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    A Pop To Sis

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    Apoptosis is a programmed and regulated form of cell death that is important for development, tissue homeostasis, and immune defense. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and membrane blebbing. In contrast, necrosis is unregulated cell death that results from external factors and causes inflammation. Apoptosis occurs through intrinsic and extrinsic pathways that converge on caspase activation to execute cell death. It plays roles in development, hormone responses, and eliminating infected or damaged cells.

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    A Pop To Sis

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    Apoptosis is a programmed and regulated form of cell death that is important for development, tissue homeostasis, and immune defense. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and membrane blebbing. In contrast, necrosis is unregulated cell death that results from external factors and causes inflammation. Apoptosis occurs through intrinsic and extrinsic pathways that converge on caspase activation to execute cell death. It plays roles in development, hormone responses, and eliminating infected or damaged cells.

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    A Pop to Sis

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    Apoptosis is a programmed and regulated form of cell death that is important for development, tissue homeostasis, and immune defense. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and membrane blebbing. In contrast, necrosis is unregulated cell death that results from external factors and causes inflammation. Apoptosis occurs through intrinsic and extrinsic pathways that converge on caspase activation to execute cell death. It plays roles in development, hormone responses, and eliminating infected or damaged cells.

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    15 views23 pages

    A Pop To Sis

    Uploaded by

    baby_shopgurl3738
    Apoptosis is a programmed and regulated form of cell death that is important for development, tissue homeostasis, and immune defense. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and membrane blebbing. In contrast, necrosis is unregulated cell death that results from external factors and causes inflammation. Apoptosis occurs through intrinsic and extrinsic pathways that converge on caspase activation to execute cell death. It plays roles in development, hormone responses, and eliminating infected or damaged cells.

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    of 23

    Apoptosis

    Group 3 Section C2
    Paraguya, Lanisa
    Pariñas, Orlando II
    Pasajol, Margarita
    Pascua, Vanessa
    Objectives
    • To define Apoptosis
    • To differentiate apoptosis from necrosis
    • To determine the different cellular features of
    both apoptosis and necrosis
    • To discuss the role of apoptosis in
    embryogenesis, development and differentiation
    of tissues, AIDS, Cancer and immune defense
    • To discuss the different laboratory indices that
    will define cells undergoing apoptosis
    Definition: APOPTOSIS
    • A prearranged pathway of cell death whereby the cell
    commits suicide for the benefit of the organism
    • Also known as programmed cell death (PCD), is an
    important counterpart to mitosis for the regulation of
    cell numbers during development, in homeostatic cell
    turnover in the adult, and in many other settings
    • Characterized by a series of distinct morphological
    and biochemical alterations to the cell such as DNA
    fragmentation, chromatin condensation, cell
    shrinkage, and plasma membrane blebbing
    Apoptosis is important in many of the
    following developmental and
    physiological processes:
    • Causes regression of anatomical structures in fetal
    development
    • Eliminates self-recognizing lymphocyte clones in
    immunologic processes
    • Prevents overpopulation in continuously renewing
    tissues
    • Maintains the balance of cellularity in the response of
    the tissues to hormones
    • Deletes mutant cells or those with DNA damage
    • Eliminates cells infected with viruses
    Stimuli that prompt a cell to
    commit apoptosis:
    • Hypoxia
    • Defective energy or ATP production
    • Physical agents or drugs
    • Chemical agents or drugs
    • Infectious agents
    • Immunological reactions
    • Genetic derangements
    • Nutritional imbalance
    Morphologic Features
    APOPTOSIS Vs NECROSIS
    • Death of single cells • Death of many cells
    • Cytoplasmic blebbing • Plasma membrane disruption
    • Chromatin condensation
    • Nuclear swelling and lysis
    • Cell shrinkage
    •
    • Cell swelling
    Lysosomes and other cytoplasmic
    organelles intact • Lysosomal breakdown
    • Nuclear DNA breaks into fragments • Cell lysis and disintegration
    • Rapid phagocytosis of apoptotic • Phagocytosis by macrophage
    bodies by macrophages and
    adjacent cells • Often cause a damaging
    • No inflammatory response inflammatory response in
    surrounding tissues
    Characteristics distinguishing
    apoptosis from necrosis
    Defining features Apoptosis Necrosis
    Physiologic/pathologic
    features
    Cellular role Usually normal Abnormal, accidental
    Process Active, energy-dependent Passive, results from
    lack/loss of energy
    Distribution Dispersed, affects Contiguous, simultaneous,
    individual cells and massive affects in
    damaged tissue areas
    Triggers 100s of physiologic and Sudden transfer of energy,
    noxious stimuli specific toxins, or ATP
    depletion
    Induction Slow (hours), stochastic Rapid (secs, mins)
    Tissue inflammation Absent Present
    Cell removal Rapid and discrete Slow
    Characteristics distinguishing
    apoptosis from necrosis
    Defining features Apoptosis Necrosis
    Morphologic features
    Cellular membranes Integrity preserved, Loss of integrity, with
    blebbing of intact plasma spilling of cell constituents
    membrane
    Cell volume Decreased, as well as the Increased
    formation of small,
    fragmented “apoptotic
    bodies” or inclusions
    Organelle structure Late preservation, with Swelling of nucleus and
    exception of nuclear other organelles
    condensation and
    fragmentation
    Chromatin Discrete, organized Pattern conserved
    condensation, margination
    and fragmentation (e.g.
    pyknotic nuclei)
    Characteristics distinguishing
    apoptosis from necrosis
    Defining features Apoptosis Necrosis
    Biochemical and molecular
    features
    Mitochondrial permeability Moderate Severe
    transition
    Mitochondrial membrane Transient loss Permanent loss
    potential (delta psi-m)
    Requirement fro ATP Yes No

    Membrane phospholipid Exteriorization of Unchanged


    asymmetry phosphatidylserine from inner to
    outer leaflet of plasma membrane
    Cell pH Acidification Unchanged

    DNA cleavage Initial specific large cleavage Random DNA cleavage


    products of 300, then 50, kbp,
    followed by internucleosomal
    cleavage leading to DNA ladder
    pattern of 180 bp unit repeats
    Caspase dependence Yes No
    Apoptosis is induced via two main
    routes
    1. The mitochondria (the intrinsic pathway)
    2. The activation of death receptors (the
    extrinsic pathway)
    • Both pathways converge to induce the
    activation of caspases, the final executioners
    of cell death
    Pathways
    • The extrinsic pathway is initiated through the
    stimulation of the transmembrane death
    receptors, such as the Fas receptors, located
    on the cell membrane. In contrast, the
    intrinsic pathway is initiated through the
    release of signal factors by mitochondria
    within the cell.
    Caspases
    • cysteine-aspartic proteases
    • have been termed the final "executioner" of
    apoptosis
    CASPASES
    Two types:
    1.initiator (apical) caspases-
    e.g. CASP2, CASP8, CASP9 and CASP10
    2.effector (executioner) caspases-
    e.g. CASP3, CASP6, CASP7
    The caspase cascade can be activated
    by:

    • granzyme B (released by cytotoxic T


    lymphocytes and NK cells) which is known to
    activate caspase-3 and -7
    • death receptors (like Fas, TRAIL receptors
    and TNF receptor) which can activate caspase-8
    and -10
    • the apoptosome (regulated by cytochrome
    c and the Bcl-2 family) which activates caspase-
    9.
    Clinical correlation
    • Alzheimer’s Disease

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