Bcl-2 protects against oxidative stress while inducing premature senescence

López‐Díazguerrero, Norma Edith; López-Araiza, Hugo; Conde-Pérezprina, Juan C.; Bucio, Leticia; Cárdenas-Aguayo, María del Carmen; Ventura, Josep L.; Covarrubias, Luis; Gutiérrez‐Ruiz, María Concepción; Zentella, Alejandro; Königsberg, Mina

doi:10.1016/j.freeradbiomed.2005.11.002

Cited by 41 publications

(38 citation statements)

References 47 publications

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“…Various pathways have been proposed to explain senescence induction; the most studied is replicative senescence due to telomere shortening (Cristofalo et al 2004;Rodier et al 2009Rodier et al , 2010, along with other prematureinduced senescence provoked by diverse stimuli such as oxidative stress and radiation exposure (Toussaint et al 2000;López-Diazguerrero et al 2006;Lee et al 2011), autophagy impairment (Kang et al 2011;Fujii et al 2012), proteasome inhibition (Torres et al 2006;Bitto et al 2010), and oncogenic stress (Bartkova et al 2006). Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Lung fibroblasts were obtained according to a protocol previously established (López-Diazguerrero et al 2006); pools of lungs from three animals were used for each cell culture. Cells were grown at 37°C, 5 % CO 2 in MEM supplemented with 10 % FBS (GIBCO-BRL), 100 U/mL penicillin, and 100 μg/mL streptomycin (GIBCO-BRL).…”

Section: Cell Culturementioning

confidence: 99%

“…To prevent quiescence due to contact inhibition, cell cultures that achieved confluence were trypsinized and the entire population was seeded in a larger well (six-well multi-chambers) (Corning, Acton, MA, USA). The entire population of cells in a well was quantified and scored in order to measure the proliferation rate as described elsewhere (López-Diazguerrero et al 2006).…”

Section: Replicative Senescence (Rs)mentioning

confidence: 99%

“…An aliquot of 1 μCi [ 3 H]-thymidine (NEN, USA) was used as previously described (López-Diazguerrero et al 2006). p16 and β-galactosidase immunofluorescence experiments Seven days after isolation, primary lung fibroblasts were trypsinized and seeded on coverslips at a cell density of 3 × 10 3 cells/coverslip.…”

Section: Replicative Senescence (Rs)mentioning

confidence: 99%

“…These pathways can be stimulated by telomere erosion during what has been called replicative senescence (RS) (Blazer et al 2002;Dimri et al 2005); nevertheless, it has been suggested that senescence in vivo might be prematurely attained mainly as a response to different stressors independently of cellular duplications number, i.e., independently of telomere shortening . Senescence can be induced by diverse stimuli such as stress-induced premature senescence (SIPS) after H 2 O 2 treatment (Chen et al 2005;López-Diazguerrero et al 2006), exposition to UV and gamma radiation , or hyperoxia (Toussaint et. al.…”

Section: Introductionmentioning

confidence: 99%

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Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli

Maciel-Barón

Morales-Rosales

Aquino-Cruz

et al. 2016

AGE

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Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as an important feature during tumor suppression mechanisms and a contributor to aging. Senescent cells have an altered secretion pattern called Senescence-Associated Secretory Phenotype (SASP) that comprises a complex mix of factors including cytokines, growth factors, chemokines, and matrix metalloproteinases. SASP has been related with local inflammation that leads to cellular transformation and neurodegenerative diseases. Various pathways for senescence induction have been proposed; the most studied is replicative senescence due to telomere attrition called replicative senescence (RS). However, senescence can be prematurely achieved when cells are exposed to diverse stimuli such as oxidative stress (stressinduced premature senescence, SIPS) or proteasome inhibition (proteasome inhibition-induced premature senescence, PIIPS). SASP has been characterized in RS and SIPS but not in PIIPS. Hence, our aim was to determine SASP components in primary lung fibroblasts obtained from CD-1 mice induced to senescence by PIIPS and compare them to RS and SIPS. Our results showed important variations in the 62 cytokines analyzed, while SIPS and RS showed an increase in the secretion of most cytokines, and in PIIPS only 13 were incremented. Variations in glutathione-redox balance were also observed in SIPS and RS, and not in PIIPS. All senescence types SASP displayed a pro-inflammatory profile and increased proliferation in L929 mice fibroblasts exposed to SASP. However, the behavior observed was not exactly the same, suggesting that the senescence induction pathway might encompass dissimilar responses in adjacent cells and promote different outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

Section: Replicative Senescence (Rs)mentioning

confidence: 99%

Section: Replicative Senescence (Rs)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli

Maciel-Barón

Morales-Rosales

Aquino-Cruz

et al. 2016

AGE

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Bik subcellular localization in response to oxidative stress induced by chemotherapy, in Two different breast cancer cell lines and a Non‐tumorigenic epithelial cell line

Trejo-Vargas

Hernández-Mercado

Ordóñez-Razo

et al. 2015

J of Applied Toxicology

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Cancer chemotherapy remains one of the preferred therapeutic modalities against malignancies despite its damaging side effects. An expected outcome while utilizing chemotherapy is apoptosis induction. This is mainly regulated by a group of proteins known as the Bcl-2 family, usually found within the endoplasmic reticulum or the mitochondria. Recently, these proteins have been located in other sites and non-canonic functions have been unraveled. Bik is a pro-apoptotic protein, which becomes deregulated in cancer, and as apoptosis is associated with oxidative stress generation, our objective was to determine the subcellular localization of Bik either after a direct oxidative insult due to H2 O2 , or indirectly by cisplatin, an antineoplastic agent. Experiments were performed in two human transformed mammary gland cell lines MDA-MB-231 and MCF-7, and one non-tumorigenic epithelial cell line MCF-10A. Our results showed that in MCF-7, Bik is localized within the cytosol and that after oxidative stress treatment it translocates into the nucleus. However, in MDA-MB-231, Bik localizes in the nucleus and translocates to the cytosol. In MCF10A Bik did not change its cellular site after either treatment. Interestingly, MCF10A were more resistant to cisplatin than transformed cell lines. This is the first report showing that Bik is located in different cellular compartments depending on the cancer stage, and it has the ability to change its subcellular localization in response to oxidative stress. This is associated with increased sensitivity when exposed to toxic agents, thus rendering novel opportunities to study new therapeutic targets allowing the development of more active and less harmful agents.

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Biomarkers of Aging

Bai

2018

Advances in Experimental Medicine and Biology

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Biomarkers of aging are a biological parameter that can predict the functional status of an individual in the absence of disease and can be used to better predict morbidity and mortality, compared to using the chronological age alone. Most of aging biomarkers were gene, molecules, and protein, which were found in basic scientific researches, such as telomeres, proteomics, cytokines, etc. However, it is almost impossible for single biomarkers to fully reveal the mechanism of aging. Because of the complexity of aging process, the biomarkers of aging may need to be composed of multiple genes, proteins, and metabolites. The biological age is based on the setting of biological markers, which is a parameter for evaluating the functional status of the individual. Aging is not only dependent on the process of time. The chronological age is only the evaluation indicators of time scale in the aging process. Therefore, biological age can be more representative of the true degree of aging than chronological age, which provides a quantitative standard for individualized aging. According to the factor score, we established biological age score (BAS) = 0.248 (CA) + 0.195 (IMT) - 0.196 (EDV) - 0.167 (E/A) - 0.166 (MVEL) + 0.188 (PP) + 0.182(FIB) + 0.193 (CYSC) through 7 aging biomarkers selected from 108 variables. The study found the rate of aging was gradually increased before the age of 75 years old and afterward entered a stable plateau. In the future, the new approach may be needed to investigate the mechanisms and evaluation of aging.

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Bcl-2 protects against oxidative stress while inducing premature senescence

Cited by 41 publications

References 47 publications

Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli

Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli

Bik subcellular localization in response to oxidative stress induced by chemotherapy, in Two different breast cancer cell lines and a Non‐tumorigenic epithelial cell line

Biomarkers of Aging

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