobiology is poorly understood. Here, we have examined the effects of heat stress (40°C for 72 h incubation) in human lung adenocarcinoma (A549), mouse melanoma (B16F10), and non-cancerous mouse origin adipose tissue cells (L929). Hyperthermia increased the level of ROS, γ-H2AX and HSP70 and decreased mitochondrial membrane potential in the cells. Heat stress impaired cell division, caused G1 arrest, induced cellular senescence, and apoptosis in all the tested cell lines. The cells incubated at 40°C for 72 h displayed a significant decrease in the f-actin level and cellular traction as compared with cells incubated at 37°C. Also, the cells showed a larger focal adhesion area and stronger adhesion at 40°C than at 37°C. The mitotic cells at 40°C were unable to round up properly and displayed retracting actin stress fibers. Hyperthermia down-regulated HDAC6, increased the acetylation level of microtubules, and perturbed the chromosome alignment in the mitotic cells at 40°C. Overexpression of HDAC6 rescued the cells from the G1 arrest and reduced the delay in cell rounding at 40°C suggesting a crucial role of HDAC6 in hyperthermia mediated responses. This study elucidates the significant role of cellular traction, focal adhesions, and cytoskeletal networks in mitotic cell rounding and chromosomal misalignment. It also highlights the significance of HDAC6 in heat-evoked senile cellular responses.

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“…The THz power density must not be too high to avoid detrimental thermal effects on the sample. Many studies have shown the effect of heating on cells, such as tissue damage [ 23 , 24 ], heat-induced cellular death [ 25 , 26 ], and DNA damage [ 27 , 28 ]. Thus, the THz beam should not be focused tightly to prevent an increase in the temperature on the sample.…”

Section: Introductionmentioning

confidence: 99%

THz irradiation inhibits cell division by affecting actin dynamics

et al. 2021

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Biological phenomena induced by terahertz (THz) irradiation are described in recent reports, but underlying mechanisms, structural and dynamical change of specific molecules are still unclear. In this paper, we performed time-lapse morphological analysis of human cells and found that THz irradiation halts cell division at cytokinesis. At the end of cytokinesis, the contractile ring, which consists of filamentous actin (F-actin), needs to disappear; however, it remained for 1 hour under THz irradiation. Induction of the functional structures of F-actin was also observed in interphase cells. Similar phenomena were also observed under chemical treatment (jasplakinolide), indicating that THz irradiation assists actin polymerization. We previously reported that THz irradiation enhances the polymerization of purified actin in vitro; our current work shows that it increases cytoplasmic F-actin in vivo. Thus, we identified one of the key biomechanisms affected by THz waves.

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Severe, short-duration (0–3 min) heat shocks (50–52°C) inhibit the repair of DNA damage

Cited by 15 publications

References 35 publications

Non-thermal effect of terahertz wave radiation on DNA damage repair in living cells

Non-thermal effect of terahertz wave radiation on DNA damage repair in living cells

Hyperthermia induced disruption of mechanical balance leads to G1 arrest and senescence in cells

THz irradiation inhibits cell division by affecting actin dynamics

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