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1

Scutellarein ameliorates tongue cancer cells via mitochondria

100%

Jing G., Zheng J., Wang X., Li H., Jiao X.

Open Medicine

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2014

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vol. 9

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issue 2

193-199

EN

To investigate the mechanism in Scutellarein-induced apoptosis of SAS human tongue cancer cells, inhibitory effects of Scutellarein on SAS cells were detected by MTT assay. Cell apoptosis was analyzed by flow cytometry. Ultrastructural changes of SAS cells were observed by transmission electron microscopy (TEM). Mitochondrial transmembrane potential (ΔΨm) were analyzed by JC-1 [5,5,6,6-Tetrachloro-1,1,3,3-tetraethylbenzimidazolylcarbocyanine iodide]. Western blotting was used to examine the expression level of Bcl-2, Bax and caspase-3 in SAS cells treated with Scutellarein. Scutellarein inhibited the proliferation of SAS cells in a time and dose-dependent manner and increased the percent of apoptotic cells. The mitochondrial cristae were swollen and had vacuolar degeneration. ΔΨm decreased when the concentration of scutellarein increased. Scutellarein effectively up-regulated the expression of mitochondrial Bax and caspase-3 and down-regulated the expression of Bcl-2. Scutellarein induces apoptosis of SAS human tongue cancer cells via activating mitochondrial signaling pathway.

2

Vimentin cleavage in end-stage renal disease is not related to apoptosis

100%

Liebscher F., Arnold T., Liang Y., Reiter T., Böhmig G., Oehler R.

Open Medicine

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2013

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vol. 8

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issue 3

297-301

EN

Anti-vimentin auto-antibodies contribute to chronic allograft nephropathy. They exist in sera of end-stage renal disease patients on hemodialysis (ESRD) already before renal transplantation. We found recently that a 49 kDa vimentin fragment is increased in lymphocytes of ESRD patients which is presented on the cell surface. In vitro studies showed that such a fragment is formed during apoptosis by active caspase-3. We hypothesized that vimentin degradation in leukocytes of ESRD patients correlates to caspase-3 activation in vivo. Lymphocytes and monocytes were isolated from ESRD patients and from healthy volunteers and analyzed for vimentin expression and caspase-3 activation. In addition, apoptosis was induced in vitro and quantified by flow cytometry. ESRD monocytes have shown only the full length 60 kDa vimentin isoform. ESRD lymphocytes, however, showed in addition a strongly increased expression of the 49 kDa vimentin in all samples. Caspase-3 activation was found in 60% of ESRD lymphocytes and 66% of ESRD monocytes but not in healthy volunteers. UV-mediated induction of apoptosis was not associated with vimentin degradation. These experiments could confirm increased vimentin degradation in ESRD lymphocytes. However, we could not validate any correlation to apoptosis.

3

LDOC-1 and PARP-1 mRNA expression in leukocytes of father and son with cutaneous malignant melanoma

88%

Salemi M., Soma P., Condorelli R., Recupero D., Calogero A.

Open Medicine

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2013

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vol. 8

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issue 2

204-207

EN

Apoptosis is central to the biology of cutaneous malignant melanoma (CMM). The leucine zipper, down regulated in cancer 1 (LDOC-1) gene, is known to be a regulator of the nuclear factor kappa B (NF-kB) through inhibition of the same NF-kB. The poly (ADP-ribose) polymerase-1 (PARP1) gene plays an important role for the efficient maintenance of genome integrity. PARP-1 protein is required for the apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus. We report here two interesting cases of family melanoma, a father and son 84 and 40 years old, respectively. The histological evaluation of the lesions of both men revealed diffused superficial melanoma with epithelioid cells. We evaluated the differential expression of LDOC-1 and PARP-1 mRNA in peripheral blood leukocytes of both the father and son. We found that both LDOC-1 and PARP-1 genes were down-regulated in both patients compared with those of controls. These data suggest that low levels of expression of LDOC-1 and PARP-1 mRNA may be associated with familial melanoma.

4

Apoptosis quantification at the respiratory epithelium level in asthma

88%

Grigoraş A., Grigoraş C., Mihăescu T., Vereş L., Cotuţiu C., Floarea-Strat A.

Open Medicine

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2010

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vol. 5

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issue 5

556-564

EN

The „changes” occurring in the expression of the factors involved in the apoptotic chain at the level of the respiratory epithelium in asthma is still an unsolved issue. At this level an important role is played by the mitochondria and the factors that influence the membrane permeability, especially the Bcl-2 super family. The purpose of this study is to evaluate both the changes in the expression of the Bcl-2 and of the Bax proapoptotic factors at the respiratory epithelium level in 21 patients with bronchial asthma of different degrees of severity of disease (aaccording to GINA - Global Initiative For Asthma). To accomplish this, fragments of the bronchial mucosa were obtained through fiberbronchoscopy, being afterwords hystologically prepare in view of the immunomarking with anti Bcl-2 and anti-Bax antibodies. Microscopic examination revealed an important decrease in the level of proapoptotic factor Bcl-2 in patients with persistent severe forms of the disease and a significant decrease in the expression of the proapototic Bax factor at the respiratory epithelium level even in the early stages of the disease. Knowing all the factors involved in apoptosis at the respiratory epithelium level in bronchial asthma, as well as of their expression changes will be at the core of new therapeutical approaches to of this disease.

5

The effect of vitamin C on amiodarone-induced toxicity in rat thymocytes

88%

Cekic S., Pavlovic D., Sarac M., Kamenov B., Dimic A., Pavlovic V.

Open Medicine

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2011

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vol. 6

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issue 1

58-63

EN

Although, the antiarrhythmic effect of amiodarone (AMD) is well characterized, the mechanism of its toxicity on extracardiac tissues is still poorly understood. Several antioxidants have been shown to prevent AMD-induced toxicity by antioxidant and/or non-antioxidant mechanisms. In the current study, we evaluated the possible protective effect, in vitro, of vitamin C on AMD-induced toxicity in rat thymocytes. Rat thymocytes were cultured with increasing AMD concentrations (1–20 μM) with or without vitamin C (1000 μg/ml), for 24 hours. Cells treatment with AMD resulted in a concentration-dependent increase of hypodiploid cells and a significant decrease in cellular glutathione content. Vitamin C combined with AMD significantly decreased the proportion of hypodiploid cells and markedly increased the cellular glutathione content, compared with AMD treatment alone. These results suggest that treatment with vitamin C may prevent AMD-induced toxicity in rat thymocytes by restoring cellular glutathione content.

6

Protein Disulfide Isomerase Superfamily in Disease and the Regulation of Apoptosis

63%

Grek C., Townsend D. M.

Endoplasmic Reticulum Stress in Diseases

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2014

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vol. 1

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issue 1

EN

Cellular homeostasis requires the balance of a multitude of signaling cascades that are contingent upon the essential proteins being properly synthesized, folded and delivered to appropriate subcellular locations. In eukaryotic cells the endoplasmic reticulum (ER) is a specialized organelle that is the central site of synthesis and folding of secretory, membrane and a number of organelletargeted proteins. The integrity of protein folding is enabled by the presence of ATP, Ca++, molecular chaperones, as well as an oxidizing redox environment. The imbalance between the load and capacity of protein folding results in a cellular condition known as ER stress. Failure of these pathways to restore ER homeostasis results in the activation of apoptotic pathways. Protein disulfide isomerases (PDI) compose a superfamily of oxidoreductases that have diverse sequences and are localized in the ER, nucleus, cytosol, mitochondria and cell membrane. The PDI superfamily has multiple functions including, acting as molecular chaperones, protein-binding partners, and hormone reservoirs. Recently , PDI family members have been implicated in the regulation of apoptotic signaling events. The complexities underlying the molecular mechanisms that define the switch from pro-survival to pro-death response are evidenced by recent studies that reveal the roles of specific chaperone proteins as integration points in signaling pathways that determine cell fate. The following review discusses the dual role of PDI in cell death and survival during ER stress.

Refine search results

Scutellarein ameliorates tongue cancer cells via mitochondria

Vimentin cleavage in end-stage renal disease is not related to apoptosis

LDOC-1 and PARP-1 mRNA expression in leukocytes of father and son with cutaneous malignant melanoma

Apoptosis quantification at the respiratory epithelium level in asthma

The effect of vitamin C on amiodarone-induced toxicity in rat thymocytes

Protein Disulfide Isomerase Superfamily in Disease and the Regulation of Apoptosis