Cold induces reactive oxygen species production and activation of the NF‐kappa B response in endothelial cells and inflammation in vivo

Awad, Ezzat M.; Khan, Shafaat Yar; Sokolikova, Barbora; Brunner, Patrick M.; Olcaydu, Damla; Wojta, Johann; Breuss, Johannes M.; Uhrín, Pavel

doi:10.1111/jth.12357

Cited by 39 publications

(31 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been reported that cold stress increased the production of ROS in animal model and cellular and mitochondrial experiments, respectively (Ali et al 2010;García-Díaz et al 2015;Awad et al 2013). Our results suggest that TRPA1 is mainly involved in the production of ROS via [Ca 2+ ] c elevation pathway induced by cold stress in lung epithelial cell.…”

Section: Production Of Reactive Oxygen Species Is Through the Activatsupporting

confidence: 52%

Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

Sun

Wang

Cao

et al. 2016

Cell Stress and Chaperones

View full text Add to dashboard Cite

Reactive oxygen species (ROS) are responsible for lung damage during inhalation of cold air. However, the mechanism of the ROS production induced by cold stress in the lung is still unclear. In this work, we measured the changes of ROS and the cytosolic Ca 2+ concentration ([Ca 2+ ] c ) in A549 cell. We observed that cold stress (from 20 to 5°C) exposure of A549 cell resulted in an increase of ROS and [Ca 2+ ] c , which was completely attenuated by removing Ca 2+ from medium. Further experiments showed that cold-sensing transient receptor potential subfamily member 1 (TRPA1) agonist (allyl isothiocyanate, AITC) increased the production of ROS and the level of [Ca 2+ ] c in A549 cell. Moreover, HC-030031, a TRPA1 selective antagonist, significantly inhibited the enhanced ROS and [Ca 2+ ] c induced by AITC or cold stimulation, respectively. Taken together, these data demonstrated that TRPA1 activation played an important role in the enhanced production of ROS induced by cold stress in A549 cell.

show abstract

Section: Production Of Reactive Oxygen Species Is Through the Activatsupporting

confidence: 52%

Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

Sun

Wang

Cao

et al. 2016

Cell Stress and Chaperones

View full text Add to dashboard Cite

show abstract

“…To investigate the time course of NF-κB activation in HUVECs in response to TNFα, we assessed the translocation of the NF-κB subunit p65 over the course of two days using a commercially available antibody and fluorescence microscopy. ROS levels were evaluated based on a fluorescence method applying H2-DCF44 and in comparison to control cells.…”

Section: Resultsmentioning

confidence: 99%

“…We employed inhibitors of NF-κB signaling, including PHA-40833 and plumericin34 that target IKK2 (a kinase targeting the inhibitors of NF-κB), and other inhibitors that act against ROS, including the anti-oxidant NAC3536 and diphenyleneiodonium chloride (DPI), a known inhibitor of NADPH oxidase45. We contemporaneously applied TNFα and each of these inhibitors to HUVECs, and measured their effects on translocation of the NF-κB subunit p65 and generation of ROS, using the fluorescent methods described previously44. TNFα-non treated HUVECs incubated with inhibitors were considered as controls.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Premature senescence of endothelial cells upon chronic exposure to TNFα can be prevented by N-acetyl cysteine and plumericin

Khan

Awad

Oszwald

et al. 2017

Sci Rep

107

View full text Add to dashboard Cite

Cellular senescence is characterized by a permanent cell-cycle arrest and a pro-inflammatory secretory phenotype, and can be induced by a variety of stimuli, including ionizing radiation, oxidative stress, and inflammation. In endothelial cells, this phenomenon might contribute to vascular disease. Plasma levels of the inflammatory cytokine tumor necrosis factor alpha (TNFα) are increased in age-related and chronic conditions such as atherosclerosis, rheumatoid arthritis, psoriasis, and Crohn’s disease. Although TNFα is a known activator of the central inflammatory mediator NF-κB, and can induce the intracellular generation of reactive oxygen species (ROS), the question whether TNFα can induce senescence has not been answered conclusively. Here, we investigated the effect of prolonged TNFα exposure on the fate of endothelial cells and found that such treatment induced premature senescence. Induction of endothelial senescence was prevented by the anti-oxidant N-acetyl cysteine, as well as by plumericin and PHA-408, inhibitors of the NF-κB pathway. Our results indicated that prolonged TNFα exposure could have detrimental consequences to endothelial cells by causing senescence and, therefore, chronically increased TNFα levels might possibly contribute to the pathology of chronic inflammatory diseases by driving premature endothelial senescence.

show abstract

“…Os tumores eram avaliados duas a três vezes por semana, tendo seu tamanho indicado em cm 3 . Os camundongos eram eutanasiados após seu crescimento tumoral e tiveram seu RNAm extraído e comparado para a produção de gal-3, onde tumores derivados de células parentais e scramble tiveram expressão semelhante e tumores derivados de células shRNA para gal-3 demonstraram menor expressão do RNAm de gal-3.…”

Section: 17) a Gal-3 Apresenta Alterações Pós-traducionais Em Normóunclassified

Análise da expressão de galectina-3 em células de glioma expostas a condições hipóxicas e seu papel no desenvolvimento de tumores in vivo

Ikemori¹

View full text Add to dashboard Cite

AGRADECIMENTOSAgradeço a todos os que me acompanharam nesta longa jornada, especialmente meus pais, que me apoiaram nestes longos anos de estudo.Agradeço meu orientador, professor doutor Roger Chammas, sem o qual este trabalho nunca teria sido realizado. Aos os meus amigos do grupo de 6) RESULTADOS ______________________________________________536.1) Demonstração da indução de hipóxia _______________________53 6.2) Acúmulo de HIF-1α nuclear _______________________________57 6.3) Distribuição de gal-3 -NG97ht ____________________________59 6.4) Necessidade de fatores intermediários na indução de gal-3 ______66 6.5) Indução de gal-3 dependente de NF-κB _____________________67 6.6) Aumento das formas de ponto isoelétrico mais básico de gal-3 ___69 Sumário 6.7) Detecção de duas isoformas diferentes de gal-3 _______________72 6.8) Aumento da e vacúolos acídicos em hipóxia -NG97ht __________73 6.9) A morte induzida por privação de oxigênio e nutrientes apresenta caráter necrótico -NG97ht ___________________________________75 6.10) Avaliação do knockdown do RNAm de gal-3 -NG97ht _________77 6.11) A participação da gal-3 extracelular -NG97ht _______________79 6.12) Expressão protéica de gal-3 -U251, U87MG e T98G _________81 6.13) Avaliação da indução de gal-3 por q-RT-PCR -U251, U87MG e T98G ____________________________________________________83 6.14) Avaliação das taxas de morte celular -U251, U87MG e T98G __85 6.15) Expressão de gal-3 em privação de oxigênio e nutrientes -U87MG _________________________________________________________87 6.16) Avaliação da localização subcelular de gal-3 -T98G e U87MG _________________________________________________________88 6.17) Gal-3 apresenta alterações pós-traducionais -U87MG ________97 6.18) Aumento de ROS e vacúolos acídicos -U87MG e T98G _______99 6.19) Transdução das células das linhagens T98G e U87MG _______101 6.20) Avaliação da morte em células com knockdown de gal-3 -U87MG e T98G ___________________________________________________103 6.21) Inoculação de células shRNA para gal-3 em camundongos nude proteína é um fator chave na proteção destas células contra a morte celular induzida pela privação de oxigênio e nutrientes, mimetizando condições necróticas de pseudopaliçada in vivo, destacando-se as habilidades antiapoptóticas desta proteína. Embora uma de suas possíveis funções tenha sido elucidada, os mecanismos de atuação e de indução da gal-3 ainda são obscuros. Deste modo, este projeto visa explorar os papéis pró-tumorais da gal-3, podendo torná-la um possível alvo em terapias anti-neoplásicas, entendendo melhor seus mecanismos de proteção contra a morte celular e controle de expressão em ambientes hipóxicos, além de estudar suas possíveis funções in vivo no desenvolvimento de tumores, e também estendendo seus estudos para outras linhagens de glioblastoma. Nossos resultados demonstraram que a gal-3 está co-localizada com mitocôndrias nestas linhagens de glioma, podendo sofrer alterações pós-traducionais em hipóxia, como a fosforilação e que houve acúmulo de HIF-1α nucl...

show abstract

Cold induces reactive oxygen species production and activation of the NF‐kappa B response in endothelial cells and inflammation in vivo

Cited by 39 publications

References 52 publications

Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

Premature senescence of endothelial cells upon chronic exposure to TNFα can be prevented by N-acetyl cysteine and plumericin

Análise da expressão de galectina-3 em células de glioma expostas a condições hipóxicas e seu papel no desenvolvimento de tumores in vivo

Contact Info

Product

Resources

About