Apoptosis, Cell Death and Inflammation

Witko‐Sarsat, Véronique

doi:10.1159/000296505

Cited by 10 publications

(10 citation statements)

References 38 publications

(20 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Apoptosis is the principal mechanism by which cells are physiologically eliminated in metazoan organisms (7). During apoptotic death, cells are digested by caspases and packaged into apoptotic bodies as a mechanism to avoid immune activation.…”

Section: Introductionmentioning

confidence: 99%

“…During apoptotic death, cells are digested by caspases and packaged into apoptotic bodies as a mechanism to avoid immune activation. Necrosis, previously hypothesized as a passive, unorganized method of cell death, has emerged as an alternate form of programmed cell death whose activation may have important biological consequences, including the induction of an inflammatory response (7). Autophagy has also been reported as a possible mechanism for non-apoptotic death despite evidence from a number of species showing that autophagy represents a survival strategy in times of stress.…”

Section: Introductionmentioning

confidence: 99%

“…Autophagy has also been reported as a possible mechanism for non-apoptotic death despite evidence from a number of species showing that autophagy represents a survival strategy in times of stress. Recent advances have been important for the definition of the function and mechanism of programmed necrosis and the role of autophagy in cell survival and suicide (7). …”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of autophagy by 3-MA enhances endoplasmic reticulum stress-induced apoptosis in human nasopharyngeal carcinoma cells

Song

Liu

et al. 2013

Oncology Letters

View full text Add to dashboard Cite

Radiotherapy and adjuvant cisplatin chemotherapy are the mainstream treatments for nasopharyngeal carcinoma (NPC), which effectively improve the outcome and reduce tumor recurrence. However, the resistance mechanism(s) involved in radiotherapy and chemotherapy, which is the main barrier in NPC treatment, remains undefined. Therefore, there is an urgent requirement for the identification of new therapeutic strategies or adjuvant drugs. In the present study, the effects of autophagy inhibitors on endoplasmic reticulum (ER) stress-induced autophagy was investigated. Combining 3-methyladenine (3-MA) with cisplatin (DDP), ionizing radiation (IR), 2-deoxy-D-glucose (2-DG) or tunicamycin (TM) resulted in enhanced cell death, as revealed by MTT and colony formation assays. Flow cytometry results demonstrated that the sensitivity of NPC cells to DDP- and IR-induced apoptosis was not significant. DDP, IR, 2-DG and TM induced ER stress and autophagy. Using fluorescence microscopy, 3-MA was identified to increase the apoptotic cell death induced by DDP, IR, 2-DG or TM. In addition, 3-MA inhibited the increased autophagy induced by DDP, IR, 2-DG or TM, as demonstrated by western blot analysis and immunocytochemistry results. Results of the present study indicate that autophagy acts as a protective mechanism response to the apoptosis induced by DDP, IR, 2-DG or TM.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of autophagy by 3-MA enhances endoplasmic reticulum stress-induced apoptosis in human nasopharyngeal carcinoma cells

Song

Liu

et al. 2013

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…Importantly, we found that the bacterial GroEL, but not self-HSP60, could generate CD4 + CD25 + Foxp3 + T cells from naïve T cells, indicating that the production of Treg cells depends on the type of HSP. Taken together, our findings imply that the exogenous HSPs derived from gut microflora can constitutively function as a regulatory factor to control immune homeostasis at peripheral mucosal sites, providing a link between innate and adaptive immune systems [36][37][38] .…”

Section: Discussionmentioning

confidence: 64%

Bacterial Heat Shock Protein 60, GroEL, Can Induce the Conversion of Naïve T Cells into a CD4+ CD25+ Foxp3-Expressing Phenotype

Ohue¹,

Hashimoto²,

Nakamoto³

et al. 2011

J Innate Immun

View full text Add to dashboard Cite

Recent publications report that heat shock proteins (HSPs) can endow regulatory responses to the systemic immune system when administered via the mucosal route, leading to an amelioration of atherosclerosis and allergy. However, it remains poorly understood if HSP antigens exist in the luminal contents of the gastrointestinal tract and which types of HSP induce regulatory responses. Here we addressed these problems, considering that numerous gut microflora and foods are natural sources of HSPs. SDS-PAGE and immunoblotting with the anti-HSP60 antibody demonstrated the intact and degraded forms of HSP60 mainly in appendix and large intestine of the gastrointestinal tract. No reactivity with this antibody was observed for any of the luminal contents derived from germ-free animals, suggesting gut microflora to be a source of the intestinal HSPs because of lack of HSPs in animal chow diet. GroEL, a typical member of bacterial HSP60, showed a tendency to stimulate splenocytes in germ-free mice, compared to that in conventional mice, suggesting that resident commensal bacterial GroEL may stimulate HSP-reactive T cells as regulatory cells in conventional animals. Importantly, GroEL, but not mouse-derived HSP60, caused naïve T cells to differentiate into CD4⁺ CD25⁺ Foxp3⁺ T cells, indicating that the production of regulatory T cells depends on the type of HSP. Thus, HSPs derived from commensal microbes can be utilized to stimulate immunoregulatory pathways for the maintenance of intestinal homeostasis.

show abstract

“…Rapamycin blocks the signals of multiple cytokines and inhibits the calcium-dependent and -independent signaling pathways in T and B lymphocytes, thereby suppressing the immune response and inflammation. Inflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), can induce apoptosis in different cell types [17]. Rapamycin has been found to increase autophagy by inhibition of the mammalian target of rapamycin (mTOR) [18,19].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Autophagy Induced by Rapamycin in Rat Acute Spinal Cord Injury Model

Wang

Liu

Muharram

et al. 2014

Neuroimmunomodulation

View full text Add to dashboard Cite

Background/Aims: To explore the effects of rapamycin-induced autophagy on apoptosis in a rat model of acute spinal cord injury (SCI), and to explore the effect of rapamycin on apoptosis in primary spinal cord cell culture. Methods: SCI was induced at T10 in female adult Sprague-Dawley rats. After injury was induced, the rats were injected with rapamycin and/or methylprednisolone and were sacrificed at various days after injury. Apoptosis and autophagy were examined with TUNEL staining and electron microscopy. Hind limb function was assessed by the Gale scale. Results: The expression of the apoptosis-related protein caspase-3 did not significantly increase until 21 days following injury, while increases in LC3II and LC3I began 10 days after injury, but then declined. TUNEL staining and electron microscopy confirmed that following injury autophagy occurred before apoptosis, but by 14 days after the injury, the level of autophagy had decreased significantly while the level of apoptosis showed a continued increase. Following treatment with rapamycin, apoptosis was significantly higher than in the vehicle control group, but significantly lower than in the sham-operated group, showing a protective effect of rapamycin. Gale scale grades in rats treated with rapamycin were significantly higher compared with the vehicle control group, suggesting a functional effect of rapamycin-induced inhibition of apoptosis. Conclusions: The results indicate thatrapamycin significantly improved the prognosis of acute SCI in rats by inhibiting cell apoptosis. Rapamycin might be useful as a therapeutic agent for acute SCI.

show abstract

Apoptosis, Cell Death and Inflammation

Cited by 10 publications

References 38 publications

Inhibition of autophagy by 3-MA enhances endoplasmic reticulum stress-induced apoptosis in human nasopharyngeal carcinoma cells

Inhibition of autophagy by 3-MA enhances endoplasmic reticulum stress-induced apoptosis in human nasopharyngeal carcinoma cells

Bacterial Heat Shock Protein 60, GroEL, Can Induce the Conversion of Naïve T Cells into a CD4+ CD25+ Foxp3-Expressing Phenotype

Neuroprotective Effects of Autophagy Induced by Rapamycin in Rat Acute Spinal Cord Injury Model

Contact Info

Product

Resources

About