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MSK > Tissue Architecture > Flashcards

Tissue Architecture Flashcards

1
Q

What are the functions of the cytoskeleton on the subcellular, cellular, and tissue level?

A
  • subcellular: organization, tensile strength, chromosome segregation, cell polarity, vesicular movement
  • cellular: cell morphology/shape, motility, cell adhesion, division
  • tissue: muscle contraction
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2
Q
  • type of filament
  • actin filaments (F-actin)
  • present in all cell types
  • generally unstable
  • essential for cell movements: locomotion, phagocytosis, cell division, contraction, etc.
A

microfilaments

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3
Q

What are modifications to actin proteins by other bound proteins?

A
  • stabilization
  • strengthen
  • cross-linking
  • organizing
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4
Q

What are drugs that affect actin filaments, what affect do they have?

A
  • phalloidin: binds and stabilizes filaments (death cap mushroom, used in microscopy)
  • cytochalasin: caps filament plus ends, prevents polymerization there
  • latrunculin: binds actin monomers and prevents their polymerization
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5
Q
  • type of cytoskeleton filament
  • crucial role in organization in all eukaryotic cells
  • long, stiff, hollow tubes
  • can undergo rapid assembly and disassembly
  • (+/-) sides like actin, dimers are added to (+) end
  • push/pull cells a part during cell division
  • shape, organize, and act are roads to move things around
  • comprise flagella and cilia
A

microtubules

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6
Q

What are drugs that affect microtubules and what is their action?

A
  • taxol: binds and stabilizes microtubules
  • colchicine, colcemid: binds tubulin and prevents their polymerization
  • vinblastine, vincristine: binds tubulin dimers and prevents their polymerization

(some of these meds are occasionally used in cancer tx to prevent formation of microtubules to prevent cell division)

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7
Q
  • type of filament
  • rope-like properties give these high tensile strength
  • often further stabilized by accessory proteins: cross-link filaments into bundles, link to microtubules, actin filaments, and cell junctions
  • form mesh-like structure called nuclear lamina
  • gives strength/stability to cell/tissue
A

intermediate filaments

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8
Q

Intermediate Filaments:

A
  • keratin
  • vimentin and vimentin-related filaments
  • neurofilaments
  • nuclear lamins
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9
Q
  • condition due to lack of nuclear lamins which causes cellular instability
  • mutations in type A lamin
  • sx: accelerated aging
A

Hutchinson-Gilford Progeria Syndrome (HGPS)

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10
Q
  • components are produced intracellularly and secreted/aggregate
  • matrix that interacts w/ cells/tissues via adhesion proteins
  • functions: anchor/engluf cells to define boundaries, cell polarity, cell survival/proliferation, cell movement
  • composition and properties controlled/vary by tissue type, location of cell, etc.
  • protein groups: proteoglycans, collagens, multi-adhesive matrix proteins
A

extracellular matrix and basal lamina

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11
Q
  • main structural protein in ECM/connective tissue and basal laminae
  • composed of trimeric proteins
  • associate as fibers, sheets, or transmembrane structures
  • affected by nutrient deficiencies and genetic conditions
A

collagen

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12
Q

How is collagen made/processed in the cell in terms of locations:

Rough ER:

Lumen of ER:

Lumen of ER and Golgi:

Secretory vesicle:

Extracellular:

A

Rough ER: synthesis of preprocollagen; insertion of procollagen molecule into lumen of ER

Lumen of ER: hydroxylation of proline and lysine residues; glycosylation of selected hydroxylysine residues

Lumen of ER and Golgi: self-assembly of the tropocollagen molecule, initiated by disulfide bond formation in th carboxy-terminal extensions; triple helix formation

Secretory vesicle: procollagen prepared for secretion from cell

Extracellular: cleavage of the propeptides, removing the amino and carboxy-terminal extensions, and self-assembly of the collagen molecules into fibrils and then fibers

TLDR: synthesized in the ER, processed in Golgi, further processed extracellularly

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13
Q

What is the mechanism of action of vitamin C deficiency leading to scurvy?

A
  • vitamin C deficiency leads to decreased hydroxylation of the proline/lysine residues comprising procollagen
  • this leads to failure of the procollagen to form the triple helix, leading to tissue instability
  • sx: decreased wound healing, loss of teeth, anemia, pale skin, sunken eyes
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14
Q

What are the 4 types of cell connections/junctions?

A
  • anchoring junctions
  • occluding junctions
  • channel-forming junctions
  • signal-relaying junctions
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15
Q
  • type of cell junction
  • link cells together and strengthens contact between cells and the ECM
  • ex: adheren junctions, desmosomes, hemidesmosomes
A

anchoring junctions

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16
Q
  • type of cell junction
  • seal gaps between cells through cell to cell contact, making an impermeable barrier for diffusion
  • ex: tight junctions
A

occluding junctions

17
Q
  • type of cell junction
  • link cytoplasm of adjacent cells allowing transport of molecules to occur between cells
  • ex: gap junctions
A

channel-forming junctions

18
Q
  • type of cell junction
  • ex: synapses in the nervous system
A

signal-relaying junctions

19
Q

What are the 4 major types of cell adhesion molecules (CAMs)?

A
  • cadherins: cell-cell
  • intergrins: cell-ECM or cell-cell
  • selectins: cell-cell in circulatory system (leukocytes/endothelial)
  • Ig superfamily: variable based on tissue
20
Q
  • type of cell adhesion molecule group
  • Ca2+ dependent adhesion
  • important in formation of junctions between cells (epithelial sheets), for example, desmosomes and adherens junctions
  • naming is based on location
A

cadherins

21
Q
  • subgroup of cadherins
  • type I (ex: E-cadherin, N-cadherin, R-cadherin): Ca2+ dependent homophilic adhesion function, cytoplasmic domains interact w/ beta-catenin, alpha-catenin, and p120
  • type II (ex: VE-cadherin): linked to the actin cytoskeleton, a/w adherens junctions
A

class cadherins

22
Q
  • subgroup of cadherins
  • T-cadherin and LI-cadherin
  • function as homophilic adhesion proteins w/o interaction w/ catenins or link to actin cytoskeleton
A

atypical cadherins

23
Q
  • type of cell adhesion molecule group
  • 15alpha and 8beta subunits form over 20 heterodimeric integrins
  • couple the ECM (fibronectin, collagen lamin) to cell cytoskeleton (intracellular actin)
  • cell-cell interactions via beta2 family (these molecules on leukocytes allow for adhesion and transmigration to sites of infection)
  • can activate signaling pathways and initiate multiple cellular responses
A

integrins

24
Q
  • type of cell adhesion molecule group
  • calcium dependent glycoproteins
  • bind to extracellular carbohydrates/ligands/integrins
  • important role in host defense mechanism (increased presentation during immune response, WBC has carbs and integrins (beta2) on the surface which act as ligands for these molecules)
  • ex: endothelial (E), leukocyte (L), and platelet (P)
A

selectins

25
Q
  • type of cell adhesion molecule group
  • family of more than 25 calcium-independent transmembrane glycoproteins
  • functions: immune cell interactions; homophilic/heterophilic binding; self recognition, binding, or adhesion processes of cells; stable adherent junctions; can give a cell polarity
  • ICAM, VCAM-1, PECAM-1, NCAM: contain variable number of immunoglobulin-like domains, expressed on vascular endothelial cells and bind to various integrin molecules
  • MAdCAM-1: contain Ig-like and mucin-like domains, expressed on mucosal endothelium to direct lymphocyte entry into mucosa
A

Ig superfamily of CAMs

MSK (33 decks)

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