Organ- and Tissue-specific Alterations in the Anti-apoptotic Protein Bcl-2 in CD1 Female Mice of Different Ages

López-Araiza, Hugo; Ventura, Josep L.; López‐Díazguerrero, Norma Edith; González‐Márquez, Humberto; Gutiérrez‐Ruiz, María Concepción; Zentella, Alejandro; Königsberg, Mina

doi:10.1007/s10522-005-6038-x

Cited by 9 publications

(6 citation statements)

References 22 publications

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“…Findings from the current study show that resistance exercise induced an increase in beclin-1, which was accompanied by decreased Bcl-2 and Bcl-xL protein concentration. It is important to note that several authors have shown that the expression of Bcl-2 and Bcl-xL increases with aging in many tissues [11,42]. Furthermore, the relative Bad/Bcl-2 ratio, a parameter of apoptotic cell death, decreased with the training program.…”

Section: Discussionmentioning

confidence: 98%

Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects

Mejías-Peña

Estébanez

Rodriguez‐Miguelez

et al. 2017

Aging

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Aging is associated with a decline in autophagy and a state of low-grade inflammation which further affects apoptosis and autophagy. Importantly, these alterations could reverse with regular physical activity. This study assessed the effects of a resistance exercise training program on autophagy, NLRP3 inflammasome, and apoptosis in peripheral blood mononuclear cells (PBMCs) from old subjects. Twenty-six healthy women and men (age, 69.6±1.5 yr) were randomized to a training (TG) or a control (CG) group. TG performed an 8-week resistance training program, while CG followed their daily routines. Protein expression of beclin-1, Atg12, Atg16 and LAMP-2 increased following the training program, while expression of p62/SQSTM1 and phosphorylation of ULK-1 at Ser757 were significantly lower. Resistance exercise also induced a decrease in NLRP3 expression and in the caspase-1/procaspase-1 ratio. Expression of Bcl-2 and Bcl-xL, as well as the Bad/BcL-2 ratio were reduced, and there was a significant decrease in the protein content of caspase-3. The results obtained seem to indicate that 8-week resistance training stimulates autophagy, prevents NLRP3 inflammasome activation, and reduces apoptosis in PBMCs from elderly subjects. These data could have a significant impact in prevention and rehabilitation programs currently employed in elderly population.

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Section: Discussionmentioning

confidence: 98%

Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects

Mejías-Peña

Estébanez

Rodriguez‐Miguelez

et al. 2017

Aging

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“…Small variations in Bcl2 levels can capture tissue specific variations as well as variations during various developmental stages [43]. Bcl2 over-expression (3-fold) resulted in inhibition of Bax activation and slightly delayed release of mitochondrial cytochrome c. Subsequent formation of XIAP-Smac and apoptosome complex were also delayed.…”

Section: Resultsmentioning

confidence: 99%

Monte Carlo Study Elucidates the Type 1/Type 2 Choice in Apoptotic Death Signaling in Healthy and Cancer Cells

Raychaudhuri

2013

Cells

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Apoptotic cell death is coordinated through two distinct (type 1 and type 2) intracellular signaling pathways. How the type 1/type 2 choice is made remains a central problem in the biology of apoptosis and has implications for apoptosis related diseases and therapy. We study the problem of type 1/type 2 choice in silico utilizing a kinetic Monte Carlo model of cell death signaling. Our results show that the type 1/type 2 choice is linked to deterministic versus stochastic cell death activation, elucidating a unique regulatory control of the apoptotic pathways. Consistent with previous findings, our results indicate that caspase 8 activation level is a key regulator of the choice between deterministic type 1 and stochastic type 2 pathways, irrespective of cell types. Expression levels of signaling molecules downstream also regulate the type 1/type 2 choice. A simplified model of DISC clustering elucidates the mechanism of increased active caspase 8 generation and type 1 activation in cancer cells having increased sensitivity to death receptor activation. We demonstrate that rapid deterministic activation of the type 1 pathway can selectively target such cancer cells, especially if XIAP is also inhibited; while inherent cell-to-cell variability would allow normal cells stay protected.

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“…The aged cells were acquired resistance to certain apoptotic molecules such as bcl-2 expression (López-Araiza et al 2006). Bcl-2 gene expression is regulated by c-myb (Weston 1998).…”

Section: Discussionmentioning

confidence: 99%

“…However, many authors reported that ageing cells show more resistance and an increased cell survival ratio against oxidative stress (Yeo et al 2000;Suh et al 2002;Lee et al 2008Lee et al , 2009. Aged cells have the capacity to survive environmental stress by altering many types of changeable gene such as bcl-2 and Hsp60 (López-Araiza et al 2006;Lee et al 2008). It was previously reported that aged cells have a higher cell survival capacity to oxidative stress, which involves a blockage of the translocation of Hsp60 followed by SAPK/JNK inactivation, than young cells (Lee et al , 2009.…”

Section: Introductionmentioning

confidence: 99%

c-myb has a character of oxidative stress resistance in aged human diploid fibroblasts: regulates SAPK/JNK and Hsp60 pathway consequently

Lee

Bhattarai

et al. 2009

Biogerontology

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This study examined whether c-myb acts as a survival molecule in aged cells. A previous in vitro ageing model suggested that aged cells have a higher cell capacity for survival after exposure to oxidative stress, which involves blockage of the translocation of Hsp60 from the mitochondria to the cytoplasm followed by SAPK/JNK inactivation, than young cells. In human diploid fibroblasts (HDFs), c-myb expression increased gradually with ageing, and this increase had a significant influence on the cell survival capacity after exposure to oxidative stress. To clarify the role of c-myb in oxidative stress, young cells under 21 passages, which lacked c-myb expression, were transfected with adenovirus-mediated c-myb for express c-myb. These c-myb-over-expressed young cells showed increased cell viability upon exposure to oxidative stress to a similar extent to that of the aged cells. In addition, these c-myb-over-expressed young cells did not exhibit SAPK/JNK activation, Hsp60 displacement and cytochrome C release, as was observed in aged cells. The aged cells that had c-myb suppressed using siRNA c-myb showed reduced cell viability and increased apoptosis in a manner to that observed in young cells. From this study, c-myb blocked SAPK/JNK and Hsp60 translocation upon exposure to oxidative stress. This result suggests that c-myb might act as a modulator of cell survival in the ageing process by suppressing apoptosis in aged cells.

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Organ- and Tissue-specific Alterations in the Anti-apoptotic Protein Bcl-2 in CD1 Female Mice of Different Ages

Cited by 9 publications

References 22 publications

Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects

Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects

Monte Carlo Study Elucidates the Type 1/Type 2 Choice in Apoptotic Death Signaling in Healthy and Cancer Cells

c-myb has a character of oxidative stress resistance in aged human diploid fibroblasts: regulates SAPK/JNK and Hsp60 pathway consequently

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