Factors controlling ovarian apoptosis

2000 ◽  
Vol 78 (12) ◽  
pp. 1003-1012 ◽  
Author(s):  
C V Andreu-Vieyra ◽  
H R Habibi

Apoptosis is a form of programmed cell death that is essential for the development of the embryo and adult tissue plasticity. In adults, it is observed mainly in those tissues undergoing active differentiation such as the hematopoietic system, testis, ovary, and intestinal epithelium. Apoptosis can be triggered by many factors, such as hormones, cytokines, and drugs, depending on the type of the cell. While the intracellular signaling mechanisms may vary in different cells, they all display similar morphological and biochemical features at the later stages of the apoptotic process. This review focuses on the factors controlling ovarian apoptosis, emphasizing observations made on GnRH-induced apoptotic process in goldfish follicles.Key words: apoptosis, ovary, GnRH.

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Jianan Zhao ◽  
Yiyang Hu ◽  
Jinghua Peng

AbstractMost currently recommended therapies for metabolic dysfunction-associated fatty liver disease (MAFLD) involve diet control and exercise therapy. We searched PubMed and compiled the most recent research into possible forms of programmed cell death in MAFLD, including apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis. Here, we summarize the state of knowledge on the signaling mechanisms for each type and, based on their characteristics, discuss how they might be relevant in MAFLD-related pathological mechanisms. Although significant challenges exist in the translation of fundamental science into clinical therapy, this review should provide a theoretical basis for innovative MAFLD clinical treatment plans that target programmed cell death.


2020 ◽  
Vol 10 (9) ◽  
pp. 594
Author(s):  
Giuseppe Giglia ◽  
Giuditta Gambino ◽  
Pierangelo Sardo

Neuroblastoma (NBM) is a deadly form of solid tumor mostly observed in the pediatric age. Although survival rates largely differ depending on host factors and tumor-related features, treatment for clinically aggressive forms of NBM remains challenging. Scientific advances are paving the way to improved and safer therapeutic protocols, and immunotherapy is quickly rising as a promising treatment that is potentially safer and complementary to traditionally adopted surgical procedures, chemotherapy and radiotherapy. Improving therapeutic outcomes requires new approaches to be explored and validated. In-silico predictive models based on analysis of a plethora of data have been proposed by Lombardo et al. as an innovative tool for more efficacious immunotherapy against NBM. In particular, knowledge gained on intracellular signaling pathways linked to the development of NBM was used to predict how the different phenotypes could be modulated to respond to anti-programmed cell death-ligand-1 (PD-L1)/programmed cell death-1 (PD-1) immunotherapy. Prediction or forecasting are important targets of artificial intelligence and machine learning. Hopefully, similar systems could provide a reliable opportunity for a more targeted approach in the near future.


2006 ◽  
Vol 20 (4) ◽  
pp. E7 ◽  
Author(s):  
Florence Lefranc ◽  
Robert Kiss

✓ Malignant gliomas, among which glioblastomas constitute the largest group, are characterized by a dramatically diffuse infiltration into the brain parenchyma with, as a consequence, the fact that no patient with glioblastoma multiforme (GBM) has been cured to date. Migrating GBM cells are resistant to apoptosis (Type I programmed cell death), and thus to radiotherapy and conventional chemotherapy, because of the constitutive activation of several intracellular signaling pathways, of which the most important identified to date are the pathways controlled by phosphatidylinositol 3-kinase, Akt, and the mammalian target of rapamycin (mTOR). Migrating GBM cells seem to be less prone to resist autophagy (Type II programmed cell death), and disruption of the pathway controlled by mTOR induces marked autophagic processes in GBM cells. Temozolomide is the most efficacious cytotoxic drug employed today to combat glioblastoma, and this drug exerts its cytotoxic activity through proautophagic processes. Thus, autophagy represents a kind of Trojan horse that can be used to bypass, at least partly, the dramatic resistance of glioblastoma to radiotherapy and proapoptotic-related chemotherapy.


2019 ◽  
Vol 9 (9) ◽  
pp. 221 ◽  
Author(s):  
Salvo Danilo Lombardo ◽  
Mario Presti ◽  
Katia Mangano ◽  
Maria Cristina Petralia ◽  
Maria Sofia Basile ◽  
...  

Immunotherapy is a promising new therapeutic approach for neuroblastoma (NBM): an anti-GD2 vaccine combined with orally administered soluble beta-glucan is undergoing a phase II clinical trial and nivolumab and ipilimumab are being tested in recurrent and refractory tumors. Unfortunately, predictive biomarkers of response to immunotherapy are currently not available for NBM patients. The aim of this study was to create a computational network model simulating the different intracellular pathways involved in NBM, in order to predict how the tumor phenotype may be influenced to increase the sensitivity to anti-programmed cell death-ligand-1 (PD-L1)/programmed cell death-1 (PD-1) immunotherapy. The model runs on COPASI software. In order to determine the influence of intracellular signaling pathways on the expression of PD-L1 in NBM, we first developed an integrated network of protein kinase cascades. Michaelis–Menten kinetics were associated to each reaction in order to tailor the different enzymes kinetics, creating a system of ordinary differential equations (ODEs). The data of this study offers a first tool to be considered in the therapeutic management of the NBM patient undergoing immunotherapeutic treatment.


Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 7028
Author(s):  
Chandrasekar Balachandran ◽  
Kenta Yokoi ◽  
Kana Naito ◽  
Jebiti Haribabu ◽  
Yuichi Tamura ◽  
...  

In our previous paper, we reported that amphiphilic Ir complex–peptide hybrids (IPHs) containing basic peptides such as KK(K)GG (K: lysine, G: glycine) (e.g., ASb-2) exhibited potent anticancer activity against Jurkat cells, with the dead cells showing a strong green emission. Our initial mechanistic studies of this cell death suggest that IPHs would bind to the calcium (Ca2+)–calmodulin (CaM) complex and induce an overload of intracellular Ca2+, resulting in the induction of non-apoptotic programmed cell death. In this work, we conduct a detailed mechanistic study of cell death induced by ASb-2, a typical example of IPHs, and describe how ASb-2 induces paraptotic programmed cell death in a manner similar to that of celastrol, a naturally occurring triterpenoid that is known to function as a paraptosis inducer in cancer cells. It is suggested that ASb-2 (50 µM) induces ER stress and decreases the mitochondrial membrane potential (ΔΨm), thus triggering intracellular signaling pathways and resulting in cytoplasmic vacuolization in Jurkat cells (which is a typical phenomenon of paraptosis), while the change in ΔΨm values is negligibly induced by celastrol and curcumin. Other experimental data imply that both ASb-2 and celastrol induce paraptotic cell death in Jurkat cells, but this induction occurs via different signaling pathways.


2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  

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