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CV-1 > Cardiac Cell Biology > Flashcards

Cardiac Cell Biology Flashcards

1
Q

WHat do skeletal muscle and cardiac muscle have in common

A

basal lamina

striated

contractile proteins similar

mechanism of contraction is similar

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2
Q

What are some factors about cardiac muscles that are unique against skeletal?

A

involuntary

smaller

1-2central uclei

branched

more vascular

more mitochondria (2x)

more myoglobin

more lipid droplets

intercalated discs

CICR

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3
Q

WHich is cardiac and which is skeletal?

A

Left is cardiac and right is skeletal

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4
Q

describe a cardiac myocyte

A

CMs branch (arrowheads)

intercolated discs (arrows) form boundaries between CMs

cross-striations are obscure, relative to skeltal muscle

nuclei centrally located

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5
Q

What is seen in the green outline what is within it?

A

myocytes! myofibrils!

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6
Q

How are sarcomeres aligned in cardiac muscle? are there more or less mitochondria in cardiac compared to skeletal? Where is the nucleus?

A
  • sarcomeres aligned as skeeltal musle
  • many more mito
  • lots of glycogen
  • central nucleus
  • endothelial cell (mkaing a capillary)
  • profuse mitochondria
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7
Q

WHat is the blue and what is the orange? What is the yellow?

A

blue is basal lamina between 2 adjacent cardiomyocytes

orange is Sarcoplasmic Reticulum which surrounds each myofibril

there are 6 thin filaments per thick filament

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8
Q

What is the function of the intercalated discs (IDs)?

A
  • sarcolemmal specializations that mediate CM-CM binding
  • they enable CMs to work as a single unit as if they were in syncytium
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9
Q

How do IDs connect? (structure)

A

they connect in a starcase fashion

  • transverse part: transmits force
    • a modified Z-band (Z-line)
  • consists of fascia adherens, comprised of N-cadherins, and desmososmes
  • lateral part: mediates CM-CM signaling
    • gap junctions (nexi) and a few desmosomes
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10
Q

WHat is the yellow? what is the blue ?

A
  • yellow-last I bands attaching to the modified Z-line
  • blue-gap junctions are along this lateral border

IDs cross adjacent in stepwise fashion

the fascia adherens is a zonula adhernes that doesn’t encircle the cell

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11
Q

what is the fascia aderens?

A

N-cadherins and desmosomes

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12
Q

WHat is this image illustrating?

A

N-cadherin in the intercelular space

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13
Q

WHat junctions make up the lateral part of the intercalated disc?

A

gap and desmosome junctions

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14
Q

1 connexon is made up of _______

A

1 connexon is made u of 6 connexins

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15
Q

How does excitation (electrical) occur?

A
  • Action potential: depolarization of the T tubules leads to depolarization of the SR
  • phase 2 AP: L-type Cav1.2 leads to Ca influx (CICR)
    • subunit through which Ca ions enter
    • Encoded by CACNA1C: mutated in long QT arrhythmia
    • does not bind to SR
  • Ca binds to Ryr leading to release of Ca from the sarcoplasmic reticulum, intracellular Ca increases and binds to troponin causing the physical phase of contraction
  • The Action Potential (AP) wave caused by brief influx of Na+ into CMs initiates a wave of depolarization along the sarcolemma, which proceeds into the T-tubules. This results in opening of L-type Ca++ channel proteins in the T-tubule membrane – notably Cav1.2 – which causes slightly increased Ca++ levels inside the CM, near the SR. This induces a Ca++-induced Ca++ release from the SR – termed a “CICR” – mediated by the binding of Ca++ (not binding of Cav1.2) to ryanodine receptors (RyR) in the SR membrane. Highlights of this process that should be noted are as follows:
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16
Q

How does contraction occur?

A
  • Ca binds troponin C causing tropomyosin to move
  • ATP hydrolysis activates the myosin head
  • The myosin head binds actin
  • Power stroke: myosin pulls actin into A-band, thus sarcomere shortens leading to contraction
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17
Q

What are the diffeences between Cav1.1 and Cav1.2

A

Cav1.1 is in skeletal muscle, Cav1.2 is in cardiac muscle

In skeltal muscle Cav1.1 binds istelf to the SR via Ryr. This binding does not happen between Cav1.2 and Ryr, instead a little Ca comes in causing a calcium induced calcium release fromt eh SR which will initiate contractile phase of cardiac muscle

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18
Q

What happens to the length of teh A band and I band?

A

A band length stays the same and I band length shortens

19
Q

How does relaxation occur?

A
  • L-type Ca channel inactivates
  • Phospholamban (PL) is phosphorylated, so that SERCA can pump Ca back into the SR
20
Q

Ho does B adrengergic stimulation lead to relaxation

A

The B adrenergic receptor modulates the contractile response

cAMP levels are increased

protein kinases are activated

phosphorylation of phospholamban

phosphorylation of phospholamban permits Ca uptake by SR

this leads to relaxation

21
Q

How does B adrenergic stimulation lead to enhanced contractile force?

A
  • The B adrenergic receptor modulates the contractile response
  • cAMP levels increased
  • protein kinases activated
  • phosphorylation of L-type Ca channel
  • phosphorylation of L-type channel leads to increased Ca uptake into myocyte
  • enhanced contractile force
22
Q

what impact do the sympathetics have on the heart and great vessels?

A

increase HR positive chronotropic

23
Q

what impact do the parasympathetics have on the heart and great vessels?

A

decrease HR and negative chronotropic

24
Q

what is the vagal neurotransmitter and how does it work? what are the effects?

A
  • the vagal neurotransmitter=achetychloine
  • activates muscarinis AchRs that inturn, inhibit adenyl cyclase
  1. negatice chronotropism: via muscarinic AcHcRs in SA node (slowing of heart)
  2. Negative Inotropism: reduced contractile force (B-adrenergic antagonist)
25
Q

The heart has regional histologic differences what the the different regions?

A

ventricular myocardium

atria, SA, AV nodes

Bundle of His

Cardiac fibroblasts

26
Q

What are the atria, SA, AVnodes like histologically?

A

they are smaller CMs with fewer striations

  • atrial myocytes have granules (G) with atrial natriuretic factor (ANF aka ANP)
  • ANF is pleiotropic: vasodlation etc
    *
27
Q

WHat is the Bundle of His like histologically?

A

specialized for conduction

endotheln leads to cardiac myocyte leads to purkinje fiber

28
Q

what are cardiac fibroblasts liek histologically?

A
  • the hearts most abundant cell type
  • but myocytes are much larger, hence occupy most of the hearts volume
29
Q

What is the chronology of a heart attack?

A
  1. immediate: myocyte death (MB-CK and cTnI) (creatine kinase and troponin)
  2. +15 hours: inflammation
  3. +2-3 days: wound healing
    1. collagen deposition, leading to fibrosis
  4. +3-4 days: angiogenesis
    1. clinical enhancement via VEGF, FGF
  5. Scar deposition
30
Q

What happens to cardiomyocytes during a heart attack?

A

cardiomyocytes die!

about 1 billion among a total of 5 billion (lose 20% of structure)

current research is looking into if the heart can regenerate!

31
Q

WHat happens to CM turnover with age? how does it compare throughout the heart?

A

is decreases with age, <1% annualy

the rate of turnover is similar in all parts of the heart

32
Q

What 7 cellulary therapies are thought to possibly regenerate the heart?

A
  1. skeletal muscle myoblasts
  2. cardiac fibroblasts (endogenous)
  3. pre-existing cardiomycytes
  4. adult stem cells (transplanted)
  5. bone marrow cells (transplanted)
  6. CMs from pluripotent stem cells (iPSCs)
33
Q

Can skeletal myoblasts (skeletal muscle stem cells) re-muscularize the injured heart?

A

transplanted satellite cells cause arrhythma

34
Q

Are Cardiac fibroblasts CM stem cells?

A

No

Fibroblasts respond to injury by making a scar

scars are permanent and they can’t contract

this is not good

35
Q

Can pre-existing CMs proliferate to fix the heart?

A

Maybe

  • adult CM proliferation can . be induced by
    • inhibiting tumor supressors
    • pro-proliferative agents
      • phase 1 trials are planned to evaluate Neuregulin
36
Q

Can endogenous adult stem cells re-muscularize the damaged heart?

A

apparently not, but can these cells can be induced?

  • their existence is still controversial
  • they might exist in ‘niches’ near BVs and/or in the epicardium
  • they’re identified by a stem cell marker (c-kit)
37
Q

what about transplanting c-kit cells?

A

phase 1 clinical trials isolate c kit cells from R atrium orIV septum via catheter and expand in culture. then transplant them. the result is that they function partly

38
Q

what about transplanting bone marrow cells?

A

**ckit+ cells from bone marrow

no new muscle, no harm done. modest increase in heart function, but transient. the best bet would be to transplant MSCs

39
Q

WHat about transplanting CMs from iPSCs?

A

the definitely do make beating CMs! but there are a few major concerns including tumor formation, CM immaturity, ability to integrate with host myocardium

40
Q

the structural and molecular features of adult CMs confer heart function, which is aerobically powered by ______

A

mitochondria, lipids and vascularization

41
Q

rhythmic heartbeat is conferred by ______

A

intercolated discs

42
Q

how does excitation/contraction differ between skeletal and cardiac myocytes?

A

Ca channel subunits are different

CICR is unique to the heart

Localization of Ca channel proteins relative to SR is different

contraction is similar

43
Q

In the heart ____________ are modulated via B-adrenergic, sympathetic and vagal pathways

A

strength of contraction, relaxation, and HR

44
Q

What are the best options for regeneration of CMs in the diseased heart?

A

best options for re-muscularization:

  • iPSC-CMs or new CMs from pre-existing CMs

CV-1 (7 decks)

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