T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

Chen, Jinghong; Cao, Junling; Chu, Yangyang; Wang, Zhilun; Yang, Zhantian; Wang, Honglin

doi:10.1631/jzus.b0820013

Cited by 78 publications

(50 citation statements)

References 26 publications

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“…In contrast to other studies [30,31], neither caspase-3 nor Fas were detectable in the type of the human chondrocytes investigated. Still apoptosis was observed at a rate of 18% in monolayer cultures and 10% in microgravity cultures.…”

Section: Apoptosiscontrasting

confidence: 99%

Characterization of Human Chondrocytes Exposed to Simulated Microgravity

Ulbrich

Westphal²,

Pietsch³

et al. 2010

Cell Physiol Biochem

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Background: Tissue engineering is a strategy of cartilage regeneration, but scaffolds, required for 3D growth of chondrocytes, are still a problem. Methods: Searching for possibilities to improve scaffold-free engineering of cartilage, we characterized human chondrocytes incubated on a random positioning machine (RPM) to simulate microgravity (µg). Results: When cultured in simulated µg, human chondrocytes start forming 3D cell assemblies within 5 days. After 24h, we could not detect caspase-3, Fas, p53 or Bcl-2 proteins in these cells, Annexin V flow cytometry, however, revealed 18% of apoptotic chondrocytes in 1g cultures but only 10% on the RPM. Both rates of apoptosis were not changed, when vascular endothelial growth factor (VEGF) or basic fibroblast growth factor (bFGF) was added. 24 h, simulated microgravity also had significantly decreased collagen type I and X, but did not change collagen type IV and laminin, while collagen type II, chondroitin sulfate and aggrecan were elevated as compared with 1g controls. The production of collagen type II/X, chondroitin sulfate and aggrecan was modified, when external bFGF or VEGF had been applied. Conclusion: Chondrocytes exposed to simulated µg seem to change their extracellular matrix production behavior, while they rearrange their cytoskeletal proteins prior to forming 3D aggregates.

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Section: Apoptosiscontrasting

confidence: 99%

Characterization of Human Chondrocytes Exposed to Simulated Microgravity

Ulbrich

Westphal²,

Pietsch³

et al. 2010

Cell Physiol Biochem

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“…Western blot analysis was done as previously described with minor modifications to detect the expressions of caspases-3, PARP, Bcl-2, Bcl-xL, Bad, Bax, and survivin proteins (Chen et al, 2008). After treatment for 24 h, the cells were washed thrice with ice-cold PBS.…”

Section: Western Blot Analysismentioning

confidence: 99%

Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Wang

Zheng

et al. 2009

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate the effects of curcumin on release of cytochrome c and expressions of Bcl-2, Bax, Bad, Bcl-xL, caspase-3, poly ADP-ribose polymerase (PARP), and survivin of HT-29 cells. Methods: HT-29 cells were treated with curcumin (0~80 μmol/L) for 24 h. The release of cytochrome c from the mitochondria and the apoptosis-related proteins Bax, Bcl-2, Bcl-xL, Bad, caspase-3, PARP, and survivin were determined by Western blot analysis and their mRNA expressions by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Curcumin significantly induced the growth inhibition and apoptosis of HT-29 cells. A decrease in expressions of Bcl-2, Bcl-xL and survivin was observed after exposure to 10~80 μmol/L curcumin, while the levels of Bax and Bad increased in the curcumin-treated cells. Curcumin also induced the release of cytochrome c, the activation of caspase-3, and the cleavage of PARP in a dose-dependent manner. Conclusion: These data suggest that curcumin induced the HT-29 cell apoptosis possibly via the mitochondria-mediated pathway.

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“…Recent cytotoxicological studies, most of them employing human cell lines, have shown that trichothecenes are able to trigger intracellular pathways leading to apoptosis and necrotic processes (Bouaziz et al 2008;Chen et al 2008;Islam et al 2008;Königs et al 2008;Pestka 2008). The elucidation of the mechanisms of toxicity has focused on differential responses of mRNA and proteins following in vitro exposure.…”

Section: Introductionmentioning

confidence: 99%

Trichothecene-induced cytotoxicity on human cell lines

et al. 2009

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Trichothecene cytotoxicity of type A (T-2 toxin and HT-2 toxin), type B (deoxynivalenol, DON, and nivalenol, NIV), and type D (satratoxins G and H) compounds was determined comparatively by using eight permanent human cell lines (Hep-G2, A549, CaCo-2, HEp-2, A204, U937, RPMI 8226, and Jurkat). Viability of cells was measured by a water-soluble tetrazolium (WST-1) reagent cell proliferation assay assessing mitochondrial metabolic activity. Toxicity was expressed as the toxin concentration inhibiting 50% of cell viability (IC50). Depending on the chemotype of the tested trichothecenes, relative cytotoxic activity differed by a factor of 100-1,000, and the corresponding IC50 values were in the range from 2.2 nmol/l (satratoxin H on Jurkat and U937 cells) to 4,900 nmol/l (deoxynivalenol on HEp-2 cells). In contrast, the specific toxicity of each individual mycotoxin towards different cell lines was within remarkable close limits, and between-cell line differences were much smaller than previously reported. For the cell lines tested, IC50 values were 4.4-10.8 nmol/l for T-2 toxin, 7.5-55.8 mol/l for HT-2 toxin, 600-4,900 nmol/l for DON, 300-2,600 nmol/l for NIV, and 2.2-18.3 nmol/l for satratoxins G/H. In addition, for the first time, the toxic activity of trichothecenes on primary cell culture of human endothelial cells (HUVEC) was tested. The susceptibility of this cell line was comparable to the other cell lines tested, with IC50 values ranging from 16.5 nmol/l (T-2 toxin) to 4,500 nmol/l (DON). The results suggest that the current focus of cytotoxicological studies on trichothecenes on lymphoid cell lines may lead to an underestimate of their potential on other target cell systems.

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T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

Cited by 78 publications

References 26 publications

Characterization of Human Chondrocytes Exposed to Simulated Microgravity

Characterization of Human Chondrocytes Exposed to Simulated Microgravity

Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Trichothecene-induced cytotoxicity on human cell lines

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