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Cell ageing and senescence

Description

University S377 Mind Map on Cell ageing and senescence, created by Sarah Smith on 09/16/2015.
Sarah Smith
Mind Map by Sarah Smith, updated more than 1 year ago
Sarah Smith
Created by Sarah Smith over 6 years ago
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Resource summary

Cell ageing and senescence
  1. Progerias
    1. Werner's syndrome
      1. Ataxia telangiectasia
      2. What changes?
        1. Expression of proteins and mRNA
          1. Nuclear and mitochondrial genomes
            1. MtDNA more exposed to damage: not complexed with histones, almost all is coding, repair not as efficient
              1. cytochrome oxidase is critically important
            2. Energy metabolism
              1. enlarged mitochondria, decline in membrane potential, increase in production of ROS
              2. Protein processing
                1. Glycation - assoc with diabetes and alzeimers
                  1. Protein cross-linking and advanced glycosylation end products (AGES)
                2. Accumulation of aggregated/damaged proteins and lipids
                  1. accumulation of misfolded proteins and peptides (amyloid fibrils/plaques) associated with disease
                    1. type II diabetes, alzheimers, parkinsons
                  2. Cessation of division of proliferative cells
                    1. Functional alterations
                    2. Network Theory, Free-Radical Theory, telomere theory
                      1. Free Radicals
                        1. Reactive Oxygen Species (ROS) Table 18.1 Page 102
                          1. Hydrogen peroxide
                            1. Lipid peroxide
                              1. Nitric oxide (also RNS)
                                1. Peroxynitrite (also RNS)
                                  1. Main source: oxidative metabolism
                                    1. Superoxide radicals Fig 18.1 Page 103
                                  2. Metals (i.e. iron and copper)
                                    1. ATOMS OR MOLECULES WITH UNPAIRED ELECTRONS
                                      1. Exogenous agents: UV and ionizing radiation, some chemicals
                                        1. Effects
                                          1. DSBs and altered bases, i.e. 8-oxoguanosine
                                            1. Lipid peroxidation
                                              1. Proteins: formation of carbonyl groups, 3-nitrotyrosine, amino acid radicals
                                                1. Oxidative Stress
                                                2. Defenses
                                                  1. Molecules that scavenge ROS and RNS
                                                    1. Proteins that bind metal ions
                                                      1. Enzymes that convert FRs to less reactive or inactive forms
                                                        1. Table 18.2 Page 106
                                                          1. Enzymes that repair DNA damage
                                                            1. Protein degradation systems
                                                              1. Stress response proteins
                                                            2. Replicative Senescence
                                                              1. Cells cannot divide indefinitely
                                                                1. Proliferative reserve capacity
                                                                2. Senescent cells
                                                                  1. Larger, with larger nuclei
                                                                    1. Table 18.3 Page 112
                                                                    2. Causes?
                                                                      1. Shortening of telomeres, DNA damage, decondensation of chromatin, overactivation of mitotic stimuli and activation of some oncogenes
                                                                        1. telomere shortening doesn't always occur
                                                                          1. Telomere shortening detected by ATM results in withdrawal from the cell cycle and possibly apoptosis (p53)
                                                                            1. Transfection with genes for telomerase can make a cell immortal
                                                                              1. BUT: no correlation between telomere length and lifespan or replicative capacity in vitro. Telomere length is not consistent for all chromosomes in a cell
                                                                                1. may be "sentinels that respond to cellular stress - particularly OXIDATIVE STRESS
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