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The Indispensable Soma Hypothesis in Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
It is also possible to examine the reprogramming of somatic cells into induced pluripotent stem cells (iPSCs). This is one way whereby somatic cells can be reprogrammed and so be used when needed by somatic tissues [129]. An intriguing possibility is the reprogramming of somatic cells into specifically neural stem cells via microRNAs (which provide the interface between external stimulation, such as cognitive information, and the cellular milieu) [130]. Although there are many still unanswered questions regarding this process, such as the stress response triggered by the reprogramming process (the reprogramming-induced senescence (RIS) [131], this is a useful concept to consider as it shows that the aged soma is not necessarily irreparable. Epigenetic regulation (via chromatin modification for instance) can assure a successful repair sequence and thus increase the life span [129]. We know that chromatin modifiers play a positive role in neural health [132]. One such chromatin modulator is the barrier-to-autointegration factor (BAF) which plays a role both in gonad development [133] and in neurodevelopment [134]. Stimuli originating from the environment constantly influence the epigenome and remodel our responses to these stimuli. The process of aging is subjected to epigenetic regulations [135]. Taking these facts a little more into the realm of speculation, we may assume that aging somatic cells may be reprogrammed through the action of microRNAs (which operate following suitable external, cognitive, technology-assisted stimulation) into functioning neurons [136] and thus improve overall brain function. This must result in a reduction of age-related degeneration, and also represents an example where germline repair resources have been diverted to the neuron [137].
Proteomic and bioinformatic analysis of condyloma acuminata: mild hyperthermia treatment reveals compromised HPV infectivity of keratinocytes via regulation of metabolism, differentiation and anti-viral responses
Published in International Journal of Hyperthermia, 2019
Yu-Zhe Sun, Jia-Feng Li, Zhen-Dong Wei, Hang-Hang Jiang, Yu-Xiao Hong, Song Zheng, Rui-Qun Qi, Xing-Hua Gao
On the other hand, the study revealed that multiple biological processes involved with viral responses were enhanced and proteins with anti-viral activities such as 2'-5'-oligoadenylate synthase 1 (OAS1), Interferon-induced GTP-binding protein Mx1 (MX1), Barrier-to-autointegration factor 1 (BANF1), Calnexin (CANX) as well as the AP-1 complex subunit sigma-1A (AP1S1) were induced by hyperthermia. These proteins have been reported to be crucial for anti-viral responses involving viral genome degradation [29,30], interferon activation [31,32], viral replication inhibition [33,34] as well as antigen presentation [35,36]. Therefore, we proposed that by induction of these key factors, hyperthermia has the potential to interfere with HPV DNA replication and expression as well as HPV antigen presentation and, in this way, boost the immunologic clearance of HPV infections.
Investigating the toxic effects induced by iron oxide nanoparticles on neuroblastoma cell line: an integrative study combining cytotoxic, genotoxic and proteomic tools
Published in Nanotoxicology, 2019
Dalel Askri, Valérie Cunin, David Béal, Sylvie Berthier, Benoit Chovelon, Josiane Arnaud, Walid Rachidi, Mohsen Sakly, Salem Amara, Michel Sève, Sylvia G. Lehmann
Moreover, among the 5 DEP specific to the nano form of Fe, the protein ‘Barrier-to-autointegration factor’ BANF1 was reported in a study published in 2014 by Edelmann et al. to be disturbed and down regulated following the exposure of BEAS-2B type human lung cells to copper NPs (Edelmann et al. 2014). Other proteins were also affected and are involved in cytoskeletal signaling pathways, epithelial remodeling, ILK, EIF2 and RhoA, etc. These proteins have various molecular functions: death and cell survival, protein synthesis, post- translational, protein folding, cellular development and proliferation, cell cycle and cell morphology.