Jump to content

Endothelial activation: Difference between revisions

Edit links
From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
m →‎Further reading: Journal cites, Added 1 doi to a journal cite
→‎See also: Added relevant section covering the mechanical, flow-induced sensing and behavior that determines vascular homeostasis, inflammation, and coagulation via endothelial activation.
Line 1: Line 1:
'''Endothelial activation''' is a [[proinflammatory]] and [[Coagulation|procoagulant]] state of the [[endothelial cell]]s lining the [[Lumen (anatomy)|lumen]] of [[blood vessel]]s.<ref name="li-2016">{{cite journal |vauthors=Li X, Fang P, etal |title = Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation | journal = Arteriosclerosis, Thrombosis, and Vascular Biology |date=April 2016 | pmid = 27127201 |doi = 10.1161/ATVBAHA.115.306964 |pmc=4882253 |volume=36 |pages=1090-100}}</ref> It is most characterized by an increase in interactions with [[white blood cell]]s (leukocytes), and it is associated with the early states of [[atherosclerosis]] and [[sepsis]], among others.<ref name="Alom">{{cite journal|vauthors=Alom-Ruiz SP, Anilkumar N, Shah AM | title=Reactive oxygen species and endothelial activation | journal=Antioxid Redox Signal | year= 2008 | volume= 10 | issue= 6 | pages= 1089–100 | pmid=18315494 | doi=10.1089/ars.2007.2007 }}</ref> It is also implicated in the formation of [[deep vein thrombosis]].<ref name="Whatis">{{cite journal|vauthors=Bovill EG, van der Vliet A | title=Venous valvular stasis-associated hypoxia and thrombosis: what is the link? | journal=Annu Rev Physiol | year= 2011 | volume= 73 | issue= | pages= 527–45 | pmid=21034220 | doi=10.1146/annurev-physiol-012110-142305 }}</ref> As a result of activation, enthothelium releases [[Weibel–Palade body|Weibel–Palade bodies]].<ref name="Lopez">{{cite journal|vauthors=López JA, Chen J | title=Pathophysiology of venous thrombosis | journal=Thromb Res | year= 2009 | volume= 123 | issue= Suppl 4 | pages= S30-4 | pmid=19303501 | doi=10.1016/S0049-3848(09)70140-9 }}</ref>
'''Endothelial activation''' is a [[proinflammatory]] and [[Coagulation|procoagulant]] state of the [[endothelial cell]]s lining the [[Lumen (anatomy)|lumen]] of [[blood vessel]]s.<ref name="li-2016">{{cite journal |vauthors=Li X, Fang P, etal |title = Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation | journal = Arteriosclerosis, Thrombosis, and Vascular Biology |date=April 2016 | pmid = 27127201 |doi = 10.1161/ATVBAHA.115.306964 |pmc=4882253 |volume=36 |pages=1090-100}}</ref> It is most characterized by an increase in interactions with [[white blood cell]]s (leukocytes), and it is associated with the early states of [[atherosclerosis]] and [[sepsis]], among others.<ref name="Alom">{{cite journal|vauthors=Alom-Ruiz SP, Anilkumar N, Shah AM | title=Reactive oxygen species and endothelial activation | journal=Antioxid Redox Signal | year= 2008 | volume= 10 | issue= 6 | pages= 1089–100 | pmid=18315494 | doi=10.1089/ars.2007.2007 }}</ref> It is also implicated in the formation of [[deep vein thrombosis]].<ref name="Whatis">{{cite journal|vauthors=Bovill EG, van der Vliet A | title=Venous valvular stasis-associated hypoxia and thrombosis: what is the link? | journal=Annu Rev Physiol | year= 2011 | volume= 73 | issue= | pages= 527–45 | pmid=21034220 | doi=10.1146/annurev-physiol-012110-142305 }}</ref> As a result of activation, enthothelium releases [[Weibel–Palade body|Weibel–Palade bodies]].<ref name="Lopez">{{cite journal|vauthors=López JA, Chen J | title=Pathophysiology of venous thrombosis | journal=Thromb Res | year= 2009 | volume= 123 | issue= Suppl 4 | pages= S30-4 | pmid=19303501 | doi=10.1016/S0049-3848(09)70140-9 }}</ref>

== Mechanical sensing and responses for endothelial activation pathways ==
Elevating shear stress induces a vascular response by triggering nitric oxide synthesis and mechanotransduction pathways of endothelial cells<ref>{{Cite journal|last=Rodríguez|first=Iván|last2=González|first2=Marcelo|date=2014-09-16|title=Physiological mechanisms of vascular response induced by shear stress and effect of exercise in systemic and placental circulation|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4165280/|journal=Frontiers in Pharmacology|volume=5|doi=10.3389/fphar.2014.00209|issn=1663-9812|pmc=PMC4165280|pmid=25278895}}</ref>. The synthesis of nitric oxide facilitate shear stress mediated dilation in blood vessels and maintains a homeostatic status<ref>{{Cite journal|last=Lu|first=Deshun|last2=Kassab|first2=Ghassan S.|date=2011-10-07|title=Role of shear stress and stretch in vascular mechanobiology|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163429/|journal=Journal of the Royal Society Interface|volume=8|issue=63|pages=1379–1385|doi=10.1098/rsif.2011.0177|issn=1742-5689|pmc=PMC3163429|pmid=21733876}}</ref>. Additionally, physiologic shear stress levels at the vessel wall upregulate the presence of antithrombotic agents through the mechano-signal transduction of mechano-recepting transmembrane proteins, junctional proteins, and subendothelial mechanosensors<ref>{{Cite journal|last=Papaioannou|first=Theodore G.|date=2005 Jan-Feb|title=Vascular wall shear stress: basic principles and methods.|url=https://www.ncbi.nlm.nih.gov/pubmed/15807389|journal=Hellenic J Cardiol|volume=46|pages=9-15|via=}}</ref>. Shear stress causes endothelial cell deformation which activates transmembrane ion channels<ref>{{Cite journal|last=Lee|first=Juhyun|last2=Packard|first2=René R. Sevag|last3=Hsiai|first3=Tzung K.|date=2015-10|title=Blood flow modulation of vascular dynamics|url=https://www.ncbi.nlm.nih.gov/pubmed/26218416|journal=Current Opinion in Lipidology|volume=26|issue=5|pages=376–383|doi=10.1097/MOL.0000000000000218|issn=1473-6535|pmc=PMC4626080|pmid=26218416}}</ref>. Elevated wall shear stress caused by exercise is understood to promote mitochondrial biogenesis in the vascular endothelium indicating the benefits regular exercise may have on vascular function<ref>{{Cite journal|last=Kim|first=Boa|last2=Lee|first2=Hojun|last3=Kawata|first3=Keisuke|last4=Park|first4=Joon-Young|date=2014|title=Exercise-mediated wall shear stress increases mitochondrial biogenesis in vascular endothelium|url=https://www.ncbi.nlm.nih.gov/pubmed/25375175|journal=PloS One|volume=9|issue=11|pages=e111409|doi=10.1371/journal.pone.0111409|issn=1932-6203|pmc=PMC4222908|pmid=25375175}}</ref>. Alignment is recognized as an important mechanism and determinant of shear-stress induced vascular response; in vivo testing of endothelial cells has demonstrated that their mechanotransductive response is direction dependent as endothelial nitric oxide synthesis is preferentially activated under parallel flow while perpendicular flows activates inflammatory pathways like reactive oxygen species production and nuclear factor-κB<ref>{{Cite journal|last=Wang|first=Chong|last2=Baker|first2=Brendon M.|last3=Chen|first3=Christopher S.|last4=Schwartz|first4=Martin Alexander|date=2013-9|title=Endothelial cell sensing of flow direction|url=https://www.ncbi.nlm.nih.gov/pubmed/23814115/|journal=Arteriosclerosis, Thrombosis, and Vascular Biology|volume=33|issue=9|pages=2130–2136|doi=10.1161/ATVBAHA.113.301826|issn=1524-4636|pmc=PMC3812824|pmid=23814115}}</ref>. Therefore, disturbed/oscillating flow and low flow conditions, which create an irregular and passive shear stress environment, result in inflammatory activation due to a limited alignment capability of the endothelial cells. Regions in the vasculature with low shear stress are vulnerable to elevated monocyte adhesion and endothelial cell apoptosis<ref>{{Cite journal|last=Berk|first=Bradford C.|date=2008-02-26|title=Atheroprotective signaling mechanisms activated by steady laminar flow in endothelial cells|url=https://www.ncbi.nlm.nih.gov/pubmed/18299513|journal=Circulation|volume=117|issue=8|pages=1082–1089|doi=10.1161/CIRCULATIONAHA.107.720730|issn=1524-4539|pmid=18299513}}</ref>. However, unlike oscillatory flow, both laminar(steady) and pulsatile flow and shear stress environments are often considered together as mechanisms of maintaining vascular homeostasis and preventing inflammation, reactive oxygen species formation, and coagulatory pathways<ref>{{Cite journal|last=Hsieh|first=Hsyue-Jen|last2=Liu|first2=Ching-Ann|last3=Huang|first3=Bin|last4=Tseng|first4=Anne HH|last5=Wang|first5=Danny|date=2014|title=Shear-induced endothelial mechanotransduction: the interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications|url=https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-21-3|journal=Journal of Biomedical Science|language=En|volume=21|issue=1|pages=3|doi=10.1186/1423-0127-21-3|issn=1423-0127|pmc=PMC3898375|pmid=24410814}}</ref>. High, uniform laminar shear stress is known to promote a quiescent endothelial cell state, provide anti-thrombotic effects, prevent proliferation, and decrease inflammation and apoptosis. At high shear stress levels (10 Pa), the endothelial cell response is distinct from upper normal/physiological values; high wall shear stress causes a promatrix remodeling, proliferative, anticoagulant, and anti-inflammatory state<ref>{{Cite journal|last=Dolan|first=Jennifer M.|last2=Sim|first2=Fraser J.|last3=Meng|first3=Hui|last4=Kolega|first4=John|date=2012-04-15|title=Endothelial cells express a unique transcriptional profile under very high wall shear stress known to induce expansive arterial remodeling|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3330730/|journal=American Journal of Physiology - Cell Physiology|volume=302|issue=8|pages=C1109–C1118|doi=10.1152/ajpcell.00369.2011|issn=0363-6143|pmc=PMC3330730|pmid=22173868}}</ref>. Yet, very high wall shear stress values (28.4 Pa) prevent endothelial cell alignment and stimulate proliferation and apoptosis although the endothelial response to shear stress environments was determined to be dependent on the local wall shear stress gradient<ref>{{Cite journal|last=Dolan|first=Jennifer M.|last2=Meng|first2=Hui|last3=Singh|first3=Sukhjinder|last4=Paluch|first4=Rocco|last5=Kolega|first5=John|date=2011-6|title=High Fluid Shear Stress and Spatial Shear Stress Gradients Affect Endothelial Proliferation, Survival, and Alignment|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809045/|journal=Annals of biomedical engineering|volume=39|issue=6|pages=1620–1631|doi=10.1007/s10439-011-0267-8|issn=0090-6964|pmc=PMC4809045|pmid=21312062}}</ref>.


==See also==
==See also==

Revision as of 07:58, 13 November 2018

Endothelial activation is a proinflammatory and procoagulant state of the endothelial cells lining the lumen of blood vessels.[1] It is most characterized by an increase in interactions with white blood cells (leukocytes), and it is associated with the early states of atherosclerosis and sepsis, among others.[2] It is also implicated in the formation of deep vein thrombosis.[3] As a result of activation, enthothelium releases Weibel–Palade bodies.[4]

Mechanical sensing and responses for endothelial activation pathways

Elevating shear stress induces a vascular response by triggering nitric oxide synthesis and mechanotransduction pathways of endothelial cells[5]. The synthesis of nitric oxide facilitate shear stress mediated dilation in blood vessels and maintains a homeostatic status[6]. Additionally, physiologic shear stress levels at the vessel wall upregulate the presence of antithrombotic agents through the mechano-signal transduction of mechano-recepting transmembrane proteins, junctional proteins, and subendothelial mechanosensors[7]. Shear stress causes endothelial cell deformation which activates transmembrane ion channels[8]. Elevated wall shear stress caused by exercise is understood to promote mitochondrial biogenesis in the vascular endothelium indicating the benefits regular exercise may have on vascular function[9]. Alignment is recognized as an important mechanism and determinant of shear-stress induced vascular response; in vivo testing of endothelial cells has demonstrated that their mechanotransductive response is direction dependent as endothelial nitric oxide synthesis is preferentially activated under parallel flow while perpendicular flows activates inflammatory pathways like reactive oxygen species production and nuclear factor-κB[10]. Therefore, disturbed/oscillating flow and low flow conditions, which create an irregular and passive shear stress environment, result in inflammatory activation due to a limited alignment capability of the endothelial cells. Regions in the vasculature with low shear stress are vulnerable to elevated monocyte adhesion and endothelial cell apoptosis[11]. However, unlike oscillatory flow, both laminar(steady) and pulsatile flow and shear stress environments are often considered together as mechanisms of maintaining vascular homeostasis and preventing inflammation, reactive oxygen species formation, and coagulatory pathways[12]. High, uniform laminar shear stress is known to promote a quiescent endothelial cell state, provide anti-thrombotic effects, prevent proliferation, and decrease inflammation and apoptosis. At high shear stress levels (10 Pa), the endothelial cell response is distinct from upper normal/physiological values; high wall shear stress causes a promatrix remodeling, proliferative, anticoagulant, and anti-inflammatory state[13]. Yet, very high wall shear stress values (28.4 Pa) prevent endothelial cell alignment and stimulate proliferation and apoptosis although the endothelial response to shear stress environments was determined to be dependent on the local wall shear stress gradient[14].

See also

References

  1. ^ Li X, Fang P, et al. (April 2016). "Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation". Arteriosclerosis, Thrombosis, and Vascular Biology. 36: 1090–100. doi:10.1161/ATVBAHA.115.306964. PMC 4882253. PMID 27127201.
  2. ^ Alom-Ruiz SP, Anilkumar N, Shah AM (2008). "Reactive oxygen species and endothelial activation". Antioxid Redox Signal. 10 (6): 1089–100. doi:10.1089/ars.2007.2007. PMID 18315494.
  3. ^ Bovill EG, van der Vliet A (2011). "Venous valvular stasis-associated hypoxia and thrombosis: what is the link?". Annu Rev Physiol. 73: 527–45. doi:10.1146/annurev-physiol-012110-142305. PMID 21034220.
  4. ^ López JA, Chen J (2009). "Pathophysiology of venous thrombosis". Thromb Res. 123 (Suppl 4): S30-4. doi:10.1016/S0049-3848(09)70140-9. PMID 19303501.
  5. ^ Rodríguez, Iván; González, Marcelo (2014-09-16). "Physiological mechanisms of vascular response induced by shear stress and effect of exercise in systemic and placental circulation". Frontiers in Pharmacology. 5. doi:10.3389/fphar.2014.00209. ISSN 1663-9812. PMC 4165280. PMID 25278895.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  6. ^ Lu, Deshun; Kassab, Ghassan S. (2011-10-07). "Role of shear stress and stretch in vascular mechanobiology". Journal of the Royal Society Interface. 8 (63): 1379–1385. doi:10.1098/rsif.2011.0177. ISSN 1742-5689. PMC 3163429. PMID 21733876.{{cite journal}}: CS1 maint: PMC format (link)
  7. ^ Papaioannou, Theodore G. (2005 Jan-Feb). "Vascular wall shear stress: basic principles and methods". Hellenic J Cardiol. 46: 9–15. {{cite journal}}: Check date values in: |date= (help)
  8. ^ Lee, Juhyun; Packard, René R. Sevag; Hsiai, Tzung K. (2015-10). "Blood flow modulation of vascular dynamics". Current Opinion in Lipidology. 26 (5): 376–383. doi:10.1097/MOL.0000000000000218. ISSN 1473-6535. PMC 4626080. PMID 26218416. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  9. ^ Kim, Boa; Lee, Hojun; Kawata, Keisuke; Park, Joon-Young (2014). "Exercise-mediated wall shear stress increases mitochondrial biogenesis in vascular endothelium". PloS One. 9 (11): e111409. doi:10.1371/journal.pone.0111409. ISSN 1932-6203. PMC 4222908. PMID 25375175.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  10. ^ Wang, Chong; Baker, Brendon M.; Chen, Christopher S.; Schwartz, Martin Alexander (2013-9). "Endothelial cell sensing of flow direction". Arteriosclerosis, Thrombosis, and Vascular Biology. 33 (9): 2130–2136. doi:10.1161/ATVBAHA.113.301826. ISSN 1524-4636. PMC 3812824. PMID 23814115. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  11. ^ Berk, Bradford C. (2008-02-26). "Atheroprotective signaling mechanisms activated by steady laminar flow in endothelial cells". Circulation. 117 (8): 1082–1089. doi:10.1161/CIRCULATIONAHA.107.720730. ISSN 1524-4539. PMID 18299513.
  12. ^ Hsieh, Hsyue-Jen; Liu, Ching-Ann; Huang, Bin; Tseng, Anne HH; Wang, Danny (2014). "Shear-induced endothelial mechanotransduction: the interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications". Journal of Biomedical Science. 21 (1): 3. doi:10.1186/1423-0127-21-3. ISSN 1423-0127. PMC 3898375. PMID 24410814.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  13. ^ Dolan, Jennifer M.; Sim, Fraser J.; Meng, Hui; Kolega, John (2012-04-15). "Endothelial cells express a unique transcriptional profile under very high wall shear stress known to induce expansive arterial remodeling". American Journal of Physiology - Cell Physiology. 302 (8): C1109–C1118. doi:10.1152/ajpcell.00369.2011. ISSN 0363-6143. PMC 3330730. PMID 22173868.{{cite journal}}: CS1 maint: PMC format (link)
  14. ^ Dolan, Jennifer M.; Meng, Hui; Singh, Sukhjinder; Paluch, Rocco; Kolega, John (2011-6). "High Fluid Shear Stress and Spatial Shear Stress Gradients Affect Endothelial Proliferation, Survival, and Alignment". Annals of biomedical engineering. 39 (6): 1620–1631. doi:10.1007/s10439-011-0267-8. ISSN 0090-6964. PMC 4809045. PMID 21312062. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)

Further reading


Stub icon

This cardiovascular system article is a stub. You can help Wikipedia by expanding it.

Retrieved from "https://en.wikipedia.org/w/index.php?title=Endothelial_activation&oldid=868604139"