Vascular permeability to plasma, plasma proteins, and cells: an update

Purpose of reviewThe blood vasculature supplies tissues with nutrients, clears waste products, and carries and directs leukocytes to inflammatory sites. To accomplish these functions, microvessels regulate the extravasation of small molecules, plasma proteins and inflammatory cells. The mechanisms responsible for these events have been the subject of intense investigation and, often, dispute. Recent findingsRecent progress has contributed to a better understanding of the mechanisms by which microvessels of different types and in different vascular beds regulate the passage of small and large molecules and cells. Roles are shown for the glycocalyx, caveolae, perictyes, sphingosine-1-phosphate, and newly discovered signaling pathways. SummaryVascular permeability is important for maintaining homeostasis and is greatly increased in acute and chronic inflammation, wound healing, and growing tumors. New work has contributed importantly to the mechanisms responsible for regulating permeability.

[1]  M. Saint-Geniez,et al.  TGF-β Is Required for Vascular Barrier Function, Endothelial Survival and Homeostasis of the Adult Microvasculature , 2009, PloS one.

[2]  G. Hu,et al.  Neutrophil caveolin-1 expression contributes to mechanism of lung inflammation and injury. , 2008, American journal of physiology. Lung cellular and molecular physiology.

[3]  Elisabetta Dejana,et al.  The control of vascular integrity by endothelial cell junctions: molecular basis and pathological implications. , 2009, Developmental cell.

[4]  Janice A. Nagy,et al.  The neurotransmitter dopamine inhibits angiogenesis induced by vascular permeability factor/vascular endothelial growth factor , 2001, Nature Medicine.

[5]  Giuseppe Cirino,et al.  Akt1 is critical for acute inflammation and histamine-mediated vascular leakage , 2009, Proceedings of the National Academy of Sciences.

[6]  D. Lominadze,et al.  Balance of S1P1 and S1P2 signaling regulates peripheral microvascular permeability in rat cremaster muscle vasculature. , 2009, American journal of physiology. Heart and circulatory physiology.

[7]  H. Dvorak,et al.  Thrombospondin‐1 modulates vascular endothelial growth factor activity at the receptor level , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[8]  S. Coughlin,et al.  Sphingosine-1-phosphate in the plasma compartment regulates basal and inflammation-induced vascular leak in mice. , 2009, The Journal of clinical investigation.

[9]  H. Dvorak,et al.  Vascular permeability and pathological angiogenesis in caveolin-1-null mice. , 2009, The American journal of pathology.

[10]  H. Dvorak,et al.  Vascular permeability, vascular hyperpermeability and angiogenesis , 2008, Angiogenesis.

[11]  H. Dvorak,et al.  VEGF-A and the induction of pathological angiogenesis. , 2007, Annual review of pathology.

[12]  D. Mukhopadhyay,et al.  Dopamine regulates phosphorylation of VEGF receptor 2 by engaging Src-homology-2-domain-containing protein tyrosine phosphatase 2 , 2009, Journal of Cell Science.

[13]  M. Bogyo,et al.  VEGF-A induces angiogenesis by perturbing the cathepsin-cysteine protease inhibitor balance in venules, causing basement membrane degradation and mother vessel formation. , 2009, Cancer research.

[14]  E. Damiano,et al.  The Recovery Time Course of the Endothelial Cell Glycocalyx In Vivo and Its Implications In Vitro , 2009, Circulation research.

[15]  U. Welsch,et al.  Antithrombin reduces shedding of the endothelial glycocalyx following ischaemia/reperfusion. , 2009, Cardiovascular research.

[16]  José A Fernández,et al.  Protection of vascular barrier integrity by activated protein C in murine models depends on protease-activated receptor-1 , 2009, Thrombosis and Haemostasis.

[17]  G. Palade,et al.  STRUCTURAL MODULATIONS OF PLASMALEMMAL VESICLES , 1968, The Journal of cell biology.

[18]  J. Briegel,et al.  TNF-α induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin , 2008, Basic Research in Cardiology.

[19]  B. Lal,et al.  Internalization of eNOS and NO delivery to subcellular targets determine agonist-induced hyperpermeability , 2009, Proceedings of the National Academy of Sciences.

[20]  T. Hla,et al.  Regulation of vascular physiology and pathology by the S1P2 receptor subtype. , 2008, Cardiovascular research.

[21]  A. Malik,et al.  Critical role of Cdc42 in mediating endothelial barrier protection in vivo. , 2008, American journal of physiology. Lung cellular and molecular physiology.

[22]  S. Harper,et al.  Angiopoietin-1 alters microvascular permeability coefficients in vivo via modification of endothelial glycocalyx , 2009, Cardiovascular research.

[23]  J Ean,et al.  Efficacy and safety of recombinant human activated protein C for severe sepsis. , 2001, The New England journal of medicine.

[24]  H. Dvorak,et al.  The vesiculo‐vacuolar organelle (VVO): a distinct endothelial cell structure that provides a transcellular pathway for macromolecular extravasation , 1996, Journal of leukocyte biology.

[25]  A. Malik,et al.  Bone Marrow Progenitor Cells Induce Endothelial Adherens Junction Integrity by Sphingosine-1-Phosphate–Mediated Rac1 and Cdc42 Signaling , 2009, Circulation research.