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    APOPTOSIS

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    johnthar929
    Apoptosis is a natural and programmed process of cell death that occurs under genetic control. It plays an important role in development, tissue homeostasis, and removing damaged or infected cells. The process involves activation of cysteine proteases called caspases that trigger a cascade of events within the cell leading to its death. Apoptosis is regulated by proteins like Bcl-2, Bax, and p53 and can be stimulated by both external signals and internal signals within the cell. Dysregulation of apoptosis can lead to diseases associated with excessive or insufficient cell death.

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    APOPTOSIS

    Uploaded by

    johnthar929
    9 views13 pages
    Apoptosis is a natural and programmed process of cell death that occurs under genetic control. It plays an important role in development, tissue homeostasis, and removing damaged or infected cells. The process involves activation of cysteine proteases called caspases that trigger a cascade of events within the cell leading to its death. Apoptosis is regulated by proteins like Bcl-2, Bax, and p53 and can be stimulated by both external signals and internal signals within the cell. Dysregulation of apoptosis can lead to diseases associated with excessive or insufficient cell death.

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    Apoptosis is a natural and programmed process of cell death that occurs under genetic control. It plays an important role in development, tissue homeostasis, and removing damaged or infected cells. The process involves activation of cysteine proteases called caspases that trigger a cascade of events within the cell leading to its death. Apoptosis is regulated by proteins like Bcl-2, Bax, and p53 and can be stimulated by both external signals and internal signals within the cell. Dysregulation of apoptosis can lead to diseases associated with excessive or insufficient cell death.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    9 views13 pages

    APOPTOSIS

    Uploaded by

    johnthar929
    Apoptosis is a natural and programmed process of cell death that occurs under genetic control. It plays an important role in development, tissue homeostasis, and removing damaged or infected cells. The process involves activation of cysteine proteases called caspases that trigger a cascade of events within the cell leading to its death. Apoptosis is regulated by proteins like Bcl-2, Bax, and p53 and can be stimulated by both external signals and internal signals within the cell. Dysregulation of apoptosis can lead to diseases associated with excessive or insufficient cell death.

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    of 13

    APOPTOSIS

    • Apoptosis- Programmed cell


    death
    • Greek word- falling off /
    Dropping off -1972
    • Form of coordinated & internally
    planned cell death
    • Greater significance in – variety
    of physiologic & pathologic
    conditions
    • Occur – under genetic control –
    cell suicide
    • Genes of – own cells play important role
    • Natural process
    • 1. Proper development of tissues:
    • Eg : death of neurons in CNS – during
    brain development & synapse formation
    • Fetal development – degeneration of –
    many tissues – web in fingers
    • 2. Normal functioning of adult tissues:
    • Cyclic breakdown of endometrium – start
    of –menstruation
    • Epithelial cells tht- lose their connection –
    basal lamina & surrounding cells -undergo
    • 3. Apoptosis to destroy the cells that represent – threat to –
    integrity of – organism
    • Apoptosis of the cells – infected with virus
    • Cells with DNA damage
    • Cancer cells
    STIMULAI
    Activation – cysteine Smac
    proteases in cell –CASPASES –
    triggers – apoptosis
    Normally – inactive form
    Stimulated by external &
    internal stimuli

    In mitochondria – apoptosis
    factor – located in –
    intermembrane space –
    migrates to – nucleus –
    destroys – DNA
    • REGULATION OF APOPTOSIS
    • ONCE – initiated – certain intracellular proteins provide – signal for – final
    programmed cell death – determine – outcome
    • BCL-2 –
    • Located – outer mitochondrial membrane
    • Control apoptotic process by binding to various cytosolic proteins
    • Binds with – BAX & BAD – proteins – ( known to promote APOPTOSIS )
    • Also bind BCL-XL – protein- inhibits APOPTOSIS
    • Another binding protein – in cytosol – pro- apoptotic protease activating
    factor (apzaf-1)
    • Other Apoptotic regulator protein
    • TP53
    • Caspases
    • BAX
    • Certain Viruses – adenovirus, papilloma, hepatitis B
    MAJOR STEPS OF APOPTOSIS
    Surface receptor –
    present on –Cytotoxic T
    cells , when comes in Hydrolysis of
    contact with target cell- sphingomyelin on cell
    activated membrane – generates
    – ceramide
    Physiologic process of apoptosis which occur
    in three main steps
    1.Involve single / cluster of cells
    2. Apoptotic cell become – round /
    oval & reduce in size
    3. Cytoplasm – reduced, organelles –
    almost normal
    4. Cell membrane – convolutes with
    formation of membrane bound
    spherical structures – apoptotic
    bodies
    That contain compacted organelles
    5. Chromatin condensation – occurs-
    around – periphery of nucleus
    6. Phagocytosis of apoptotic bodies –
    occurs by – macrophages
    • Glycoprotein molecule –
    THROMBOSPONDIN –
    • Posphoprotein –
    PHOSPHATIDYLSERINE –
    Appear on – outer surface
    of apoptotic bodies –
    which facilitate
    recognition by
    macrophages for
    phagocytosis
    • Detection
    • DNA fragmentation assay by electrophoresis
    • TUNEL staining
    • Demonstration of chromatic condensation by
    H&E/Feulgen/Acridine orange
    • Estimation of cytosolic cytochrome –C ,
    activated caspase,
    • Application
    • Disorders with reduced apoptosis (survival of abnormal cells)
    • Cancer
    • Autoimmune diseases

    • Disorders with increased apoptosis (excessive loss of cells)


    • Neurodegenerative disease – Alzheimers , Parkinson’s
    disease
    • Ischemic injury – MI & stroke

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