2. Academic Validation
  3. Identification of Antiangiogenic Potential and Cellular Mechanisms of Napyradiomycin A1 Isolated from the Marine-Derived Streptomyces sp. YP127

Identification of Antiangiogenic Potential and Cellular Mechanisms of Napyradiomycin A1 Isolated from the Marine-Derived Streptomyces sp. YP127

  • J Nat Prod. 2017 Aug 25;80(8):2269-2275. doi: 10.1021/acs.jnatprod.7b00211.
Ji Sun Hwang 1,  Geum Jin Kim 2,  Hyun Gyu Choi 2,  Min Cheol Kim 3,  Dongyup Hahn,  Joo-Won Nam 2,  Sang-Jip Nam 4,  Hak Choel Kwon 3,  Jungwook Chin 1,  Sung Jin Cho 1 5,  Hayoung Hwang 1,  Hyukjae Choi 2
Affiliations

Affiliations

  • 1 New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation (DGMIF) , Daegu 41061, Korea.
  • 2 College of Pharmacy, Yeungnam University , Gyeongsan-si, Gyeongsangbukdo 38541, Korea.
  • 3 Natural Products Research Center, Korea Institute of Science and Technology (KIST) Gangneung Institute , Gangneung, Gangwon-do 25451, Korea.
  • 4 Department of Chemistry and Nano Science, Ewha Womans University , Seoul 03760, Korea.
  • 5 Leading-edge Research Center for Drug Discovery and Development for Diabetes and Metabolic Disease, Kyungpook National University Hospital , Daegu 41404, Korea.
PMID: 28749137 DOI: 10.1021/acs.jnatprod.7b00211
Abstract

Angiogenesis is the process of new blood vessel formation. Excessive angiogenesis is a critical factor in the progression of Cancer, macular degeneration, and Other chronic inflammatory diseases. When investigating the effects of crude extracts of cultured marine Microorganisms, an extract of the cultured Streptomyces sp. YP127 strain was found to inhibit human umbilical vein endothelial cell (HUVEC) tube formation. Bioassay-guided fractionation and spectroscopic data analyses led to the identification of napyradiomycin A1 (1) as an antiangiogenic component of the extract. Compound 1 inhibited HUVEC tube formation in a concentration-dependent manner. It inhibited endothelial cell proliferation but did not affect human dermal fibroblast proliferation. Compound 1 also suppressed migration and invasion of vascular endothelial cells. In addition, compound 1 suppressed vascular endothelial cadherin expression and increased the permeability of the endothelial cell membrane. These results suggested that compound 1 modulates cell permeability and inhibits the angiogenesis of endothelial cells.

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