Cell Bio Apop/Cell Cycle (6)

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mse263
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232198
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Cell Bio Apop/Cell Cycle (6)
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2013-09-01 10:55:34
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Cell Biology
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MBS Exam 1
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  1. Hypertrophy
    an increase in cell size; also used to describe tissues and organs that have enlarged (NOT an altered proliferative state)
  2. altered Proliferation states that are REVERSIBLE:
    • Regeneration
    • Metaplasia
    • Hyperplasia
    • Dysplasia
    • • altered growth states in tissues can reverse back to normal or at least stop progressing if the stimulus that provoked the proliferation is removed
  3. Regeneration
    a one-for-one replacement of cells; type of reversible proliferation state
  4. Hyperplasia
    • increase in number of fully differentiated/functions cells in a tissue (more than normal; in response to some kind of stimulus, eg. injury)
    • • disease examples: Restenosis [following vascular surgery], Grave's disease
  5. Restenosis following vascular surgery
    • • if endothelial cells don’t regenerate quickly enough after a balloon angioplasty, then smooth muscle cells can become hyperplastic
    • • this is problematic b/c excessive smooth muscle cells causes re-blockage (restenosis) of the blood vessel that was JUST opened
  6. Grave's disease
    • • a form of hyperthyroidism
    • • hyperplasia occurs: too many thyroid cells that are all fully differentiated
    • • with the increase of cells comes an increase of thyroid hormone production --> leads to increased metabolic rate, weight loss, bulging eyes, and strabismus
  7. Hyperthyroidism
    • overproduction of thyroid hormones --> increased metabolic rate, increased ocular pressure
    • • Grave's Disease = most common form of hyperthyroidism
  8. Metaplasia
    adaptive substitution of one cell type by another cell type; ALWAYS pathogenic
  9. What are the two places metaplasia is commonly seen in?
    • 1) Lung – in smokers, heat and smoke cause normal cells to be replaced by other, more protective cells
    • 2) Cervix: Chronic Inflammatory Pelvic Disease
    • • normal columnar is replaced by a stratified squamous epithelium
    • • more protective squamous epithelium lacks cilia and can't move mucus along well creating a rich environment for bacterial/viral replication
  10. Dysplasia
    • changes in mitotic rate of cells, loss of positional control, and loss in the uniformity of cell shape (pleiotropy)
    • • often a precursor to cancer
    • • seen in the exocervix where it is often a precursor to CERVICAL CANCER (reason for pap smears)
  11. cancer
    malignant neoplasia or malignant tumor; cell has to lose both proliferation controls and positional controls to be cancerous
  12. Neoplasia
    • proliferation continues even in the absence of an external stimulus (NOT CANCER)
    • • NON-reversible proliferation state
  13. Benign Neoplasia
    • loss of proliferation control only; "benign" tumors, like fibroids
    • • when there the loss of proliferation control, but NO loss of position control; means that a tumor will result but can't spread
  14. Uterine Fibroids
    • clinical correlate: BENIGN NEOPLASIA
    • • these are benign tumors that grow in the uterus
    • • positional control is retained.
    • • tumors cause severe pain, bleeding and infertility
  15. Malignant Neoplasia
    • loss of BOTH proliferation and positional controls
    • • (eg. metastatic tumors, "cancer")
  16. Cancer
    clinical correlate: MALIGNANT NEOPLASIA
  17. CENTROMERES ARE ATTACHED TO __________ AND CYTOKINESIS IS ORCHESTRATED BY ____________
    Centromeres are attached to microTUBULES and cytokinesis is orchestrated by microFILAMENTS
  18. position of a cell within a tissue can determine its:
    • proliferation rate
    • • partly b/c information in the extracellular matrix helps regulate cell proliferation
    • • eg. epithelial cells in intestinal crypt
  19. What are the four phases of the cell cycle?
    • G1prepares cell for replicating DNA; cell is busy doubling its contents in preparation for an eventual cell division
    • S
    • G2
    • M
  20. G1
    prepares cell for replicating DNA; cell is busy doubling its contents in preparation for an eventual cell division
  21. Restriction (R) Point
    • checkpoint between G1 and S where the cell has the option to exit the cell cycle & enter a quiescent state called G0
    • • cells go into G0 based on their nutritional state, positional information, density/contact/ shape/stretch information, and matrix information
  22. Rb protein
    • normally inactive (hypophosphorylated) and complexed w/ TFs needed for cell proliferation
    • • this prevents them from binding to DNA
    • • during correct passage through the R checkpoint, cyclin D/cdk4-6 and cyclin E/cdk2 complexes phosphorylate Rb, changing its conformation and releasing the TFs
  23. Describe the active/inactive state of the Rb protein:
    • • active: UNphosphorylated, complexed with TFs
    • • inactive: phosphorylated, NOT complexed with TFs
    • • in tumor cells, the Rb protein is missing or defective.
  24. How does the R checkpoint work?
    • 1) external signals (growth factors) stimulate synthesis of cyclins D & E
    • • cyclin D partners w/ cdk4 or 6
    • • cyclin E partners w/ cdk2
    • 2) when enough cyclin D/cdk4-6 and cyclin E/cdk2 are activated, they phosphorylate Rb protein
    • 3) the TFs released from Rb bind to DNA and activate transcription that encodes proteins which push cells through the R-point --> into S-phase
    • • once DNA synthesis starts a protease is activated & destroys cyclins D & E inactivating kinase complexes
  25. S
    DNA replication
  26. G2
    prepares cell for segregation/division of genome and cytoplasm
  27. M
    chromosome segregation (mitosis) and separation of daughter cells (cytokinesis)
  28. What are the purposes of checkpoints in the cell cycle?
    • • monitor the health of the nuclear genome (i.e., DNA damage, completeness of DNA replication, alignment of chromosomes
    • • monitor availability of key nutrients and cytokines in the environment
  29. In what kind of cells is the R (restriction) point defective?
    CANCER cells; they plough through & if they start making DNA and don't have enough material they'll happily die
  30. MPF
    • regulates mitosis; made up of two cyclins: cyclin B & cdk1
    • • the key substrates for cyclin B-cdk1 are laminas and histones
    • • think back to lecture 1: at the start of mitosis, laminas are phosphorylated, causing nuc. membrane disassembly, while the histones are phosphorylated, cause chromosome CONdensation
  31. Which cyclin partners with which cdk?
  32. Tissues with the greatest frequencies of ___ _________ also exhibit the greatest frequency of apoptosis
    • cell proliferation
    • • seen in thymus, spleen, small intestine, epidermis, & ovarian follicles
  33. Necrosis
    • •'accidental' cell death
    • •triggered by sustained ischemia, physical or chemical trauma (eg. ionic shock)
    • •cells and organelles swell, organelles damaged, •chromatin randomly degraded
    • •cells LYSE
    • •INFLAMMATORY RESPONSE OCCURS
  34. Apoptosis
    • •programmed cell death triggered by specific signals that activate specific genes
    • •cells shrink, organelles intact, & chromatin is degraded systematically
    • •membrane blebs (chunks of cell) can be phagocytosed by neighboring cells
    • •NO INFLAMMATORY RESPONSE
  35. PKD (polycystic kidney disease)
    • clinical correlate: APOPTOSIS
    • •autosomal dominant
    • •results in uncontrolled APOPTOSIS of kidney cells.
    • •get kidney tissue full of cysts b/c cells that have died from apoptosis leave spaces that become filled with fluid --> creating cysts.
  36. What are the 3 phases of Apoptosis?
    • 1) Induction: intrinsic or extrinsic
    • 2) Modulation
    • 3) Execution: caspases --> endonucleases
    • (I'm Meredith Elman)
  37. What are PHYSIOLOGIC activators of apoptosis induction (5)?
    • intrinsic and extrinsic pathway inducers:
    • • intrinsic = growth factor withdrawal, survival factor withdrawal, glucocorticoids
    • • extrinsic = TNF-alpha, FasL
  38. What are DAMAGE-RELATED activators of apoptosis induction (5)?
    viral infection, heat shock, toxins, tumor suppressors, oxidants/free radicals
  39. What are THERAPY-ASSOCIATED activators of apoptosis induction (2)?
    UV/gamma radiation, chemotherapeutic drugs
  40. What are the intrinsic pathway inducers of apoptosis?
    • •growth factor withdrawal
    • •survival factor withdrawal
    • •glucocorticoids
    • -intrinsic often called mitochondrial pathway
  41. How does the intrinsic pathway work?
    • • upon mild ischemia, removal of nutrients, there is a withdrawal of growth factors (& the like)
    • • when apoptosis signal is received, pro-apoptotic Bcl-2 proteins (eg. BAD) are DEphosphorylated
    • • they bind to others on the outer mitochondrial membrane
    • • this results in loss of mitochondria membrane channel control and cytochrome C is released
    • • helps cleave caspase 9 --> begins caspase amplification
  42. What are extrinsic pathway inducers of apoptosis?
    • •TNF-alpha
    • •FasL (Fas ligand)
  43. How does the extrinsic pathway work?
    • • via receptor mediated apoptosis
    • • 2 death receptors may be expressed on a cell's membrane: TNF-alpha & FasL (fas ligand system, or FasL receptor)
    • -almost all cells have TNF-alpha receptors in their membrane
    • • a cell presenting a ligand will live
    • • cells with receptors will DIE
    • • once bound the receptor's death domain is activated and initiates caspase cascade
  44. Bcl
    both pro- and anti-apoptotic family of proteins
  45. Burkitt's Lymphoma
    • clinical correlate: apoptosis modulation, BcL proteins
    • •individual produces LOTS of pro-life Bcl proteins (eg. Bcl-2, Bcl-X1) but low levels apoptosis-inducing Bcl proteins (eg. BAD)
    • •results in excessive overgrowth of cells
  46. What activates the caspase pathway in the intrinsic & extrinsic pathways of apoptosis induction?
    • • intrinsic: Bcl protein dephosphorylation, complexing, and openings of mitrochondrial membrane channels to release cytochrome C
    • • extrinsic: binding of a TNF-alpha or FasL ligand to their respective receptors
  47. What are two differences and one similarity between the extrinsic and intrinsic pathways?
    • 1) intrinsic pathway is activated by: growth factor/survival factor withdrawal, glucocorticoids, viruses, DNA damage-causing events, toxins, oxidized compounds (free radicals), and ischemia
    • • extrinsic pathway is activated by TNF-alpha or Fas ligand binding to their receptors on the cell surface
    • 2) intrinsic, NOT the extrinsic pathway, can be modulated by the Bcl family proteins
    • 3) similarity: both pathways result in massive amounts of caspase-3 activity --> the chief executioner of cells undergoing apoptosis
  48. caspase 3
    cleaves cytoskeletal fibers and activates specific endonuclease that makes the ladder; common enzyme in apoptosis cascade
  49. How do the eye and testes confer immunological privilege?
    • • via the EXTRINSIC pathway
    • • all T-cells have Fas RECEPTORS on their surface
    • • blood vessels lining immune privileged sites constitutively express Fas-LIGAND on their endothelial cells
    • • when T-cells enter blood vessels lining privileged sites, Fas receptor on T-cells interacts with Fas-Ligand on endothelial cells
    • • T cells are induced to undergo apoptosis
  50. Hashimoto Disease
    HYPOthyroidism: apoptosis of thyroid cells leads to compromised thyroid function
  51. Dysregulated apoptosis is the hallmark of which conditions?
    • • Syndactyly + polydactyly
    • • cancers expansion
    • • cachexia (“wasting”) seen in some late-stage cancer patients
    • • Polycystic Kidney Disease
    • • Hashimoto’s (autoimmune form of hypothyroidism)
  52. Stroke
    • • clinical correlate: anti-apoptosis drugs
    • • inhibitors of apoptosis (IAPs) exist in humans; neuronal IAP can protect stroke victims from excessive loss of neurons if given in time

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