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BMS 460 > Cell Membrane > Flashcards

Cell Membrane Flashcards

1
Q

junctional complexes

A

peripheral proteins in the plasma membrane that attach adjacent epithelial cells on their lateral surfaces

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2
Q

terminal bar

A

unresolved (can’t be visualized) group of junctional complexes. using light microscopy, looks like a little bar or spot where the lateral surfaces of epithelial cells meets the apical surface

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3
Q

terminal web

A

a filamentous structure found at the apical surface of epithelial cells, possesses microvilli (between the epithelial cells and the microvilli)

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4
Q

describe the glycocalyx

A
  • extracellular domain of the plasma membrane that is glycosylated by CHO portions of glycolipids and transmembrane glycoproteins (“sugar shell”)
  • in the electron micrograph, it shows up as an enzyme layer on top of the microvilli
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5
Q

functions of the glycocalyx

A
  • protection and lubrication
  • contains enzymes
  • cell-cell interaction
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6
Q

homing

A

a type of cell-cell interaction in which leukocytes are allowed to leave blood vessels and mediate inflammatory responses. this is allowed by the glycocalyx (and the transmembrane proteins that it possesses?)

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7
Q

passive transport

A

movement of molecules or ions across the membrane down their concentration or electrochemical gradient; no energy required

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8
Q

active transport

A

protein-mediated movement of molecules or ions across the membrane against their concentration or electrochemical gradient; energy required

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9
Q

primary active transport

A

transport of a substance across the membrane directly coupled to ATP hydrolysis

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10
Q

secondary active transport

A

simultaneous movement of two substances across the membrane indirectly coupled to ATP hydrolysis
- cotransport (symport): both substances in the same direction
- countertransport (antiport): substances move in opposite directions

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11
Q

example of cotransport

A
  • remember, this is secondary active transport in which ions move in the same direction
  • Na+-glucose transporter in small intestinal epithelial cells (move both glucose and sodium into cells)
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12
Q

example of countertransport

A
  • remember, this is secondary active transport in which ions move in opposite directions
  • Na+-Ca2+ transporter in heart muscle cells (calcium out of the cell, sodium in)
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13
Q

non-carrier-mediated transport

A

small hydrophobic molecules and small uncharged polar molecules can pass through the membrane with no carrier

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14
Q

carrier-mediated transport

A

transport proteins have a high level of specificity for the transported molecule or ion, undergo conformational changes during the transport process (can include facilitated diffusion or active transport, anything that requires a carrier)

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15
Q

examples of active transport in the myocardium

A
  • Ca2+ pump (primary, uses ATP to pump Ca2+ out of the cell
  • Na+/Ca2+ exchanger (3:1, secondary active transport, uses Na+ gradient to push Ca2+ out of the cell)
  • Na+/K+ ATPase (primary, 3:2)
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16
Q

how is the Na+/Ca2+ exchanger related to membrane potential?

A
  • when the membrane potential is negative (resting cells), Ca2+ goes out as Na+ enters the cell down its gradient
  • when the cell is depolarized and has a positive membrane potential, the exchanger works in the opposite direction, so Na+ leaves the cell as Ca2+ enters
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17
Q

what is the Na/Ca exchanger constantly doing under resting conditions

A

moves 3 Na+ ions out of the cell and 2 K+ ions in, maintaining their gradient (this pump is only slightly electrogenic!)

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18
Q

what are the 2 mechanisms by which Ca2+ gets removed from cells?

A
  • ATP-dependent Ca2+ pump that is constantly pumping Ca2+ out of the cell
  • Na+/Ca2+ exchanger, which uses the Na+ gradient to allow Na+ to enter the cell down it’s gradient, pushing Ca2+ out of the cell (antiporter, secondary active transport)
19
Q

what is the main consequence of cellular hypoxia and what processes can this cause?

A

cellular hypoxia results in decreased ATP production. this has a large effect on the Na+/K+ ATPase, which establishes the Na+/K+ gradient. when function of the ATPase decreases, Na+ builds up inside the cell. this triggers the Na+/Ca2+ exchanger because less Na+ will want to move into the cell down its gradient. as a result, intracellular Ca2+ levels rise since the exchanger is not pushing them out. increased intracellular Ca2+ increases cardiac muscle contractility. however, if the starting point of this process was hypoxia, then this cannot happen because there is not enough ATP to facilitate muscle contraction that would use the increased Ca2+ levels. thus the Ca2+ levels can cause mitochondrial damage and alter cellular function

20
Q

describe hydropic swelling as it relates to cellular hypoxia

A

cellular hypoxia primarily results in decreased ATP production. this decreases function of the Na+/K+ ATPase. we know that this results in an increase of intracellular Ca2+, but it also affects the movement of water because Na+ is no longer leaving the cell, taking water with it. an increase in osmotic pressure causes water to flow into the cell, causing the cell to swell. this hydropic swelling is an example of reversible cell injury, except in the case of rupture of the plasma membrane

21
Q

three cytoplasmic domains that regulate Cl- permeable CFTR channels

A
  • 2 ATP binding domains
  • a regulatory domain
  • the channel becomes permeable to Cl- when ATP is bound and the regulatory domain is phosphorylated
21
Q

what is CFTR

A

the CFTR protein is a membrane protein that conducts Cl- ions across epithelial membranes and is encoded by the CFTR gene. it also transports HCO3- out of the cell

22
Q

what family of transporters does the CFTR protein belong to?

A

the ABC transporter family – ATP-binding cassettes, requires ATP hydrolysis to transport ions, sugars, and amino acids

23
Q

name two important aspects of the CFTR protein

A
  • it is very efficient, so only about 10% of cells need to normally express the gene to prevent CF
  • the functions of CFTR are tissue-specific, and so is the impact of a CFTR mutation!!
24
Q

what channel does the CFTR gene regulate other than the CFTR channel?

A

Na+ ion channels, which are necessary for normal function of the lungs and pancreas

25
Q

what mutation accounts for nearly 70% of all CF cases?

A
  • the delta-F508 mutation (missing phenylalanine 508), which is in one of the ATP binding domains
  • note: CFTR gene is on chromosome 7
26
Q

what is the inheritance pattern of CF?

A

CF is the most common autosomal recessive monogenic disease, meaning it is passed via Mendelian inheritance. also, it is predominantly observed in Caucasians

27
Q

what glands does CF affect?

A

all exocrine glands, specifically submucosal glands of the respiratory tract and excretory ducts of sweat glands, also other epithelia

28
Q

how does CF affect the pancreas?

A

sticky mucus causes scarring of the pancreas, which prevents it from producing normal amounts of insulin (results in CFRD, of cystic fibrosis-related diabetes)

29
Q

problems caused by defective CFTR channel?

A
  • defective chloride and bicarbonate secretion
  • dysregulation of epithelial Na+ channels
  • the above changes cause poor clearance of mucus (because it is so thick), reduced airway surface liquid, and an exaggerated proinflammatory response that is partially driven by infection
30
Q

describe how CF impairs function of epithelial cells lining the airways

A

in normal individuals, the CFTR channel releases Cl- from epithelial cells into the airway, with water following. In addition. Na+ channels that allow Na+ to come back into the cell. in people with CF, the CFTR channel is stuck closed and does not allow Cl- to leave the cell, meaning water does not leave either, resulting in sticky mucous. the Na+ channel also take up extra Na+.

31
Q

describe how CF impairs function of epithelial cells lining excretory ducts of sweat glands

A

in normal individuals, the CFTR channel allows Cl- to come back into the epithelial cells from the lumen of the excretory duct. the Na+ channel also lets Na+ back into the cell. in people with CF, these channels do not let these ions back into the cells, leaving them in the excretory duct resulting in overly salty sweat.
NOTE: this process is occurring in the bilayer cuboid cells in the excretory duct which are normally responsible for reabsorbing NaCl. Clear cells in the coiled tubular secretory portion secrete most water and electrolytes (actually making the sweat)

32
Q

steps for a CF diagnosis

A
  1. test for high levels of immunoreactive trypsinogen (IRT)
  2. PCR for CFTR mutation
  3. if the mutation is detected, confirm with sweat test
33
Q

describe heterozygous vs. homozygous CFTR mutation

A

heterozygous: carrier, no CF phenotype
homozygous (recessive) CF phenotype

34
Q

what is IRT

A

immunoreactive trypsinogen - if the pancreatic duct is dysfunctional due to excess mucous, then the pancreatic enzymes that it is supposed to secrete will go into the blood instead, one of these being IRT

35
Q

what are some GPCR agonist ligands?

A

these are things that bind the receptor just like the intended ligand:
- photons
- ions
- odorants
- tastants
- vitamins
- hormones
- NT’s
- natural products like morphine
- human symbiotic bacteria

36
Q

describe the structure of a GPCR

A

7 transmembrane segments, ligand-binding pocket on the outside, G-protein-activating portion on the inside

37
Q

what larger group of enzymes are GPCR’s a part of?

A

GTPases - the most well known of which are the Ras superfamily, which are involved in cell differentiation, proliferation, cytoskeletal organization, vesicle trafficking, and nuclear transport

38
Q

4 major families of G proteins

A

according to their alpha subunits:
- G alpha s: stimulatory, via adenyl cyclase, increases cAMP
- G alpha i: inhibitory, via adenyl cyclase, decreases cAMP
- G alpha q: via a phospholipase, increases IP3 and DAG and releases intracellular Ca2+
- G alpha t: transducin, via a phosphodiesterase

39
Q

describe the path from ligand binding to altered gene expression

A

ligand binds to cell-surface receptor, activates associated proteins, which activates an effector enzyme to generate an intracellular second messenger

40
Q

what are two important membrane-bound enzymes?

A

adenylyl cyclase and phospholipase C

41
Q

what do small GTPases do?

A

they can act as molecular switches in intracellular signaling pathways and have many downstream targets

42
Q

manifestations of McCune-Albright syndrome

A
  • bony fibrous dysplasia, whitish skin pigmentation, early puberty, more common in boys than girls
  • rare, genetic, non-inherited
  • caused by an activating mutation in GNAS gene, causing adenylyl cyclase to be constnatly turned on, which = more cAMP
  • really affects whole endocrine system
43
Q

cause of McCune-Albright syndrome

A

an activating mutation in the GNAS gene (which makes an alpha subunit for a G protien) results in adenylyl cyclase to be constitutively activated, resulting in constant production of cAMP. this affects regulation of many endocrine glands, bone development, and producing bone in the wrong place

BMS 460 (28 decks)

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