The patterns and expression of KDR in normal tissues of human internal organs

J Mol Histol. 2011 Dec;42(6):597-603. doi: 10.1007/s10735-011-9355-1. Epub 2011 Sep 10.

Abstract

KDR has been implicated for playing an important role in the formation of new blood vessels and in solid tumor growth. It was considered as one of the most important regulators of angiogenesis and a key target in anticancer treatment. In the present study, we characterized KDR mRNA and protein expression in normal tissues of perinatal and adult tissues using One-step Real-Time RT-PCR and immunohistochemistry with a self-made anti-KDR antibody. The expression of KDR mRNA and protein in perinatal internal organs were all higher than in adult organs including brain, kidney, liver, lung and heart, respectively. KDR protein was presented in the cell plasma membrane of human internal tissues. The expression of KDR protein was raised in macrophage of spleen, and decreased in neurons of brain, myocardium, bronchial epithelial cells and alveolar epithelial cell, proximal and distal tubules cells, and hepatic cells with the maturity process of human organs. Notably, the order of KDR protein expression from highest to lowest is as follows: brain, liver, heart, kidney, and lung in adult tissues with statistically significant. It follows that how to balance the potential therapeutic side effect with human internal organs in targeted therapy of over-expressing KDR tumor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Autopsy / methods
  • Cell Membrane / metabolism
  • Female
  • Fetus / metabolism
  • Humans
  • Immunohistochemistry / methods
  • Male
  • Middle Aged
  • Neoplasms / metabolism
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Vascular Endothelial Growth Factor Receptor-2 / biosynthesis*
  • Vascular Endothelial Growth Factor Receptor-2 / genetics
  • Vascular Endothelial Growth Factor Receptor-2 / metabolism

Substances

  • RNA, Messenger
  • Vascular Endothelial Growth Factor Receptor-2