Detection of apoptosis in vivo using antibodies against caspase-induced neo-epitopes

Jakob, Sabine; Corazza, Nadia; Diamantis, Eva; Каппелер, Андреас; Brunner, Thomas

doi:10.1016/j.ymeth.2007.11.004

Cited by 46 publications

(41 citation statements)

References 40 publications

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“…Other researchers, however, used doses up to 300 mg/kg trilostane/d in rats and reported a dose-dependent increase in adrenal weight, but no adrenal necrosis [1,28,29]. Notably, our study is the first study to report long-term therapy with trilostane (4 months), as in all other studies trilostane was administered for only [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] days.…”

Section: Methodsmentioning

confidence: 75%

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Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Burkhardt

Guscetti

Boretti

et al. 2011

Domestic Animal Endocrinology

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-Ruckstuhl, N S (2011). Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats. Domestic Animal Endocrinology, 40(3):155-164. Postprint available at: http://www.zora.uzh.ch Posted at the Zurich Open Repository and Archive, University of Zurich. http://www.zora.uzh.ch Originally published at: Burkhardt, W A; Guscetti, F; Boretti, F S; Todesco, A I; Aldajarov, N; Lutz, T A; Reusch, C E; Sieber-Ruckstuhl, N S (2011). Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats. Domestic Animal Endocrinology, 40(3):155-164.Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats AbstractAdrenal necrosis has been reported as a complication of trilostane application in dogs with hyperadrenocorticism. One suspicion was that necrosis results from the increase of adrenocorticotropic hormone (ACTH) during trilostane therapy. The aim of the current study was to assess the effects of ACTH and trilostane on adrenal glands of rats. For experiment 1, 36 rats were divided into 6 groups. Groups 1.1 to 1.4 received ACTH in different doses (60, 40,20, and 10 μg/d) infused subcutaneously with osmotic minipumps for 16 wk. Group 1.5 received saline, and group 1.6 received no therapy. For experiment 2, 24 rats were divided into 3 groups. Group 2.1 and 2.2 received 5 and 50 mg/kg trilostane/d orally mixed into chocolate pudding for 16 wk. Eight control rats received pudding alone. At the end of the experiments, adrenal glands were assessed for necrosis by histology and immunohistochemistry; levels of endogenous ACTH and nucleosomes were assessed in the blood. Rats treated with 60 μg ACTH/d showed more hemorrhage and vacuolization and increased numbers of apoptotic cells in the adrenal glands than rats treated with 20 or 10 μg ACTH/d, trilostane, or control rats. Rats treated with 60 μg ACTH/d had a higher amount of nucleosomes in the blood compared with rats treated with 10 μg ACTH/d, trilostane, or saline. We conclude that in healthy rats ACTH, but not trilostane, causes adrenal degeneration in a dose-dependent manner. Results of this study support the hypothesis that adrenal gland lesions seen in trilostane-treated dogs are caused by ACTH and not by trilostane. Results of this study support the hypothesis that adrenal gland lesions seen in trilostanetreated dogs are caused by ACTH and not trilostane.

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Section: Methodsmentioning

confidence: 75%

“…Presence of apoptosis was assessed by immunohistochemistry against neoepitopes of cleaved lamin A and cleaved caspase-3 [21]. Caspase-3 is a critical effector caspase, expressed in most cells and activated through cleavage in response to nearly all apoptosis triggers [22].…”

Section: Methodsmentioning

confidence: 99%

Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Burkhardt

Guscetti

Boretti

et al. 2011

Domestic Animal Endocrinology

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“…Caspase-3 is synthesized as inactive proenzyme that is processed in cells undergoing apoptosis by self-proteolysis and/or cleavage by other upstream proteases (e.g., caspases 8, 9, and 10). The detection of active caspase-3 is widely used in many cell lines undergoing apoptosis (Jakob et al 2008;Resendes et al 2004). As shown in Fig.…”

Section: Cholesterol Loading Induces Apoptosis Of Min6mentioning

confidence: 99%

Cholesterol induces pancreatic β cell apoptosis through oxidative stress pathway

Liu

Hou

et al. 2011

Cell Stress and Chaperones

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Type 2 diabetes is often associated with high blood cholesterol. Here, we investigated the effect of cholesterol loading on MIN6 cells derived from pancreatic β cells. Exposure of MIN6 cells to cholesterol-induced apoptosis in time-and dose-dependent manner. Treatment with methyl-β-cyclodextrin that removes cholesterol from plasma membrane prevented the cells from cholesterolinduced apoptosis. Western blot analysis revealed that the levels of phosphorylated-p38 mitogen-activated protein kinase (P-p38 MAPK) and c-Jun N-terminal kinases (P-JNK) were significantly increased after the cholesterol loading, suggesting that the stress-activated protein kinase signaling was stimulated. A specific p38 inhibitor rescued MIN6 cells from cholesterol-induced apoptosis, while JNK inhibitor failed, suggesting the importance of activation of p38 MAPK signaling in response to cholesterol. The expression of Bip and CHOP, the endoplasmic reticulum (ER) stress markers, remained unaffected, indicating that the ER stress may not be involved in the cytotoxicity of cholesterol on the MΙΝ6 cells. The intracellular concentration of reactive oxygen species measured by use of 2′,7′-dichlorofluorescin diacetate was significantly increased after cholesterol loading, demonstrating the induced apoptosis was mediated through oxidative stress. Addition of reduced form of glutathione in the medium rescued MIN6 cells from apoptosis induced by cholesterol loading. Taken together, these results demonstrate that the free cholesterol loading can induce apoptosis of MIN6 cells mediated by oxidative stress and the activation of p38 MAPK signaling.

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“…Antigen retrieval was performed by boiling sections for 10 min in 10 mM citrate pH 6.0 in a pressure cooker (Jakob et al, 2008). Then, endogenous peroxidase was blocked (Peroxidase Blocking Reagents, DakoCytomation) and GSTP1 expression was detected using an antihuman GSTP1 antibody (Sigma-Aldrich, Prestige Antibodies, 1:1000) and biotinylated secondary goat anti-rabbit IgG (SigmaAldrich, 1:200).…”

Section: Immunohistochemistry For Gstp1mentioning

confidence: 99%

Thiazolide-induced apoptosis in colorectal cancer cells is mediated via the Jun kinase–Bim axis and reveals glutathione-S-transferase P1 as Achilles’ heel

et al. 2011

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Detection of apoptosis in vivo using antibodies against caspase-induced neo-epitopes

Cited by 46 publications

References 40 publications

Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Adrenocorticotropic hormone, but not trilostane, causes severe adrenal hemorrhage, vacuolization, and apoptosis in rats

Cholesterol induces pancreatic β cell apoptosis through oxidative stress pathway

Thiazolide-induced apoptosis in colorectal cancer cells is mediated via the Jun kinase–Bim axis and reveals glutathione-S-transferase P1 as Achilles’ heel

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