scholarly journals Coupling Activation of Pro-Apoptotic Caspases With Autophagy in the Meckel´s Cartilage

2018 ◽  
pp. 135-140 ◽  
Author(s):  
P. Bíliková ◽  
E. Švandová ◽  
B. Veselá ◽  
J. Doubek ◽  
A. Poliard ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Beclin 1 ◽  
Hypertrophic Chondrocytes ◽  
Caspase 8 ◽  
Major Mechanism ◽  
Histological Sections ◽  
Temporary Structure ◽  
Caspase 2 ◽  
First Time

Mammalian Meckel´s cartilage is a temporary structure associated with mandible development. Notably, its elimination is not executed by apoptosis, and autophagy was suggested as the major mechanism. Simultaneous reports point to pro-apoptotic caspases as novel participants in autophagic pathways in general. The aim of this research was to find out whether activation of pro-apoptotic caspases (-2, -3, -6, -7, -8 and -9) was associated with autophagy of the Meckel´s cartilage chondrocytes. Active caspases were examined in serial histological sections of mouse mandible using immunodetection and were correlated with incidence of autophagy based on Beclin-1 expression. Caspase-2 and caspase-8 were found in Beclin-1 positive regions, whereas caspase-3, -6, -7 and -9 were not present. Caspase-8 was further correlated with Fas/FasL and HIF-1alpha, potential triggers for its activation. Some Fas and FasL positivity was observed in the chondrocytes but caspase-8 activation was found also in FasL deficient cartilage. HIF-1alpha was abundantly present in the hypertrophic chondrocytes. Taken together, caspase-8 activation in the Meckel´s cartilage was demonstrated for the first time. Caspase-8 and caspase-2 were the only pro-apoptotic caspases detected in the Beclin-1 positive segment of the cartilage. Activation of caspase-8 appears FasL/Fas independent but may be switched on by HIF-1alpha.

scholarly journals Inclusion Complex of Zerumbone with Hydroxypropyl-β-Cyclodextrin Induces Apoptosis in Liver Hepatocellular HepG2 Cells via Caspase 8/BID Cleavage Switch and Modulating Bcl2/Bax Ratio

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Nabilah Muhammad Nadzri ◽  
Ahmad Bustamam Abdul ◽  
Mohd Aspollah Sukari ◽  
Siddig Ibrahim Abdelwahab ◽  
Eltayeb E. M. Eid ◽  
...  
Keyword(s):  
Inclusion Complex ◽  
Mitochondrial Membrane ◽  
Morphological Study ◽  
Caspase 3 ◽  
Anticancer Agent ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Solubility In Water ◽  
Anticancer Effects ◽  
First Time

Zerumbone (ZER) isolated fromZingiber zerumbetwas previously encapsulated with hydroxypropyl-β-cyclodextrin (HPβCD) to enhance ZER’s solubility in water, thus making it highly tolerable in the human body. The anticancer effects of this new ZER-HPβCD inclusion complex via apoptosis cell death were assessed in this study for the first time in liver hepatocellular cells, HepG2. Apoptosis was ascertained by morphological study, nuclear stain, and sub-G1 cell population accumulation with G2/M arrest. Further investigations showed the release of cytochrome c and loss of mitochondrial membrane potential, proving mitochondrial dysfunction upon the ZER-HPβCD treatment as well as modulating proapoptotic and anti-apototic Bcl-2 family members. A significant increase in caspase 3/7, caspase 9, and caspase 8 was detected with the depletion of BID cleaved by caspase 8. Collectively, these results prove that a highly soluble inclusion complex of ZER-HPβCD could be a promising anticancer agent for the treatment of hepatocellular carcinoma in humans.

scholarly journals Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Reproduction ◽  
2006 ◽  
Vol 132 (3) ◽  
pp. 465-475 ◽  
Author(s):  
Marina C Peluffo ◽  
Leonardo Bussmann ◽  
Richard L Stouffer ◽  
Marta Tesone
Keyword(s):  
Enzyme Activity ◽  
Corpus Luteum ◽  
Estrous Cycle ◽  
Luteal Phase ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Different Populations ◽  
Structural Regression ◽  
Caspase 2

Apoptosis is associated with the regression of the corpus luteum (CL) in many species. Since caspases play a central role in apoptosis, we studied several initiators (-2, -8, and -9) and the main effector (-3) caspase in the CL during the estrous cycle of the rat. Two different populations of CL (old and new) were identified on ovaries at estrus and diestrus II (DII). Diminished (P< 0.05) luteal progesterone content and P450scc levels suggested that functional luteolysis occurred between the new CL at DII and old CL at estrus, whereas the decline (P< 0.05) in luteal weight indicated that structural regression was occurring between old CL at estrus to DII. Immunostaining for caspase-2 in luteal and endothelial cells appeared to increase as the luteal phase progressed, peaking at DII in the old CL. However, caspase-8 and -9 immunostaining showed little change with a slight increase at estrus in the old population. Notably, caspase-3 staining appeared to peak at DII in the new CL. Enzyme activity of caspase-9 increased (P< 0.05) in the new CL at DII, followed by that of caspase-2 and -3 in old CL at estrus. Caspase-8 activity did not change at any stage. The number of apoptotic cells increased at DII in the old CL. These results suggest an important role for this protease family during early events of luteolysis in the rat estrous cycle.

scholarly journals The MicroRNA-210/Casp8ap2 Pathway Alleviates Hypoxia-Induced Injury in Myocardial Cells by Regulating Apoptosis and Autophagy

2020 ◽  
Vol 23 (6) ◽  
pp. E797-E802
Author(s):  
Kunsheng Li ◽  
Jun Pan ◽  
Qiuchang Li ◽  
Shiliang Li ◽  
Kai Li ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Caspase 3 ◽  
Transfection Efficiency ◽  
Beclin 1 ◽  
Caspase 8 ◽  
H9c2 Cells ◽  
Myocardial Cells ◽  
Western Blot Assay ◽  
H9c2 Cardiomyocytes ◽  
Associated Proteins

Aim: This study was conducted to investigate the role of the miR-210/Caspase8ap2 pathway in apoptosis and autophagy in hypoxic myocardial cells. Methods: The miR-control, miR-210 mimic, and miR-210 inhibitor were transfected into rat myocardial H9C2 cells. The transfection efficiency of exogenous miR-210 was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). H9C2 cells were then treated with CoCl2 for 24, 48, and 72 h to generate a myocardial injury model. The apoptosis of H9C2 cells was assessed by flow cytometry. Additionally, a western blot assay was used to determine the expression of the autophagy-associated proteins light chain 3 (LC3), p62 and Beclin-1, and apoptosis-associated proteins Caspase8ap2, cleaved caspase 8, and cleaved caspase 3. Results: We determined that a 48 h hypoxia treatment duration in H9C2 cardiomyocytes induced myocardial injury. Additionally, the overexpression of miR-210 significantly inhibited cell apoptosis. MiR-210 suppressed autophagy by upregulating p62 and downregulating LC3II/I in hypoxic H9C2 cells. Caspase8ap2 was a putative target of miR-210, miR-210 mediated apoptosis, and autophagy of H9C2 cells via suppressing Caspase8ap2. Furthermore, the expression of caspase 8, caspase 3, and Beclin-1 were decreased in response to miR-210. Conclusion: miR-210 exhibits anti-apoptosis and anti-autophagy effects, which alleviate myocardial injury in response to hypoxia.

scholarly journals Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

2021 ◽  
Vol 9 ◽  
Author(s):  
Yong Li ◽  
Xiaoguang Wu ◽  
Yukang Mao ◽  
Chi Liu ◽  
Yiting Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Caspase 3 ◽  
High Salt ◽  
Beclin 1 ◽  
Cardiomyocyte Apoptosis ◽  
Neonatal Rat ◽  
Caspase 8 ◽  
H9c2 Cells ◽  
Cardiac Damage

The present study aimed to explore whether high-salt diet (HSD) could cause cardiac damage independent of blood pressure, and whether nitric oxide (NO) could alleviate high-salt–induced cardiomyocyte apoptosis and autophagy in rats. The rats received 8% HSD in vivo. H9C2 cells or primary neonatal rat cardiomyocytes (NRCM) were treated with sodium chloride (NaCl) in vitro. The levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1 and autophagy related 7 (ATG7) were increased in the heart of HSD rats with hypertension (HTN), and in hypertension-prone (HP) and hypertension-resistant (HR) rats. Middle and high doses (50 and 100 mM) of NaCl increased the level of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in H9C2 cells and NRCM. The endothelial NO synthase (eNOS) level was increased, but p-eNOS level was reduced in the heart of HSD rats and H9C2 cells treated with 100 mM NaCl. The level of NO was reduced in the serum and heart of HSD rats. NO donor sodium nitroprusside (SNP) reversed the increases of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2 induced by NaCl (100 mM) in H9C2 cells and NRCM. SNP treatment attenuated the increases of cleaved-caspase 3/caspase 3, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in the heart, but had no effect on the blood pressure of HSD rats with HR. These results demonstrated that HSD enhanced cardiac damage independently of blood pressure. Exogenous NO supplementarity could alleviate the high salt–induced apoptosis and autophagy in cardiomyocytes.

scholarly journals TNF receptors regulate vascular homeostasis in zebrafish through a caspase-8, caspase-2 and P53 apoptotic program that bypasses caspase-3

2012 ◽  
Vol 6 (2) ◽  
pp. 383-396 ◽  
Author(s):  
R. Espin ◽  
F. J. Roca ◽  
S. Candel ◽  
M. P. Sepulcre ◽  
J. M. Gonzalez-Rosa ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Caspase 8 ◽  
Tnf Receptors ◽  
Vascular Homeostasis ◽  
Caspase 2

scholarly journals Luteolin Induces Apoptosis and Autophagy in Mouse Macrophage ANA-1 Cells via the Bcl-2 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Yuexia Liao ◽  
Yang Xu ◽  
Mengyao Cao ◽  
Yuanyuan Huan ◽  
Lei Zhu ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Inflammatory Diseases ◽  
Flow Cytometric Analysis ◽  
Beclin 1 ◽  
Caspase 8 ◽  
Mouse Macrophage ◽  
Expression Levels ◽  
Traditional Medicines ◽  
Flow Cytometric ◽  
Induced Apoptosis

Plants rich in luteolin have been used as Chinese traditional medicines for inflammatory diseases, hypertension, and cancer. However, little is known about the effect of luteolin on the apoptosis or autophagy of the macrophages. In this study, mouse macrophage ANA-1 cells were incubated with different concentrations of luteolin. The viability of the cells was determined by an MTT assay, apoptosis was determined by flow cytometric analysis, the level of cell autophagy was observed by confocal microscopy, and the expression levels of apoptotic or autophagic and antiapoptotic or antiautophagic proteins were detected by Western blot analysis. The results showed that luteolin decreased the viability of ANA-1 cells and induced apoptosis and autophagy. Luteolin induced apoptosis accompanied by downregulation of the expression of Bcl-2 and upregulation of the expression of caspase 3 and caspase 8. And luteolin increased FITC-LC3 punctate fluorescence accompanied by the increased expression levels of LC3-I, ATG7, and ATG12, while it suppressed the expression level of Beclin-1. Luteolin treatment resulted in obvious activation of the p38, JNK, and Akt signaling pathways, which is important in modulating apoptosis and autophagy. Thus, we concluded that luteolin induced the apoptosis and autophagy of ANA-1 cells most likely by regulating the p38, JNK, and Akt pathways, inhibiting the activity of Bcl-2 and Beclin-1 and upregulating caspase 3 and caspase 8 expression. These results provide novel insights into a therapeutic strategy to prevent and possibly treat macrophage-related diseases through luteolin-induced apoptosis and autophagy.

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