Dear Nasim,

Attached please find a publication that covers the answer to your question.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3655806/

Arterioscler Thromb Vasc Biol. Author manuscript; available in PMC 2014 Mar 1.

Published in final edited form as:

Arterioscler Thromb Vasc Biol. 2013 Mar; 33(3): 489–500.

Published online 2013 Jan 3. doi:  10.1161/ATVBAHA.112.300893

PMCID: PMC3655806

NIHMSID: NIHMS436335

Claudin-5 Controls Intercellular Barriers of Human Dermal Microvascular but not Human Umbilical Vein Endothelial Cells

Martin S. Kluger, PhD,1,* Paul R. Clark, PhD,1 George Tellides, MD, PhD,2 Volker Gerke, PhD,3 and Jordan S. Pober, MD, PhD1

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The publisher's final edited version of this article is available free at Arterioscler Thromb Vasc Biol

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Abstract

Objective

To assess the role claudin-5, an endothelial cell (EC) tight junction (TJ) protein, plays in establishing basal permeability levels in humans by comparing claudin-5 expression levels in situ and analyzing junctional organization and function in two widely used models of cultured ECs, namely human dermal microvascular (HDM)ECs and human umbilical vein (HUV)ECs.

Methods and Results

By immunofluorescence microscopy, ECs more highly express claudin-5 (but equivalently express VE-cadherin) in human dermal capillaries versus post-capillary venules and in umbilical and coronary arteries versus veins, correlating with known segmental differences in TJ frequencies and permeability barriers. Post-confluent cultured HDMECs express more claudin-5 (but equivalent VE-cadherin) and show higher transendothelial electrical resistance (TEER) and lower macromolecular flux than similarly cultured HUVECs. HDMEC junctions are more complex by transmission electron microscopy and show more continuous claudin-5 immunofluorescence than HUVEC junctions. Calcium chelation or dominant negative VE-cadherin overexpression decreases TEER and disrupts junctions in HUVECs, but not in HDMECs. Claudin-5 overexpression in HUVECs fails to increase TEER or claudin-5 continuity while claudin-5 knockdown in HDMECs, but not HUVECs, reduces TEER and increases antibody accessibility to junctional proteins.

Conclusions

Claudin-5 expression and junctional organization control HDMEC and arteriolar-capillary paracellular barriers whereas HUVEC and venular junctions utilize VE-cadherin.

Keywords: endothelial cell, tight junction, microvessel, permeability, heterogeneity

Hoping this will be helpful,

Rafik

Thank you for sending the paper.

Hi Nasim,

In our publication, we found that tight junctions were relatively fewer  inHUVECs than in ECs derived from microvessels. But TJs are inducible in HUVECs  following a protocol described in the following article: 

Paracellular Diapedesis in a Human Model of

Rapid Remodeling of Tight Junctions during

Richard M. Ransohoff and William A. Muller

Ryan C. Winger, Jennifer E. Koblinski, Takashi Kanda,

http://www.jimmunol.org/content/193/5/2427

doi: 10.4049/jimmunol.1400700

July 2014;

J Immunol

---Martin