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Pathology > Regeneration and Repair Part I > Flashcards

Regeneration and Repair Part I Flashcards

1
Q

Regeneration leads to

A

restoration of lost/damaged tissue and return to normal state

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2
Q

Repair

A

restore original tissues but results in architectural changes and deposition of fibrous scar

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3
Q

what types of cells undergo regeneration

A

tissues with high proliferative capacity:

  • hematopoietic cells
  • skin
  • GI epithelium
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4
Q

regeneration is dependent on the presence of what type of cells

A

pluripotent stem cells

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5
Q

repair combines regeneration of native tissue with

A

scar formation/fibrosis

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6
Q

the extent of repair is dependent on

A

the type and degree of injury

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7
Q

inflammation contributes to scar formation through production of

A

growth factors and cytokines

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8
Q

what is the function of ECM components (ie. collagen)

A

provides a framework needed for cell migration, angiogenesis and repair

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9
Q

cell numbers are controlled by balancing

A
  • proliferation
  • differentiation
  • death
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10
Q

proliferation

A

physiologic or pathologic stimuli regulate cellular proliferation and tissue growth

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11
Q

differentiation

A

terminally differentiated cells are incapable of replication. After death, new cells may be generated by stem cells

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12
Q

cell death/apoptosis

A

genetically determined cell destruction required for tissue homeostasis

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13
Q

what are the 3 different proliferative activity of tissue

A
  1. liable (continuously dividing)
  2. stable (quiescent)
  3. permanent (non-dividing)
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14
Q

liable tissue

A

rapid replication allows replacement of dead cells with newly formed ones

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15
Q

examples of liable tissues

A

surface epithelium GI and GU tract, hematopoietic cells

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16
Q

stable tissues

A

limited replication under normal homeostasis (quiescent, Go) may replication in response to stimuli

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17
Q

examples of stable tissue

A

parenchymal cells of liver, kidneys and pancreases; mesenchymal cells

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18
Q

what are parenchymal cells

A

functional tissue o an organ as distinguished from the connective and supporting tissue

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19
Q

what is quiescent

A

in a state or period of inactivity or dormancy

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20
Q

permanent tissues

A

cannot undergo mitotic divisions

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21
Q

examples of permanent tissues

A

neurons, skeletal and cardiac muscle cells. Injured cells are replaced by system supportive elements (ie. glial cells in CNS) or scarring (fibrosis)

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22
Q

what are stem cells

A

cells capable of self-renewal and differentiation

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23
Q

what are the 2 mechanisms that stem cells maintain their number

A
  1. obligatory asymmetric replication

2. stochastic differentiation

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24
Q

what is obligatory asymmetric replication

A

-with each stem cell division, one daughter cell retains its self-renewing capacity (new stem cell) while the other enters a differentiation pathway

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25
Q

what is stochastic differentiation

A

-each stem cell division generates EITHER two self-renewing stem cells OR two cells that will undergo lineage differentiation

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26
Q

what are the 2 types of stem cells

A
  1. embryonic stem cells

2. adult (somatic) stem cells

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27
Q

embryonic stem cells are induced by

A

pluripotent stem cells

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28
Q

where do embryonic stem cells reside

A

in the inner cell mass of blastocysts during the early stages of embryonic development

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29
Q

embryonic stem cells regenerate what kind of tissue

A

any/all tissues of the body (Pluripotent)

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30
Q

as embryonic stem cells differentiate they give rise to

A

multipotent stem cells and differentiated cells of the 3 embryonic layers

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31
Q

how do you prevent embryonic stem cell rejection

A

immune rejection can be prevented if stem cells contain the patient’s genetic material

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32
Q

describe the process of embryonic stem cell treatment

A
  1. transfer of cell nucleus to enucleated oocyte
  2. induced pluripotent stem cells (iPS cells):
    • adult cells undergo activation of genes responsible for pluripotency
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33
Q

what is the purpose of stem cell therapy

A

use cells to replace damaged or genetically defective cells (sickle cell anemia)

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34
Q

function of adult (somatic) stem cells

A

-allow regeneration (and homeostasis) in liable tissues (ie. bone marrow, skin, GI tract)

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35
Q

adult (somatic) stem cells give rise to what type of cells

A

progenitor cells which are lineage restricted and no longer have the ability to self-renew

36
Q

where do adult (somatic) stem cells residue

A

in special micro environments (niches) that support transmission of regulatory stimuli that directs stem cell self-renewal and generation of daughter cells

37
Q

where do hematopoietic stem cells (HSC) generate all cell lineages

A

in the bone marrow

38
Q

after disease, radiation or chemotherapy —– cells are able to repopulate all blood elements

A

hematopoietic stemm cells (HSC)

39
Q

what is the most important clinical use of hematopoietic stem cells

A
  • in the treatment of leukaemia/lymphoma

- stem cell transplantation

40
Q

where are skin stem cells present

A

in the hair follicle bulge, interfollicular areas of the surface epidermis and sebaceous glands

41
Q

function of skin stem cells

A

replenish the surface epidermis after skin wounding

42
Q

epidermal stem cells are tightly regulated by what

A

growth factors and cytokines

43
Q

function of cell cycle and replication

A

allows tissues to maintain homeostasis and to replenish cells during tissue regeneration and repair

44
Q

Phases of Cell Cycle

A

G1 (presynthetic)
S (DNA synthesis)
G2 (premitotic)
M (mitotic)

45
Q

what phase are quiescent cells in

A

remain in Go (not entered the cell cycle)

46
Q

what are check points

A

prevent errors/maintain tissue homeostasis by halting the cell cycle if DNA is damaged

47
Q

G1 entrance

A

transition into G1 (from Go or M) induced by growth factors

48
Q

G1/S checkpoint

A
  • the restriction point, is a rate-limiting step

- monitors DNA integrity BEFORE replication

49
Q

G2/M checkpoint

A

monitors DNA AFTER replication and allows entry into M phase

50
Q

what cells are key players in the checkpoint system

A

cyclins and cyclin-depdent kinases (CDKs)

51
Q

function of cyclins and CDKs

A

they phosphyorylate target proteins which in turn stimulate transcription of cell cycle genes –> CELL CYCLE PROGRESSION

52
Q

how do cyclins and CDKs gain catalytic activity

A

by forming complexes

53
Q

function of growth factors

A

bind cell surface receptors and regulate key physiologic processes (such as proliferation, cell survival, locomotion, angiogenesis)

54
Q

what begins the intracellular signalling cascade of

A

formation of ligand-receptor complex

55
Q

what are the 3 signalling mechanisms among cells

A
  1. autocrine
  2. paracrine
  3. endocrine
56
Q

autocrine

A

cells secrete their own ligand (autocrine loop)

57
Q

paracrine

A

one cell type produces a ligand that binds to receptors on adjacent target cells

58
Q

endocrine

A

hormones are synthesized by endocrine cells and travel through the circulation to distant target cells

59
Q

the type of cellular receptors determines the mechanisms of

A

signal transduction

60
Q

what are the different types of cellular receptors

A
  1. receptors with intrinsic tyrosine kinase activity
  2. receptors lacking intrinsic tyrosine kinase activity that recruit kinases
  3. G protein-coupled receptors
  4. Steroid hormone receptors
61
Q

where do receptors with kinase activity reside

A

on the cel surface

62
Q

what activates the receptor tyrosine kinase

A

ligand binding which induces dimerization and tyrosine phosphorylation

63
Q

function of the active kinase

A

phosphorylates downstream effector molecules that transmit the signal to the cell nucleus

64
Q

receptors with kinase activity used by

A

most growth factors (EGF, TGF-a, HGF, PDGF, VEGF, FGF)

GF signalling…think kinase receptors!!!!

65
Q

describe receptors without kinase activity

A
  • ligand-receotor binding recruits extrinsic kinase (ex. JAK)
  • JAKs bind the receptors, activate signal transducers (STATs) through phosphorylation
  • STATs enter the nucleus and activate gene transcription by directly binding DNA
66
Q

receptors without kinase activity used by

A
  • interleukins
  • interferons
  • growth hormone
67
Q

what are G-protein coupled receptors

A

composed of seven transmembrane alpha helices that signal through GTP-binding proteins

68
Q

function of p53

A

inhibit cell cycle progression (TUMOR SUPPRESSOR GENE = growth inhibiting)

69
Q

G-proteins get activated by

A

guanine nucleotide exchange factor (GEF)

GDP –> GTP

70
Q

G protein coupled receptors are the largest family of

A

plasma membrane receptors

71
Q

G protein coupled receptors are common — targets

A

pharmaceutical targets

72
Q

where do steroid hormone receptors reside

A

in cell, in cytoplasm of nucelus

73
Q

steroid hormone receptors function as

A

ligand-depdent transcription factors

74
Q

ligand activated receptors bind to

A
  • specific DNA sequences (hormone response elements) in target genes
  • interact with other transcription factors
75
Q

steroid hormone receptors bind to

A
  • estrogen
  • thyroid hormone
  • Vit D
76
Q

growth hormones induce activity of

A

transcription factors

77
Q

function of transcription factors

A

bind to DNA and allow transcription of adjacent genes

78
Q

what are the important transcription factors that regulate cell proliferation

A

c-MYC and c-JUN

P53

79
Q

function of c-MYC and c-JUN

A

induce cell cycle (ONCOGENE = growth promoting)

80
Q

extensive regeneration of the liver only occurs if

A

the basic connective tissue framework is uninjured

81
Q

partial hepatectomy triggers

A

cytokine signaling that forces the remaining hepatocyte to reenter the cell cycle and proliferate

82
Q

when is the liver able to regernate

A

after partial hepatectomy (up to 60% can be removed)

83
Q

which parenchumal organ does not have a limited regeneration capacity

A

liver

84
Q

function of p53

A

inhibit cell cycle progression (TUMOR SUPPRESSOR GENE = growth inhibiting)

85
Q

function of the active kinase

A

phosphorylates downstream effector molecules that transmit the signal to the cell nucleus

Pathology (18 decks)

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