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Resolvin D1 interferes with several of the required steps for angiogenesis
Author(s) -
Fatima Farheen,
Garrett Joshua
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.527.1
Subject(s) - angiogenesis , endothelial stem cell , metastasis , endothelium , microbiology and biotechnology , cell adhesion , blood vessel , biology , cancer research , cell adhesion molecule , cell growth , cell , immunology , cancer , chemistry , endocrinology , biochemistry , in vitro , genetics
New growth of blood vessels, angiogenesis, is essential in cancer development since the proliferation, as well as metastatic spread, of cancer cells depends on an adequate supply of oxygen and nutrients and the removal of waste products. Endothelial cells, which line the inside of the entire vasculature, play an important role in angiogenesis. Specifically, endothelial cells detach from an existing blood vessel by down‐regulating their junctional cell‐cell adhesion protein complexes, they migrate away from the existing blood vessel, and they proliferate, all in an attempt to form a new blood vessel. Resolvin D1 (RvD1) is an autocoid molecule which possesses the ability to strengthen endothelial cell‐cell adhesion leading us to hypothesize that RvD1 may inhibit some of necessary steps for angiogenesis to occur. Here we show that treatment of endothelial monolayers with RvD1 increases the amount of junctional vascular endothelial‐cadherin (VE‐Cad) and slows endothelial cell migration. We also found that RvD1 slightly decreased endothelial cell proliferation. Taken together, we found that treatment of the endothelium with RvD1 inhibits several of the essential steps required for angiogenesis to occur. This suggests that RvD1 may be a useful therapeutic in the treatment cancer as it may decrease angiogenesis, preventing cancer cell proliferation and metastasis. Support or Funding Information This work was supported in part through the Hartwick College Faculty research grants program. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .