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Molecular & Cellular Mechanisms > Eicosanoids & Lipid Mediators: Prostaglandins, Thromboxane, Leukotrienes > Flashcards

Eicosanoids & Lipid Mediators: Prostaglandins, Thromboxane, Leukotrienes Flashcards

1
Q

COX

A

cyclooxygenase enzyme (COX-1 and COX-2), contains iron, needs O2 co-factor, converts AA –> PGH2

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2
Q

NSAID

A

non-steroidal anti-inflammatory drug

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3
Q

PUFA

A

polyunsaturated fatty acid

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4
Q

Eicosanoids

A

Lipid mediators derived from 20 carbon PUFA, includes prostaglandins, thromboxane, leukotrienes

Eicosanoids are autacoid mediators

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5
Q

Omega 6 PUFA

A

arachidonic acid –> 2-series prostaglandins & thromboxane

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6
Q

Omega 3 PUFA

A

EPA (eicosapentanoic acid) –> 3-series prostaglandins & thromboxane

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7
Q

ARACHIDONIC ACID

A

REMEMBER ARACHIDONIC ACID – is the substrate for COX

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8
Q

Eicosanoid Biosynthesis

A
  1. Arachidonic acid is liberated from the PM following a stimulus
  2. COX enzymes transform AA into PGs or Tx
  3. PGs exit cells and bind to receptors to transmit signals to cells
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9
Q

Arachidonic Acid Cascade

A
  1. Phospholipase A2 releases AA
  2. COX converts AA to PGH2
  3. Tissue Isomerases convert PGH2 to PGD, PGE, PGF, PGI and TxA2
  4. PG dehydrogenase or hydrolysis
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10
Q

COX

A

Cyclooxygenase enzyme contains iron and requires O2 co-factor to convert AA to PGH2

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11
Q

Eicosanoids are made, not stored

A

Is not a form of paracrine signaling (hormones, steroids)

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12
Q

PG, Tx synthesis acts only after a stimuli activates phospholipase A2

A

Phospholipase A2 induces AA to come out of PM

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13
Q

Limiting reagents of PG/Tx synthesis

A

O2 and AA, auto-inactivation of COX enzyme, metabolic degradation of PGs and spontaneous hydrolysis of Tx and PGI2

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14
Q

Can find COX in all cells except

A

RBC

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15
Q

Eicosanoids mediate autocrine and paracrine signaling nearby the cells that make them.

A

Unlike hormones, autacoids are short-lived. PGDH limits their accumulation and circulation via the blood stream.

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16
Q

Autocrine signaling

A

Cell can make PGs/Tx and respond to PGs/Tx binding to receptor

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17
Q

Paracrine signaling

A

Cell B lacks enzymes to make PGs or Tx, responds to PG/Tx made from cell A

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18
Q

Not every cell can make every prostaglandin

A

Not every cell has every membrane receptor

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19
Q

Prostaglandin and Thromboxane Receptors are G-proteins (7 layer)

A

Gs and Gq stimulatory G-proteins

Gs associated with AC (adenyl cyclase –> cAMP)
Gq associated with PLC (phospholipase C –> DAG/IP3 –> Ca2+)

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20
Q

PGE2 (EP) and PGI2( IP) associate with Gs and AC

A

PGF2 (FP) and TxA2 (TP) associate with Gq and PLC

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21
Q

Receptors: EP2, EP4 and IP

A

RELAX smooth muscles

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22
Q

Receptors: FP and TP

A

CONSTRICT smooth muscles

23
Q

Phospholipase A2 (PLA2)

A

Liberate AA (arachidonic acid) from phospholipids

24
Q

Phospholipase C (PLC)

A

Liberates IP3 & DAG from phospholipids (PIP2)

25
Q

PGI2 name

A

Prostacyclin

26
Q

Important to have balance in constricting and relaxing eicosanoids

A

Or else you can have effects like angina pectoris

27
Q

COX-1 vs COX-2

A

COX-1 is constitutive (always expressed)

COX-2 is inducible

28
Q

COX-1 functions

A

Responds to physiological stimuli to regulate physiological functions of PGs and Tx

Has role in gut, repro and development

29
Q

NSAIDS cause a decrease in PG

A

Overuse of NSAID can cause gastric ulcer

30
Q

PGE2 in gut

A

Too little = gastric ulcer

Too much = diarrhea

31
Q

PGs in repro

A

Too little = delayed birth

Too much = pre-mature labor, birth

32
Q

PGs in development

A

PG keeps ductus arteriosus patent in fetus, NSAIDs help close it

At birth, PGE2 is removed, ductus arteriosus closes

33
Q

COX-2 exception

A

COX-2 is normally expressed and plays a prominent role in kidney physiology

34
Q

COX-2 expression

A

Prominent role responding to pathological stimuli (inflammation, cancer)

35
Q

COX-2 in kidney

A

Deficit of PGs in kidney leads to Na/H2O retention (edema) and hypertension

36
Q

Cardinal signs of inflammation

A
  1. Vasodilation, decreased platelet aggregation
  2. Increased permeability
  3. Increased temperature
  4. Increased sensitivity to pain

Redness, swelling, pain

37
Q

COX-1 and COX-2, PGs and inflammation

A
  1. Inflammation stimulates AA release
  2. COX-1 converts AA into PGE2 (increases)
  3. PGE2 causes redness, swelling, pain

Induced COX-2 follows same pathway and AMPLIFIES symptoms

38
Q

Platelets

A
  1. No nucleus
  2. Generate TxA2 (thromboxane)
  3. Constrict blood vessels and amplify platelet aggregation
39
Q

Endothelium

A
  1. Cells that line blood vessels
  2. Make PGI2 (prostacyclin)
  3. Relaxes blood vessels and inhibits platelet aggregation
40
Q

How does body regulate ratios of PGs and Tx?

A

By varying the levels of isomerases/synthases among different tissues

Different cells can make different eicosanoids

41
Q

Hemostasis

A

Maintaining blood flow

42
Q

Collagen stimulates TxA2 formation by platelets

A

Clotting mechanism, reaction to severed blood vessels

43
Q

Platelet aggregation pathway

A

PLA2 activation –> AA –> COX-1 –> PGH2 –> TxA2 –> TP receptors –> signal transduction

44
Q

PGI2 and TxA2 work in concert with each other

A

Prevent systemic effect, when TxA2 is in action, PGI2 is working downstream of it

45
Q

COX-2 can be induced by endothelial cells

A

COX-2 induction may amplify PGI2 synthesis

46
Q

COX-2 cannot be induced by platelets

A

No nucleus, no de novo transcription of proteins (unlike endothelial cells)

47
Q

Arachidonic Acid rich in beef, EPA rich in fish

A

EPA –> TxA3 which is a weak vasoconstrictor, weak platelet aggregation

Omega-3 PUFA reduce inflammatory processes, vasoconstriction, platelet aggregation

48
Q

Leukotrienes made from same pathway, substitute COX for 5-LOX (lipoxygenase)

A

Leukotrienes named because they are made by leukocytes and have a conjugated triene in structure

49
Q

Leukotriene A4 = LTA4

A

No receptor

50
Q

Leukotriene B4 = LTB4

A

BLT1,2 receptor

51
Q

Leukotriene C4 = LTC4

A

CysLT1, 2 receptor

52
Q

Leukotriene D4 = LTD4

A

CysLT1 receptor

53
Q

Leukotriene E4 = LTE4

A

CysLT receptor

54
Q

TEST ADVICE

A

Leukotrienes are always an incorrect test question answer

Molecular & Cellular Mechanisms (11 decks)

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