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Cardiovascular & Respiratory Medicine > Vascular endothelium > Flashcards

Vascular endothelium Flashcards

1
Q

Describe the structure of the vascular system

A

(not just a distribution network)
- The vascular system is one of the largest and the most extensive networks in the body
- Blood vessels are lined by endothelial cells.
- When dysfunctional, the endothelium contributes to more diseases than any other organ

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2
Q

Describe the basic structure of blood vessels

A

Three layers (except for capillaries and venules):
1. Tunica adventitia:
- Vasa vasorum
- nerves
2. Tunica media:
- Smooth muscle cells & (extrenal elastic membrane)
3. Tunica intima:
- Internal elastic membrane
- Lamina propria (smooth muscle and connective tissue)
- basement membrane
- endothelium

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3
Q

Describe the role & structure of capillaries

A
  • Capillaries is where the exchanges of nutrients and oxygen between blood and tissues occur
  • Capillaries and venules are formed by::
  • endothelium (capillary endothelial cells)
  • supported by mural cells (pericytes)
  • and a basement membrane
  • this is just a general overview of the structure- endothelial cells have heterogeneity
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4
Q

What are pericytes?

A

Pericytes are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries throughout the body.

They are important for:
- blood vessel formation
- maintenance of the blood–brain barrier
- regulation of immune cell entry to the central nervous system (CNS)
- control of brain blood flow (constriction)

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5
Q

What is the role & structure of endothelial cells?

A
  • Endothelial cells line the vascular system
  • The Endothelium acts as a vital barrier separating blood from tissues
  • Very extensive: surface area > 1000 m2; weight >100g
  • Endothelial cells are very flat, about 1-2 µm thick and 10-20 µm in diameter
  • Endothelial cells form a monolayer, one cell deep (contact inhibition)
  • Endothelial cells directly control tissue-specific cell function- allow cells to have protein mediated interactions, e.g. to prevent overgrowth)
  • In vivo, it is thought that endothelial cells live a long life and have a low proliferation rate, unless new vessels are required: angiogenesis
  • Endothelial cell regulate essential functions of blood vessels
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6
Q

What functions/ processes are regulated by the endothelium?

A
  • Vascular tone
  • Angiogenesis
  • Permeability
  • Inflammation
  • Haemostasis & thrombosis
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7
Q

What is the importance of angiocrine factors in endothelial cells?

A
  • Endothelial cells directly control tissue-specific cell function
  • All cells of the body are in contact with microvascular endothelial cells
  • Angiocrine factors from endothelial cells are essential for the maintenance of tissue homeostasis and regeneration
  • they are molecules found in blood vessels’ endothelial cells that can stimulate organ-specific repair activities in damaged or diseased organs.
  • The angiocrine profile of each tissue-specific microvascular endothelium is different; conversely, the tissue-specific microenvironment influences the phenotype of endothelial cells
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8
Q

Endothelial cells are the most abundant cell type in the normal myocardium, true or false?

A

TRUE

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9
Q

How are vessel types categorised in terms of structure?

A
  • They can either be continuous or discontinuous
  • Of the continuous types, they can either be non-fenestrated or fenestrated
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10
Q

What are some examples of non-fenestrated (continuous) blood vessels in the body?

A

vessels that make up the:
- Muscle
- Lung
- Skin
- Blood brain barrier

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11
Q

What are some examples of fenestrated (continuous) blood vessels in the body?

A

Vessels that make up the:
- Kideny glomerulus
- GI tract

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12
Q

What are some examples of fenestrated (continuous) blood vessels in the body?

A

Vessels that make up the:
- Kidney glomerulus
- GI tract

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13
Q

What are some examples of discontinuous blood vessels in the body?

A

Vessels that make up the:
- liver
- marrow sinus

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14
Q

What is meant by “Single-cell RNA sequencing”?

A
  • Single-cell RNA sequencingexamines thesequenceinformation from individualcellswith optimizednext-generation sequencingtechnologies
  • Allows us to study a single cell that expresses a gene
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15
Q

What is the “Human Cell Atlas”?

A

The Human Cell Atlas is an international collaborative consortium that charts the cell types in the healthy body, across time from development to adulthood

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16
Q

What is meant by “sprouting angiogenesis”

A

“Sprouting angiogenesis is the growth of new capillary vessels out of preexisting ones”
- process is regulated by a wide array of growth factors and signalling pathways
- The list of endothelial molecules and pathways that modulate the formation of new vessels is constantly growing
- Most of these pathways depend on the dynamic regulation of gene expression in ECs, and are determined by a complex network of transcriptional regulators

17
Q

When can “sprouting angiogenesis” occur?

A

Although normally quiescent, ECs (endothelial cells) have the ability to proliferate & form new vessels, either physiologically or due to some pathology:
Physiology:
- During development
- Menstrual cycle
- Wound healing
Pathology:
- Cancer
- Chronic inflammatory diseases
- Atherosclerosis
- Retinopathies
- Ischemic diseases
- Vascular malformations

18
Q

Describe the process of “sprouting angiogenesis”

A
  1. Degradation & proliferation:
    - Angiogenesis starts with the activation of endothelial cells by specific growth factors that bind to its receptors
    - As a result, the extracellular matrix and basement membrane, surrounding the endothelial cells, are degraded locally by activated proteases
    - Regulated by growth factors and inhibitors
  2. Outgrowth/ Migration of ECs
    - This allows the endothelial cells to invade into the surrounding matrix and, subsequently, to proliferate and migrate through the matrix
    - EC proliferation & deposition of new ECM
  3. Sprout fusion and lumen formation
    By polarization of the migrating endothelial cells a lumen is created, and an immature blood vessel is formed
  4. Stabilisation: perfusion & maturation
    - The stabilisation of the immature vessels is established by recruitment of mural cells and generation of extracellular matrix.
    - Decreased EC proliferation
    - Increased pro-quiescent signals (prevent overgrowth)
19
Q

Describe the effects of tumour angiogenesis

A
  • Tumors less than 1 mm3 receive oxygen and nutrients by diffusion from host vasculature.
  • Larger tumors require new vessel network. (cells in the centre experience hypoxia)
  • Tumor secretes angiogenic factors that stimulate migration, proliferation, and neovessel formation by endothelial cells in adjacent established vessels.
  • Newly vascularized tumor no longer relies solely on diffusion from host vasculature, facilitating progressive growth.
  • Tumour takes nutrients from the original blood vessel and is able to metastasis/ spread via this link
20
Q

What is meant by the “angiogenic switch”?

A

The angiogenic switch is the term given to the point where the number or activity of the pro-angiogenic factors exceeds that of the anti-angiogenic factors, resulting in the angiogenic process proceeding, giving rise to new blood vessels from avascular/ dormant nodules into increased tumour growth and metastasis

  • The angiogenic switch is a discrete step in tumour development that can occur at different stages in the tumour-progression pathway, depending on the nature of the tumour and its microenvironment
21
Q

Describe the features of tumour blood vessels

A
  • irregularly shaped, dilated, tortuous
  • not organized into definitive venules, arterioles and capillaries
  • leaky and haemorrhagic, partly due to the overproduction of VEGF
  • perivascular cells often become loosely associated
22
Q

Explain the role of endothelium in haemostasis & thrombosis?

A
  • Produces the procoagulant factors
  • Healthy endothelium is anti-thrombotic and anti-inflammatory
  • Loss of the normal antithrombotic and anti-inflammatory functions of endothelial cells causes thrombosis with associated inflammation: thromboinflammation
  • Occurs in many disorders, including sepsis, ischemia-reperfusion injury
23
Q

What are the causes of haemostasis inbalance that leads to activated endothelium/ atherosclerosis?

A
  • Inflammation
  • Mechanical stress
  • Viruses
  • Smoking
  • high blood pressure
  • OxLDL
  • high glucose
  • if stimulation is prolonged/ chronic= atherosclerosis
24
Q

What happens to the endothelium during atherosclerosis?

A

atherosclerosis= arteries become clogged with fatty substances called plaques

  1. Endothelial dysfunction
    - Increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by nitric oxide, prostacyclin, platelet-derived growth factor, angiotensin II, and endothelin
    - up-regulation of leukocyte adhesion molecules
    - up-regulation of endothelial adhesion molecules, which include E-selectin, P-selectin
    - and migration of leukocytes into the artery wall, which is mediated by oxidized low-density lipoprotein
  2. Fatty-streak formation
    - leads to foam cell formation- form the atherosclerosis plug
  3. Formation of an advanced, complicated lesion
    - As fatty streaks progress to intermediate and advanced lesions, they tend to form a fibrous cap that walls off the lesion from the lumen (healing response)
    - The fibrous cap covers a mixture of leukocytes, lipid, and debris, which may form a necrotic core
    - These lesions expand at their shoulders by means of continued leukocyte adhesion and entry caused by the same factors
    = Macrophage accumulation
25
Q

Describe how leukocyte recruitment can lead to atherosclerosis

A

NORMALLY:
Recruitment of blood leukocytes into tissues normally takes place during inflammation: leukocyte adhere to the endothelium of post-capillary venules and transmigrate into tissues
- In atherosclerosis, leukocytes adhere to activated endothelium of large arteries and get stuck in the subendothelial space
- Monocytes migrate into the subendothelial space, differentiate into macrophages and become foam cells (form the atherosclerosis plug/ plaque)

26
Q

Describe the effects of vascular permeability in atherosclerosis

A

The endothelium regulates the flux of fluids and molecules from blood to tissues and vice versa
- In atherosclerosis increased permeability results in leakage of plasma proteins through the junctions into the subendothelial space
- These plasma proteins: lipoprotein is trapped and oxidised to form foam cells

27
Q

Why does atherosclerosis occur at branch points?

A
  • Atherosclerotic plaques occur preferentially at bifurcations and curvatures of the vascular tree
  • The flow patterns and hemodynamic forces are not uniform in the vascular system
  • So, these sites are exposed to low or disturbed blood flow, which exerts low/oscillatory shear stress on the vessel wall
    (In straight parts of the arterial tree, blood flow is laminar and wall shear stress is high and directional)
28
Q

What is better, high sheer stress of low sheer stress in the endothelium?

A

HIGH:
High sheer stress=
Laminar blood flow which promotes:
- anti-thrombotic, anti-inflammatory factors
- endothelial survival
- Inhibition of SMC proliferation
- Nitric oxide (NO) production

but low sheer stress=
disrupted blood flow which promotes:
- Thrombosis, inflammation (leukocyte adhesion)
- endothelial apoptosis
- SMC proliferation
- Loss of Nitric oxide (NO) production (reduced dilation; more likely to form plaques)

29
Q

What is the role of NO in atherosclerosis?

A

PREVENTS ATHEROSCLEROSIS:
Multiple protective effects of nitric oxide (NO) on the vascular endothelium=
- Reduces oxidation of LDL (major component of plaque)
- Dilates blood vessels
- Reduces platelet activation
- Inhibits monocyte adhesion
- Reduces proliferation of SMC in the vessel wall
- Reduces release of superoxide radicals

Cardiovascular & Respiratory Medicine (14 decks)

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