Manipulating the mitochondria activity in human hepatic cell line Huh7 by low-power laser irradiation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F18%3A00493199" target="_blank" >RIV/68378041:_____/18:00493199 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378271:_____/18:00489933 RIV/00023001:_____/18:00076546

Výsledek na webu

<a href="http://dx.doi.org/10.1364/BOE.9.001283" target="_blank" >http://dx.doi.org/10.1364/BOE.9.001283</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1364/BOE.9.001283" target="_blank" >10.1364/BOE.9.001283</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Manipulating the mitochondria activity in human hepatic cell line Huh7 by low-power laser irradiation

Popis výsledku v původním jazyce

Low-power laser irradiation of red light has been recognized as a promising tool across a vast variety of biomedical applications. However, deep understanding of the molecular mechanisms behind laser-induced cellular effects remains a significant challenge. Here, we investigated mechanisms involved in the death process in human hepatic cell line Huh7 at a laser irradiation. We decoupled distinct cell death pathways targeted by laser irradiations of different powers. Our data demonstrate that high dose laser irradiation exhibited the highest levels of total reactive oxygen species production, leading to cyclophilin D-related necrosis via the mitochondrial permeability transition. On the contrary, low dose laser irradiation resulted in the nuclear accumulation of superoxide and apoptosis execution. Our findings offer a novel insight into laser-induced cellular responses, and reveal distinct cell death pathways triggered by laser irradiation. The observed link between mitochondria depolarization and triggering ROS could be a fundamental phenomenon in laser-induced cellular responses.

Název v anglickém jazyce

Manipulating the mitochondria activity in human hepatic cell line Huh7 by low-power laser irradiation

Popis výsledku anglicky

Low-power laser irradiation of red light has been recognized as a promising tool across a vast variety of biomedical applications. However, deep understanding of the molecular mechanisms behind laser-induced cellular effects remains a significant challenge. Here, we investigated mechanisms involved in the death process in human hepatic cell line Huh7 at a laser irradiation. We decoupled distinct cell death pathways targeted by laser irradiations of different powers. Our data demonstrate that high dose laser irradiation exhibited the highest levels of total reactive oxygen species production, leading to cyclophilin D-related necrosis via the mitochondrial permeability transition. On the contrary, low dose laser irradiation resulted in the nuclear accumulation of superoxide and apoptosis execution. Our findings offer a novel insight into laser-induced cellular responses, and reveal distinct cell death pathways triggered by laser irradiation. The observed link between mitochondria depolarization and triggering ROS could be a fundamental phenomenon in laser-induced cellular responses.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/LO1309" target="_blank" >LO1309: Buněčná terapie a tkáňové náhrady</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biomedical Optics Express

ISSN

2156-7085

e-ISSN

—

Svazek periodika

9

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

18

Strana od-do

1283-1300

Kód UT WoS článku

000426743300028

EID výsledku v databázi Scopus

2-s2.0-85042686703