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Nanoparticle–Based RNA (siRNA) Combination Therapy Toward Overcoming Drug Resistance in Cancer
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
Autophagy is considered to be a cytoprotective process involved in the normal turnover of long-lived proteins and whole organelles to maintain a healthy cellular status [157]. However, recent data strongly demonstrate that autophagy is intimately linked to apoptosis or necrosis and serves both pro-survival and pro-death functions. Autophagy regulation requires an orchestrated interplay between many signaling molecules, including mammalian target of rapamycin (mTOR) kinase, which has the most potent impact on autophagy [158,159]. Once activated, mTOR inhibits autophagy via the phosphorylation of autophagy-related proteins. AMP activated protein kinase (AMPK) activation can lead to autophagy by negatively regulating mTOR [160,161]. The tumor suppressor protein p53 can trigger autophagy by phosphorylating AMPK and further inhibiting the mTOR signaling pathway [160]. Beclin-1 also plays a critical role in autophagosome formation and crosstalk between autophagy and apoptosis [161]. The BH3 domain-mediated binding of Beclin-1 to B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-XL) inhibits autophagy. However, the c-Jun N-terminal kinase (JNK) 1- or extracellular signal-regulated kinase (ERK)-mediated phosphorylation of Bcl-2 or death-associated protein kinase-mediated phosphorylation of Beclin-1 induces the dissociation of the Beclin-1–Bcl-2/Bcl-XL complex, thus inhibiting autophagy [161–165]. Intracellular calcium ions (Ca2+) can regulate the activation of JNK and the apoptotic signaling pathway [166].
Nanoparticles and Viruses as Mitophagy Inducers in Immune Cells
Published in Bertrand Henri Rihn, Biomedical Application of Nanoparticles, 2017
Housam Eidi, Zahra Doumandji, Lucija Tomljenovic, Bertrand Henri Rihn
Espert et al. (2009) have revealed that autophagy is triggered following the binding of envelope glycoprotein (Env) to CXCR4 (chemokine receptor) in T cells and that autophagy is required for Env-induced apoptosis through CXCR4. Interestingly, Biard-Piechaczyk et al. demonstrated that HIV-infected cells that express Env-induced autophagy and accumulation of Beclin1 in uninfected CD4+ T lymphocytes via CXCR4 (Espert et al. 2006). For NPs, they interact with cell surface receptors, leading to the activation of intracellular signaling cascades that induce formation of ROS (Soenen et al. 2011). These ROS further activate stress-dependent signaling pathways, such as the mitogen-activated protein kinase (MAPK) or IκB kinase pathways, ultimately altering gene expression of the antioxidant response element via the activation of transcription factors, such as AP-1, NF-kB, or Nrf2. The end result of this signaling cascade is the ROS overproduction.
Treatment Options for Chemical Sensitivity
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The process beginning with the Beclin 1 complex gives rise to nascent autophagosome membranes. These membranes assemble around cargo, encapsulating the cargo in a vesicle that subsequently fuses with a lysosome, generating an auto-lysosome. The contents are then degraded by proteases, lipases, nucleases, and glycosidases. Lysosomal permeases release the breakdown products—amino acids, lipids, nucleosides, and carbohydrates—into the cytosol, where they are available for synthetic and metabolic pathways.
Low deacetylation degree chitosan oligosaccharide protects against IL-1β induced inflammation and enhances autophagy activity in human chondrocytes
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Ruiqi Cao, Haomiao Yu, Huibin Long, Hongrui Zhang, Chao Hao, Lin Shi, Yuguang Du, Siming Jiao, Ai Guo, Lifeng Ma, Zhuo Wang
Previous studies have shown that inflammatory cytokines such as IL-1β could cause elevated levels of reactive oxygen species (ROS) and degraded ECM synthesis concomitant with reduced autophagy in the model of OA [40–42]. In all autophagy related proteins, Beclin-1 and LC3 play central roles. Beclin-1 is involved in the initial stage of autophagolysosome formation, gives rise to an incipient autophagosome membrane [43,44]. The formation and expansion of autophagosomes require the participation of LC3, which has two forms, LC3-I and LC3-II. In the process of autophagy, LC3-I is converted to LC3-II, and then LC3-II binds to autophagic vesicles. The content of LC3-II is positively correlated with the formation of autophagosomes [45]. To investigate if inflammatory cytokine (IL-1β) has an effect on the inhibition of chondrocyte autophagy, the expression of related gene and protein was assessed in IL-1β-treated chondrocytes. As the RT-PCR and western blot assay results showed, relative expression of Beclin-1 and the ratio of LC3II/LC3I were obviously decreased after IL-1β intervention, implying that IL-1β inhibited autophagy in chondrocytes.