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The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
Upon interaction of FasL with Fas receptor (Apo-1 or CD95), the death-inducing signaling complex (DISC), which contains adaptor proteins such as FADD and procaspase-8, is formed. In some cell types, activated CASP-8 directly activates other members of the caspase family and subsequently leads to the execution of apoptosis. In other types of cells, the induction of Fas pathway is not sufficient to trigger an apoptotic response, rather this pathway cross-talk with mitochondrial pathway through proteolytic degradation of Bid producing a truncated form of Bid (tBid). Then, tBid acts through a heterodimer with BAX or BAK, leading to the activation of the mitochondrial pathway of apoptosis. In this situation, the extrinsic pathway functions as an amplifier to induce an apoptotic response [35].
Potential of Herbal Extracts and Bioactive Compounds for Human Healthcare
Published in Megh R. Goyal, Hafiz Ansar Rasul Suleria, Ramasamy Harikrishnan, The Role of Phytoconstitutents in Health Care, 2020
Ramasamy Harikrishnan, Chellam Balasundaram
In mammals, the extrinsic pathway begins with the direct initiation of apoptosis through TNF (tumor necrosis factor) induction or Fas-Fas ligand-mediated induction that involved with the TNF receptor (TNFR) family [1002]. Once macrophages activate to release TNF-α cytokine, which is a main extrinsic mediator of apoptosis. The majority of human cells are present TNF-α receptors, namely TNFR1 and TNFR2. Once TNF-α binds to TNFR1, initiate the caspase activation pathways through TNF-receptor associated death domain (TRADD) and Fas-associated death domain (FADD) proteins; however, the cIAP1/2 may probably inhibit TNF-α signals once bind to TRAF2. The FLIP can also inhibit the activation of caspase-8 [147]. TNFR1 signal pathway may promote apoptosis through a caspase-independent manner [156]. The TNF-α binds with apoptosis gives rich TNF-α cytokine production that plays to produced several autoimmune diseases. The Fas receptor is the first signal of apoptosis known as Apo-1 or CD95, which is a TNF family transmembrane protein that possibly binds to Fas ligand (FasL) [1002]. The link between Fas and FasL leads to form DISC that contains FADD and caspase-8, -10. In some cells, type I is prepared caspase-8 directly and activates other caspase family members results, which triggers the strange of apoptosis while other type II cells, that combination with Fas-DISC, starts increase to release of proapoptotic factors in mitochondria after activation of caspase-8 [1001].
Gene Delivery for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Gianluca Vadalà, Luca Ambrosio, Vincenzo Denaro
The role of Fas was further investigated by Han et al. (2009), who treated rat NP cells with Fas siRNA in vitro. The Fas receptor is involved in maintaining the immune privilege of IVD (as discussed in Section 8.7) as well as in degenerative cell apoptosis: thus, its inhibition through RNAi resulted in a diminished apoptotic NP cell death in this study (Han et al. 2009).
3-Pyridinylboronic acid normalizes the effects of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine exposure in zebrafish embryos
Published in Drug and Chemical Toxicology, 2022
Fümet Duygu Üstündağ, İsmail Ünal, Derya Cansız, Ünsal Veli Üstündağ, Hülya Kara Subaşat, A. Ata Alturfan, Pınar Mega Tiber, Ebru Emekli-Alturfan
Apoptosis is initiated by intrinsic or extrinsic pathways. The death receptors such as Fas and TNFR are involved in the extrinsic apoptotic pathway. The intrinsic pathway triggers apoptosis in response to internal stimuli including stress and DNA damage. Bax and Bcl-2 group of molecules modulate the intrinsic pathway (van Loo 2002). Fas receptor (CD95, TNF receptor superfamily member 6) is a death receptor that is localized on the surface of many cells. Fas activates a signal transduction pathway leading to apoptosis (Nagata and Golstein 1995). P53 regulates apoptosis through the transport of Fas from cytoplasmic stores. Therefore, the overexpression of p53 increases the expression of Fas in cell surface (Bennett et al.1998). However, in our study, decreased fas expression was observed in the MPTP group.
A clinical and in-silico study exploring the association of CASP-3, NF-kB, miR-187, and miR-146 in pre-eclampsia
Published in Hypertension in Pregnancy, 2021
Charu Sharma, Purvi Purohit, Manoj Khokhar, Anupama Modi, Pratibha Singh, Shashank Shekhar, Shailja Sharma, Meenakshi Gothwal, Praveen Sharma
The current study, for the first time, reports the apoptosis gene CASP3, its regulatory transcription factor NF-κB and the regulatory MicroRNAs hsa-miR-146-5p and hsa-miR-187-5p in the blood samples and placental tissue of pre-eclamptic women. Recent studies have demonstrated apoptosis to have a significant role in the etiology and progression of PE. Apoptosis, defined as programmed cell death, is an important mechanism involved in maternal-fetal immune tolerance (19). In the extrinsic pathway mechanism, a cell expressing an FAS receptor on the surface binds to its FAS ligand, which activates a cascade of pro-apoptotic elements leading to cell death. The binding of FAS Ligand to the transmembrane receptor FAS recruits Pro-CASP-8. Subsequently, Pro-CASP-8 activates to CASP8 via the cleaving by procaspase and generating the active form of CASP3. The active CASP3 recruits other downstream effectors, eventually culmination in cell death (19). Placental development relies upon effective implantation and invasion of the maternal decidua (spiral arterioles) by the placental trophoblast. In normal pregnancy, trophoblast apoptosis increases with placental growth and advancing gestation. However, apoptosis is notably exaggerated in pregnancy complications like PE that is caused due to reduction of Maternal Blood flow in the intervillous space, hypoxic damage of the villous trophoblast leading to release of syncytiotrophoblast membrane fragments (20).
Novel therapeutic approaches for cutaneous T cell lymphomas
Published in Expert Review of Clinical Immunology, 2021
Antreas Pavlidis, Christina Piperi, Evangelia Papadavid
MF and SS are characterized by an impaired function of the cellular immune system highlighted by reduced production of Th1 cytokines (IFN-γ, IL-2) and elevation of Th2 (IL-4, IL-5, IL-10) which further impair Th1 cytokine production [22]. Interestingly, it has been demonstrated that both malignant and benign T cells produce the Th2 cytokines, IL-4 and IL-13 [23] while the Th2 dominant microenvironment reduces the Th1-driven anti-tumor effect of CD8+ cells. Furthermore, tumor cells release cytokines to recruit macrophages and dendritic cells which secrete pro-survival and angiogenic factors promoting tumorigenesis. However, increased expression of IL-10 inhibits maturation of dendritic cells, allowing malignant cells to escape from immune surveillance [24]. Dysfunction of the immune regulators PD-L1 and CTLA-4 might contribute to reduction of cellular immunity and immunosuppression [25]. Moreover, reduced expression of Fas receptor by malignant T cells results in impaired apoptosis and associates with the ongoing proliferation of malignant cells [25].