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Physiology of Cells 2002 > Lecture 24: Steroid receptors > Flashcards

Lecture 24: Steroid receptors Flashcards

1
Q

Cell Surface Receptors (3)

A
  1. Ion-channel-linked Receptor
  2. G-protein-linked receptor
  3. Enzyme-linked receptor
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2
Q

Classes of Receptor (4) + example

A
  • Four (4) main classes of hormone/ neurotransmitter receptor
  1. Ligand gated ion channels
    - Nicotinic receptor
  2. GPCR (G-protein coupled receptors)
    - b-adrenergic receptors
  3. Catalytic Receptor
    - Insulin receptor
  4. Intracellular receptors
    - Glucocorticoid receptor
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3
Q

Characteristics of receptor: 5

A
  1. Ion channels, GPCR and catalytic receptors located on cell membrane (typically)
  2. Most hormone, neurotransmitters cannot enter cells
  3. Extracellular ligands bind to extracellular component of a transmembrane protein.
  4. Conformational change in protein transfers the signal across the cell membrane
  5. Some hormones and neurotransmitters CAN enter cells and have receptors located in the cytosol or nucleolus
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4
Q

Intracellular Receptors (3) + examples

A
  1. Nitric Oxide (NO) can enter cells
    - Receptor is catalytic, soluble guanalyate cyclase
  2. Thyroid hormone enters cells through a carrier protein
    - Receptor is in the nucleolus, activation changes gene transcription
  3. Steroids, the classic intracellular receptor
    - Receptors in the cytosol
    - Activation causes changes in gene transcription
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5
Q

Adrenal Glands = Three principle groups of
steroid hormones
(5 examples)

A
  1. Glucocorticoids
    - Cortisol
  2. Mineralocorticoids
    - Aldosterone
  3. Sex Steroids
    - Estrogens (estradiol)
    - Progesterone
    - Androgens (testosterone)
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6
Q

Adrenal Glands Structure + Hormones secereted

A

Capsule

  1. Zona Glomerulosa = ALDOESTERONE (mineral corticoid)
  2. Zona Fasciculata =
    GLUCOCORTICOIDS (eg cortisol)

and
ANDROGENS (DHEA and androstenedione)

  1. Zona Reticularis =GLUCOCORTICOIDS (eg cortisol)

and
ANDROGENS (DHEA and androstenedione)

  1. Medulla = EPINEPHRINE

Medullary vein

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7
Q

Control of Cortisol Production

A
  1. Production of cortisol
    controlled by:
    adrenocorticotrophic
    hormone (ACTH)
  2. ACTH release from
    pituitary controlled by
    corticotropin-releasing
    hormone (CRH) from
    hypothalimus
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8
Q

What is Cortisol: 6

A
  1. Produced in adrenal cortex
  2. Primary glucocorticoid in humans

3.Causes
- Catabolism of skeletal muscle into amino acids
-Conversion of amino acids into glucose, gluconeogenesis
- Increased blood glucose
- Anti-inflammatory and much more

  1. increase CRH → increase ACTH → increase Cortisol
  2. Cortisol inhibits ACTH and CRH release
  3. ACTH inhibit CRH release
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9
Q

Control of Cortisol:

A
  1. CRH
  2. ACTH
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10
Q

Control of Cortisol: CRH (6)

A
  1. CRH receptor is a
    CPCR linked to Gs
  2. Increases cAMP
  3. Activates PKA
  4. PKA phosphorylates
    and open Ca2+
    channels
  5. Ca2+ entry causes
    exocytosis
  6. ACTH released
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11
Q

Control of Cortisol: ACTH

A

1.ACTH receptor is a
CPCR linked to Gs

  1. Increases cAMP
  2. Activates PKA
  3. PKA phosphorylates
    enzymes involved in
    synthesis of cortisol
  4. PKA also increase
    synthesis of enzymes
    used to make cortiso
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12
Q

Release of Cortisol = 8

A

1.Steroids not stored in vesicles

  1. Lipid soluble so just diffuses out of cells
  2. Cortisol controlled by controlling production
  3. ACTH and CRH both act on GPCR linked to Gs
  4. Increase cAMP production and activate PKA
  5. PKA turns on production of cortisol AND
    transcription of the enzymes that make cortisol
  6. Release of ACTH due to PKA opening Ca2+ channels
  7. Release of CRH, just like neurotransmitters
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13
Q

Steroid Receptor Action = 2

A
  1. TRANSCRIPTIONAL ACTIVATION BY GLUCOCORTICOID HORMONE
  2. TRANSCRIPTIONAL ACTIVATION BY THYROID HORMONE
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14
Q

Mechanism of Cortisol Action: 8

A
  1. Steroid Receptor bound to chaperone proteins

2.HEAT SHOCK PROTEIN 90 (HSP90) main steroid receptor binding protein

  1. Binding of cortisol to the GLUCOCORTICOID RECEPTOR
    causes translocation to the nucleolus
  2. HSP90 is released
  3. Active receptor forms HOMODIAMER
  4. Receptor-cortosol complex bind DNA at
    GLUCOCORTICOID RESPONSE ELEMENTS (GRE)
  5. Activates RNA polymerase
  6. Gene transcription
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15
Q

PKA and Gen Expression: 5

A
  1. GPCR can also alter gene expression
  2. PKA can translocate to
    nucleolus much like MAPK
  3. Phosphorylates CREB (CRE BINDING PROTEIN)
  4. Binds to DNA at *cAMP
    RESPONSE ELEMENTS (CRE)
  5. Activates gene transcription
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16
Q

Receptor Control of Transcription: 7

A
  1. Steroids, Tyrosine kinases and GPCR can all alter gene transcription.
  2. Steroid receptors are transcription factors.
  3. Tyrosine kinases activate MAPK (and other factors)
  4. MAPK enters nucleus and activates transcription factors
    by phosphorylation
  5. Gs linked GPCR activate PKA
  6. PKA enter nucleus and activates transcription factors (CREB) by phosphorylation.
  7. DNA contains HORMONE RESPONSE ELEMENTS that bind transcription factors activated by specific hormone signals.
17
Q

Features of Signal Pathways:
2

A
  1. Ligand gated ion channels
  2. G-protein coupled receptors
18
Q

Ligand gated ion channels CHARACTERISTICS = 4

A
  1. Very fast response times, a few msec
  2. Very short acting, a few to a few hundred msec
  3. Common on nerves and muscle
  4. Signal amplification is through membrane potential
19
Q

G-protein coupled receptors CHARACTERISTICS = 5

A
  1. Fast response times, hundreds of msec
  2. Short acting, seconds to min (mostly)
  3. Common for both neurotransmitters and hormones
  4. Use small molecule second messengers
  5. Modify protein function (fast) and gene transcription (slow)
20
Q

Features of Signal Pathways = 2

A
  1. Catalytic receptors
  2. Steroid receptors
21
Q

Catalytic Receptors: Characteristics 6

A
  1. Fast to slow response times, seconds to hours
  2. Moderate to long acting, min to hours
  3. Common for growth factors and hormones
  4. Signal amplification is through protein phosphorylation
    cascades
  5. Modify protein function by phosphorylation
  6. Modify Gene expression
22
Q

Steroid Receptors = 3

A
  1. Very slow response times, hours
  2. Long acting, hours to days
  3. Actions through gene transcription

Physiology of Cells 2002 (24 decks)

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