vascular epithelium Flashcards
what are the three layers of cells lining vessels other than capillaries?
tunica adventitia (think adventures= outdours- extenrla layer) = nerves
tunica media: smooth muscle cells
tunica intima: endothelium
how small are caps compared to hair
1/ of hair in width
what is the structure of capillaries
mainly endothelium supported by mural cells (pericytes) and a basement membrane
what happens in capillaries
exchange of oxygen and nutrients with tissues
How well spread/ distributed are capillaries?
almost every cell in body is in contact with microvascular endothelial cells
in what vessel type do the majority of the endothelial cells reside?
98% in microvasculature
how do the endothelial cells know that they are supposed to form monolayers and not stack onto eachother?
due to a phenomenon called contact inhibition, when they meet eachother at junctions signals are released that stop them from proliferating further
what is the proliferation rate of endothelial cells? (not in number just word) when is an exception?
dont proliferate much in vivo, only when angiogenesis
what are some of the fucntions of blood vessels that endothelium controls?
permeability
angiogenesis
haemostasis and thrombosis
INFLAMMATION
VASCULAR TONE (ud think this is only muscles buttt actuallyyy its not!)
how do endothelial cells control all thesevascular functions?
by cytokines and factors see slide 11
in what aspects do endothelial cells differ in different organs?
structure
function
molecular differences
how is it possible for endothelial cells to be organotypic (differ amongst organs)
although same dna as all cells, different expression profiles: meaning different rnas
how is the genetic profile of different endothelial types unalysed studied and presented?
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
what is the human cell atlas
1) international collaborative consortium
2) charts cel types in the healthy body
3) from development to adulthood
how do endothelial cells become tissue specific
tissue specific MICROENVIRONMENT influences phenotype of endothelial cells
tissue specific endothelial cells produce different angiocrine factors which are ESSENTIAL for
tissue homeostasis and regeneration
what is the most abundant cell type in the heart?
endothelial cell
(Then its cardiomyocytes and then stromal cells)
what two cell type sin the heart communicate and what is the term used to describe this communication?
cardiomyocytes and endothelial cells crosstalk!
what is the most common type of angiogenesis in adults (meaning not part of development) called?
sprouting angiogenesis
define angiogenesis
formation of neo-vessels FROM PRE-EXISTING blood vessels
describe the cascade of events in angiogenesis
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
what role do transcription factors play in angiogenesis?
regulate the precise temporal and spatial co-ordination of the expression of multiple genes during angiogenesis
what are some physiological processes that involve angiogenesis
1) development
2) menstrual cycle
3) wound healing
what are 2 crucial pathologies that involve angiogenesis?
cancer
atherosclerosis
what is the angiogenic switch in cancer?
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.
some other pathologies that involve angiogenesis?
retinopathies
chronic inflammatory diseases
ischemic diseases
vascular malformations
in what ways is this angiogenesis in tumours a bad thing?
facilitates tumour growth and metastasis
how does angiogenesis influence cancer treatment?
anti-angiogenic drugs in clinic given in combination with chemotherapy for a number of solid tumors
what is the difference between haemostasis and thrombosis
haemostasis is NORMAL blood clotting in response to INJURY
thrombosis is EXCESSIVE and/or SPONTANEOUS clot formation
why may vessels’ role in control of bleeding only recently have been considered?(thrombosis, haemostasis ect)
because theres no numercal test you can do to measure/ separate the role of endothelium separate to blood
what is a common way in which VWD presets?
in dentist by small bleeds
what are the 2 treatment option in VWD (von willebrand disease)
VWF or DDAVP (stimulating endocrine cells to release VWF )
what is a symptom of patients with VWD whose pathology is clearly stemming from both blood but also ENDOTHELIUM?
SEVERE INTRACTABLE (unstopable) bleeding from the gastrointestinal tract
due to vascular malformations in the gut blood vessels
what treatment is not sufficient to control the bleedin in GI tract in VWD
VWF replacement
what is a more recently discovered role of VWF? (also mention the classic role if u dont know well)
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)
what pathogenic processes lead to activation of edothelium?
what risk facotrs are linked to these processes?
what does activation of the epithelium lead to?
inflammation
thrombosis
angiofenesis
high bp, mechanical stress
oxLDL, high glucose,
smoking, viruses,
atheorsclerosis ( in larger arteries)
what is a very important factor that increases endothelial permeability to lipoproteins?
nitric oxide
what are the 4 main mechanisms of pathology of the endothelium in atherosclerosis?
leukocyte recruitment
increase in permeability
decrease in sheer stress
angiogenesis
when and where does leukocyte recruitment occur under NORMAL circumstances
in post capillary venules during inflammation
what is the difference in structure of capillary vs post -capillary venule?
post cap ven simiral to cap but more pericytes
describe the process of leukocyte adhesion - migraiton across an endothelial surface
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
