vascular epithelium Flashcards

1
Q

what are the three layers of cells lining vessels other than capillaries?

A

tunica adventitia (think adventures= outdours- extenrla layer) = nerves
tunica media: smooth muscle cells
tunica intima: endothelium

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2
Q

how small are caps compared to hair

A

1/ of hair in width

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3
Q

what is the structure of capillaries

A

mainly endothelium supported by mural cells (pericytes) and a basement membrane

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4
Q

what happens in capillaries

A

exchange of oxygen and nutrients with tissues

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5
Q

How well spread/ distributed are capillaries?

A

almost every cell in body is in contact with microvascular endothelial cells

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6
Q

in what vessel type do the majority of the endothelial cells reside?

A

98% in microvasculature

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7
Q

how do the endothelial cells know that they are supposed to form monolayers and not stack onto eachother?

A

due to a phenomenon called contact inhibition, when they meet eachother at junctions signals are released that stop them from proliferating further

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8
Q

what is the proliferation rate of endothelial cells? (not in number just word) when is an exception?

A

dont proliferate much in vivo, only when angiogenesis

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9
Q

what are some of the fucntions of blood vessels that endothelium controls?

A

permeability
angiogenesis
haemostasis and thrombosis
INFLAMMATION
VASCULAR TONE (ud think this is only muscles buttt actuallyyy its not!)

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10
Q

how do endothelial cells control all thesevascular functions?

A

by cytokines and factors see slide 11

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11
Q

in what aspects do endothelial cells differ in different organs?

A

structure
function
molecular differences

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12
Q

how is it possible for endothelial cells to be organotypic (differ amongst organs)

A

although same dna as all cells, different expression profiles: meaning different rnas

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13
Q

how is the genetic profile of different endothelial types unalysed studied and presented?

A

by rna sequencing (since rna is what guides protein synth so is dif in each type) that is presented in Seurat Cluster graphs- each dot i a cell - each cluster of dots is an endoth cell type

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14
Q

what is the human cell atlas

A

1) international collaborative consortium

2) charts cel types in the healthy body

3) from development to adulthood

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15
Q

how do endothelial cells become tissue specific

A

tissue specific MICROENVIRONMENT influences phenotype of endothelial cells

tissue specific endothelial cells produce different angiocrine factors which are ESSENTIAL for

tissue homeostasis and regeneration

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16
Q

what is the most abundant cell type in the heart?

A

endothelial cell

(Then its cardiomyocytes and then stromal cells)

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17
Q

what two cell type sin the heart communicate and what is the term used to describe this communication?

A

cardiomyocytes and endothelial cells crosstalk!

18
Q

what is the most common type of angiogenesis in adults (meaning not part of development) called?

A

sprouting angiogenesis

19
Q

define angiogenesis

A

formation of neo-vessels FROM PRE-EXISTING blood vessels

20
Q

describe the cascade of events in angiogenesis

A

1) hypoxia causes angiogenic factor production
2) release of angiogenic factor and binding on endothelial cell receptor
3) endothelial cell activation and proliferation
4) directional migration of endothelial cells (towards new vessel)
5) ECM remodelling
6) tube formation and loop formation
7) vascular stabilisation

21
Q

what role do transcription factors play in angiogenesis?

A

regulate the precise temporal and spatial co-ordination of the expression of multiple genes during angiogenesis

22
Q

what are some physiological processes that involve angiogenesis

A

1) development
2) menstrual cycle
3) wound healing

23
Q

what are 2 crucial pathologies that involve angiogenesis?

A

cancer
atherosclerosis

24
Q

what is the angiogenic switch in cancer?

A

when a tumour grows to the point where the inner part cant get enough blood by diffusion from host vessels anymore so the hypoxia in the inner part of the tumour leads to the release of angiogenic and thus new vessels grow.

24
Q

some other pathologies that involve angiogenesis?

A

retinopathies
chronic inflammatory diseases
ischemic diseases
vascular malformations

24
Q

in what ways is this angiogenesis in tumours a bad thing?

A

facilitates tumour growth and metastasis

25
Q

how does angiogenesis influence cancer treatment?

A

anti-angiogenic drugs in clinic given in combination with chemotherapy for a number of solid tumors

26
Q

what is the difference between haemostasis and thrombosis

A

haemostasis is NORMAL blood clotting in response to INJURY

thrombosis is EXCESSIVE and/or SPONTANEOUS clot formation

27
Q

why may vessels’ role in control of bleeding only recently have been considered?(thrombosis, haemostasis ect)

A

because theres no numercal test you can do to measure/ separate the role of endothelium separate to blood

28
Q

what is a common way in which VWD presets?

A

in dentist by small bleeds

29
Q

what are the 2 treatment option in VWD (von willebrand disease)

A

VWF or DDAVP (stimulating endocrine cells to release VWF )

30
Q

what is a symptom of patients with VWD whose pathology is clearly stemming from both blood but also ENDOTHELIUM?

A

SEVERE INTRACTABLE (unstopable) bleeding from the gastrointestinal tract

due to vascular malformations in the gut blood vessels

31
Q

what treatment is not sufficient to control the bleedin in GI tract in VWD

A

VWF replacement

32
Q

what is a more recently discovered role of VWF? (also mention the classic role if u dont know well)

A

in haemostasis vwf mediates platelet adhesion to subendothelium and platelet aggregation
vwf stabilises circulating coagulation factor 8

NEW: ANGIOGENESIS
vwf controls blood vessel formation and integrity partly by regulating growth factor signalling (VEGFR, ANG-2)

33
Q

what pathogenic processes lead to activation of edothelium?

what risk facotrs are linked to these processes?

what does activation of the epithelium lead to?

A

inflammation
thrombosis
angiofenesis

high bp, mechanical stress
oxLDL, high glucose,
smoking, viruses,

atheorsclerosis ( in larger arteries)

34
Q

what is a very important factor that increases endothelial permeability to lipoproteins?

A

nitric oxide

35
Q

what are the 4 main mechanisms of pathology of the endothelium in atherosclerosis?

A

leukocyte recruitment
increase in permeability
decrease in sheer stress
angiogenesis

36
Q

when and where does leukocyte recruitment occur under NORMAL circumstances

A

in post capillary venules during inflammation

37
Q

what is the difference in structure of capillary vs post -capillary venule?

A

post cap ven simiral to cap but more pericytes

38
Q

describe the process of leukocyte adhesion - migraiton across an endothelial surface

A

1) rolling
2) slow rolling
3) arrest (pause)
now activated
4) adhesion, strengthening, spreading
5) intravascular crawling (little part of cell sfinonei namesa apo kapio junction horis na diapernaei ALI PLEVRA AKOMA)
6) paracellular and trancellular transmission

39
Q
A