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Erika amberson apoptosis extra credit


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Erika amberson apoptosis extra credit

  1. 1. ApoptosisBy Erika AmbersonCell Suicide:
  2. 2. Overview of research into apoptosis• 1800sObservation of cell death• 1908 Mechnikovwins Nobel prize forphagocytosis• 1930-40 Studies of metamorphosis• 1948-49Cell death in chick limb• 1955 Beginning of studies of lysomes• 1964-66 Necrosis & PCD described• 1971 Apoptosis term established• 1977 Cell death genes in C.elegansdiscovered• 1980-82 Caspase-3 (ced-3) identified• 1989-91 Apoptosis genes identified,ced-3 sequenced(, 2001)
  3. 3. What is Apoptosis?• Programed cell death• Orderly demise of cell• Essential for multi-cellularorganisms survival during celldivision• Important for cellulardevelopment
  4. 4. Ex: Finger webbing in humans• Body produce millionsmore cells than needed• Cells that do not formsynaptic connectionsundergo apoptosis• Some cases cells do notundergo cell death,webbing remains
  5. 5. Necrosis vs. ApoptosisCell death by injury• Cells swell• Membrane rupture• Cell lyses occurs• Inflammation• Mechanism- APT depletion,membrane injury, free radicaldamage• Areas of tissues are affectedCell death by suicide• Cell shrinkage• Membrane remain intact• Cell is phagocytosed• No inflammation• Mechanism – capasesactivated, endonuclease andproteases• Individual cell affected
  6. 6. Necrosis Vs. ApoptosisWilde, 1999
  7. 7. Stages of Apoptosis1. Cell damaged, stressed, or trigged by body signal2. Mitochondrial leakage3. Cell shrinkagea) Chromatin condensationb) Nuclear fragmentation4. Enzymatic breakdown (membrane blebbing)5. Nucleus destroyed6. Phagocytosis occurs
  8. 8. Caspase:Cysteine-aspartic proteases• Essential role in apoptosis,necrosis and inflammation• Required for immune system inmaturation of lymphocytes• Aids in cell differentiation &proliferation
  9. 9. PathwaysExtrinsic Pathway• Death receptor• Initiated from outside the cell• Activated through pro-apoptoticreceptors (ligands) on cellsurfaceIntrinsic Pathway• Mitochondrial• Initiated from within the cell• Activated in response to signalsfrom DNA damage (cell stress)
  10. 10. • Binding of Fas by Fas ligand induces recruitmentof Fas protein• Inside of cell Fas protein recruits adaptorprotein that bind procaspase 8• Caspase-8 is activated• Caspase-8 activates Caspase-3• Caspase -3 cleaves other proteins• Signal cascade occurs releasing Cytochrome- cfrom the mitochondria activating ApaF-1• ApaF-1 binds with Caspase-9 creating anApoptosome• Apoptsome activates Caspase-3 which cleavesthe actin cytoskeleton and apoptosis occurs
  11. 11. • Absence of Tropic Factor fromtrophic factor receptor• p53 protein phosphorylated• Inhibiting Bcl-2 &Bcl-XL releasingpro-apoptotic regulator Bax• Cytochrome c is released and bindsApaF-1• ApaF-1 binds with procaspase-9activating the caspase cascade• ApaF-1 binds with Caspase-9 creatingan Apoptosome• Apoptsomeactivates Caspase- 3 whichcleaves the actin cytoskeleton andapoptosis occurs
  12. 12. Diseases associated with ApoptosisInhibits Apoptosis• Cancer• HPV• Melanoma• Autoimmune Disorders• Systemic Lupus• Immune-mediate glomerulonephritis• Viral Infections• HerpesIncreases Apoptosis• AIDS• Neurodegenerative Disorders• Alzheimer’s Disease• Parkinson’s Disease• Ischemic Injury• Stroke• Myocardial infarction• Toxin-Induced liver disease• Alcohol
  13. 13. Future research…….• How cells are selected in vivo for cell death• How effector caspases are able to triggerapoptosis specifically for targeted cells andnot elicit a full blow apoptotic response• Further understanding of cell deathregulations to help treat a variety of humandisorders that are specific to programmedcell death