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AFN Pathophysiology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

Signal Transduction

A

Transmission/amplification
sorting and directing
integration
adaptation/modulation

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2
Q

4 Types of Cell Signaling

A

Autocrine
Juxtacrine
Paracrine
Endocrine

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3
Q

Autocrine Signaling

A

Cell targets itself

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4
Q

Juxtacrine Signaling

A

Acts on cells within close proximity that are connected by gap junctions. I.E. Cardiac muscle cells connected by intercalated discs

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5
Q

Paracrine Signaling

A

Acts on nearby cell, but ligands are secreted into cytoplasm and travel short distance to target cell

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6
Q

Endocrine Signaling

A

Ligands secreted into blood stream where they travel to target cell

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7
Q

Types of Signaling Pathway Receptors

A

Lipophilic ligand (doesn’t need receptor)
Transporter (water soluble ligands)
Ion channel (water soluble ligands)
GPCR (water soluble ligands)
Enzyme linked receptor (water soluble ligands)

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8
Q

Membrane receptors

A

Receptors are the detectors and initial amplifiers
when the receptor binds a ligand the receptor undergoes a conformational change which initiates signal transmission

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9
Q

Ion Channels

A

LIgand activated
GPCR-linked
2nd messenger activated

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10
Q

Kinases

A

Add phosphate to a molecule
can either activate or inactivate a protein

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11
Q

Phosphtases

A

take a phosphate away (ase)

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12
Q

Receptor Kinsases/Phosphotases

A

mostly used in growth/survival signaling.

most ligands are some type of growth factor (including growth hormone)

Main way things are turned off and on

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13
Q

Heterotrimeric G-Protein Coupled Receptors

A

HCPCR

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14
Q

HGPCR

A

2/3 of all ABX work through these receptors
Human genome project has identified about 500 HGPCRs

Ligand binds HBPCR > activation of G protein > activates 2nd messenger proteins and or activates ion channels

Almost like having kinase/phosphatase in the same unit.

Has alpha, gamma, and beta subunits.

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15
Q

Active subunit of HGPCRs?

A

alpha subunit
(most HCPCRs work through alpha subunit)

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16
Q

GEF

A

Guanine exchange factor
takes phosphate from GTP and adds phosphate to GDP on alpha subunit to activate it

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17
Q

GAP

A

GTPase activating protein (RGS protein)
takes phosphate away from alpha subunit of g protein inactivating it

Has both GEF and GAP?? (I will clarify this on Friday)

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18
Q

HGPCR Pathway Overview

A

Ligand binds receptor
ligand receptor complex activates G-protein (g protein binds GTP)
G protein disassociates from the complex
Alpha/beta/gamma subunits disassociate and interact with their
effector proteins
Hydrolysis of GTP by RGS inactivates the alpha subunit and promotes reassembly of the trimer (alpha/beta/gamma subunit)

19
Q

Types of G alpha Proteins

A

Gs
Gi
Gq

20
Q

Differential effects of GPCRs

A

Different tissues have different receptors, response depends on the type of receptor, and which 2nd messenger molecules are activated

21
Q

Gs Protein

A

Activated by: Epi, NorEpi, histamine, glucagon, ACTH, LH, FSH, TSH, and more

22
Q

Gi Proteins

A

Activated by: NorEpi, prostaglandins, opiates, angiotensin, many peptides

23
Q

Gq Protein

A

Activated by: Acetylcholine, Epi

24
Q

Gs Signaling Pathway

A

Increase cAMP
increase Ca++ influx

25
Q

Gi Signaling Pathway

A

Decrease cAMP
Increase IP3 and CA++

26
Q

Gq Signaling Pathway

A

Increase: IP3, DAG, Ca++
Polarize membrane

27
Q

G Protein Acting by Adenylyl Cyclase

A

Receptor linked to Gs activated adenylyl cyclase
converts ATP to cAMP which acts as small intracellular transporter
(Gs think stimulation of cAMP)
(cAMP is also most widely used 2nd messenger)
activates cAMP dependent protein kinase (PKA) (4cAMP to 1 PKA)
PKA phosphorylates many proteins leading to cell response

28
Q

A cellular signaling pathway that leads to increase in cAMP must occur through which G alpha protein?

A

Gs. Any increase of cAMP is modulated by Gs.

29
Q

G-Protein acting via phosphodiesterase (PDE)

A

Receptor linked to Gi activates PDE,
PDE brakes the ester bond of cyclic nucleotides (cAMP) leaving monophosphate nucleotides (AMP) without signaling function (can’t activate PKA).

Gi think inhibitory

Basically: PDE breaks down cAMP

30
Q

G protein action via PDE Example (don’t need to know for test, only to help understand the concept)

A

In vascular smooth muscle:
Gs> ^cAMP > inhibits MLCK > prevents contraction > causes vasodilation

Gi > decrase cAMP > inhibit inhibition of MLCK > prevent relaxation > cause contraction

31
Q

G-Protein acting via Phospholipase

A

Receptor linked to Gq activates membrane bound enzyme phospholipase C (PLC)

PLC converts membrane phospholipid into 2nd messengers inositol triphosphate (IP3) and diacylglycerol (DAG)

IP3 bind receptor on SR causing release of Ca++

DAG binds and partially activates protein kinase C (PKC)

Ca++ triggers many cellular events including the full activation of PKC

32
Q

Signaling via Lipid Molecules

A

Phospholipase A2 (PLA2) breaks down membrane phospholipids into arachidonic acid.

Arachidonic acid > lipoxygenase > leukotrines

Arachidonic acid > cycloxygenases (COX1/COX2) > prostaglandins, prostacylcines, & thomboxanes

*we take aspirin or NSAIDs to block cycloxygenase activity

33
Q

Effects of Leukotrines

A

vasoconstriction
brochnospasm
^ vascular permeability

34
Q

Effects of Prostaglandins / Prostacyclins

A

vasodilation
^ vascular permeability
inhibit platelet aggregation (prostacyclins)

35
Q

Effects of thromboxanes

A

vasoconstriction
platelet aggregation

Thromboxanes occur latter on in the inflammation process

36
Q

Predominant Inflammatory Signaling molecules

A

lipoxygenase
cycloxygenase
leukotrienes
prostaglandins
prostacyclins
thromboxanes

37
Q

Signaling via Gases

A

Nitric oxide (NO) synthesized by the enzymatic (NOS) degradation of arginine > 2nd messenger guanylyl cyclase > activation of cGMP > PKG signals (cGMP > PKG pathway is the same as the cAMP > PKA pathway)

Remember: gasses diffuse across membranes. NO is acting as ligand

NO is the primary signaling gas

38
Q

Why is vasodilation controlled by gas signaling?

A

There is no parasympathetic innervation of vascular smooth muscle, so vasodilation is entirely mediated by NO.

39
Q

3 ways NO is produced

A
  1. Produced by neurons (nNOS). Acts as neurotransmitter and neuromodulator in the brain.
  2. Produced by endothelial cells (eNOS): inhibits platelet aggregation and leukocyte adhesion, causes vasodilation
  3. Inducible form (iNOS): produced by wide range of tissues; induced by pro-inflammatory cytokines producing huge amounts of NO
40
Q

Lipophilic Ligands

A

Can pass through cell membrane on their own

intracellular receptors are usually in the nuclear membrane, slow metabotropic receptors.

Affect transcription/translation of proteins.

Many hormones and drugs work this way.

This pathway works from bottom of cell up, unlike the other signaling pathways.

41
Q

Signal Modulation

A

We can modulate signaling events over time by changing lots of different things. I.e number of receptors, ligand concentration, ligand specificity, receptor affinity.

An example: in opioid abuse receptors become less responsive over time

42
Q

How can single ligand I.E (NE) elicit opposite responses in identical tissues at different locations simultaneously?

A

some tissues have both beta and alpha receptors, the [NE} determines which receptors are activated.

Target response depends on the target receptors and ligand concentration.

43
Q

Agonist vs Antagonist

A

Agonist: mimics normal response

Antagonist: binding inhibits response. Two types, competitive and allosteric (noncompetitive) inhibition.

44
Q

Signal Transduction is Adaptive

A

Over time strength of stimuli and increase or decrease.
Multiple overlapping adaptive mechanisms dependent on strength and duration of stimulus.

AFN Pathophysiology (6 decks)

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