Inhibition of staurosporine-induced activation of the proapoptotic multidomain Bcl-2 proteins Bax and Bak by three invasive chlamydial species

Zhong, Youmin; Weininger, Marilyn; Pirbhai, Mustak; Dong, Feng; Zhong, Guangming

doi:10.1016/j.jinf.2005.12.028

Cited by 34 publications

(23 citation statements)

References 27 publications

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“…In addition, PorB also did not activate NOD-transfected HEK cells (66; R. Ingalls and P. Massari, unpublished observations). Collectively, similar to findings for Chlamydia trachomatis (20,22,79,80), these observations argue against a major role for NF-B transcriptional activation in the antiapoptotic effect of PorB in HeLa cells (which does not induce IB␣ degradation or p65/RelA nuclear translocation but induces p65 cleavage to interfere with the host inflammatory response) (37). Although the lack of NF-B activation might explain the lack of Bcl-2, Bcl-xL, and c-IAP-2 expression by PorB, induction of Bfl-1 expression might be induced via NF-B-independent transactivation of the bfl-1 gene, similar to what has been described for Burkitt's lymphoma cells with EBV nuclear antigen 2 via CBF1 (or RBP-J kappa), a nuclear component of the Notch signaling pathway (60).…”

Section: Discussionsupporting

confidence: 84%

Meningococcal Porin PorB Prevents Cellular Apoptosis in a Toll-Like Receptor 2- and NF-κB-Independent Manner

et al. 2010

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Meningococcal porin PorB is an inhibitor of apoptosis induced via the intrinsic pathway in various cell types.This effect is attributed to prevention of mitochondrial depolarization and of subsequent release of proapoptotic mitochondrial factors. To determine whether apoptosis is globally inhibited by PorB, we compared the intrinsic and extrinsic pathways in HeLa cells. Interestingly, PorB does not prevent extrinsic apoptosis induced by tumor necrosis factor alpha plus cycloheximide, suggesting a unique mitochondrial pathway specificity.

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Section: Discussionsupporting

confidence: 84%

Meningococcal Porin PorB Prevents Cellular Apoptosis in a Toll-Like Receptor 2- and NF-κB-Independent Manner

et al. 2010

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“…Mammalian cells respond to infection by apoptosis mediated by the proapoptotic members of the Bcl-2 family; BBC3/Puma, DSIPI, Bax, Bak, Bim/Bod, and Bad are involved in the mitochondrion-mediated pathway of apoptosis during human immunodeficiency virus, Sendai virus, and Chlamydia trachomatis infection (2,4,12,18,45,53,55). Infection with both hepatitis C virus and Japanese encephalitis virus induces DDIT3/CHOP expression and sensitizes cells to apoptosis by downregulation of Bcl-2 (4,45).…”

Section: Discussionmentioning

confidence: 99%

Biphasic Modulation of Apoptotic Pathways in Cryptosporidium parvum -Infected Human Intestinal Epithelial Cells

et al. 2009

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The impact of Cryptosporidium parvum infection on host cell gene expression was investigated by microarray analysis with an in vitro model using human ileocecal HCT-8 adenocarcinoma cells. We found changes in 333 (2.6%) transcripts at at least two of the five (6, 12, 24, 48, and 72 h) postinfection time points. Fifty-one of the regulated genes were associated with apoptosis and were grouped into five clusters based on their expression patterns. Early in infection (6 and 12 h), genes with antiapoptotic roles were upregulated and genes with apoptotic roles were downregulated. Later in infection (24, 48, and 72 h), proapoptotic genes were induced and antiapoptotic genes were downregulated, suggesting a biphasic regulation of apoptosis: antiapoptotic state early and moderately proapoptotic state late in infection. This transcriptional profile matched the actual occurrence of apoptosis in the infected cultures. Apoptosis was first detected at 12 h postinfection and increased to a plateau at 24 h, when 20% of infected cells showed nuclear condensation. In contrast, experimental silencing of Bcl-2 induced apoptosis in 50% of infected cells at 12 h postinfection. This resulted in a decrease in the infection rate and a reduction in the accumulation of meront-containing cells. To test the significance of the moderately proapoptotic state late in the infection, we inhibited apoptosis using pancaspase inhibitor Z-VAD-FMK. This treatment also affected the progression of C. parvum infection, as reinfection, normally seen late (24 h to 48 h), did not occur and accumulation of mature meronts was impaired. Control of host apoptosis is complex and crucial to the life of C. parvum. Apoptosis control has at least two components, early inhibition and late moderate promotion. For a successful infection, both aspects appear to be required.

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“…This mechanism has been studied extensively in Chlamydia [12][13][14]. Infected epithelial cells were exposed to either staurosporine (STS) or ultraviolet (UV) irradiation to determine if the bacteria can prevent apoptosis induced by these stimuli.…”

Section: Protection Of the Mitochondria And Prevention Of Cytochrome mentioning

confidence: 99%

“…Initially, it was discovered that Chlamydia trachomatis inhibits the pro-apoptotic host proteins Bax and Bak and prevents them from permeabilizing the mitochondrial membrane. Cytochrome c release and subsequent caspase activation are inhibited in infected cells [12]. Further research indicated that Chlamydia targets pro-apoptotic proteins with a BH3 domain (i.e.…”

Section: Protection Of the Mitochondria And Prevention Of Cytochrome mentioning

confidence: 99%

Staying alive: bacterial inhibition of apoptosis during infection

Faherty

Maurelli

2008

Trends in Microbiology

132

108

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The ability of bacterial pathogens to inhibit apoptosis in eukaryotic cells during infection is an emerging theme in the study of bacterial pathogenesis. Prevention of apoptosis provides a survival advantage because it enables the bacteria to replicate inside host cells. Bacterial pathogens have evolved several ways to prevent apoptosis by protecting the mitochondria and preventing cytochrome c release, by activating cell survival pathways, or by preventing caspase activation. This review summarizes the most recent work on bacterial anti-apoptotic strategies and suggests new research that is necessary to advance the field.

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Inhibition of staurosporine-induced activation of the proapoptotic multidomain Bcl-2 proteins Bax and Bak by three invasive chlamydial species

Cited by 34 publications

References 27 publications

Meningococcal Porin PorB Prevents Cellular Apoptosis in a Toll-Like Receptor 2- and NF-κB-Independent Manner

Meningococcal Porin PorB Prevents Cellular Apoptosis in a Toll-Like Receptor 2- and NF-κB-Independent Manner

Biphasic Modulation of Apoptotic Pathways in Cryptosporidium parvum -Infected Human Intestinal Epithelial Cells

Staying alive: bacterial inhibition of apoptosis during infection

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