Genomics of cardiac remodeling in angiotensin II-treated wild-type and LOX-1-deficient mice

Bum Yong Kang, Changping Hu, Sunhyo Ryu, Junaid A. Khan, Michela Biancolella, Sastry Prayaga, Ki Bae Seung, Giuseppe Novelli, Paulette Mehta, Jawahar L. Mehta

Research output: Contribution to journalArticlepeer-review


We studied the gene expression profile during cardiac hypertrophy induced by angiotensin (ANG) II in wild-type mice and the influence of LOX-1 deletion on the gene expression profile. Wild-type and LOX-1 knockout mice were given saline or ANG II infusion for 4 wk. The saline-treated LOX-1 knockout mice showed upregulation of several genes including Ddx3y and Eif2s3y. ANG II infusion enhanced expression of genes known to be associated with cardiac remodeling, such as Agt, Ace, Timp4, Fstl, and Tnfrst12a, as well as oxidant stress-related genes Gnaq, Sos1, and Rac1. Some other strongly upregulated genes identified in this study have not been previously associated with LOX-1 deletion and/or hypertension. To confirm these observations with ANG II infusion and LOX-1 deletion, cultured HL-1 mouse cardiomyocytes were exposed to ANG II or transfected with pCI-neo/LOX-1, which resulted in severalfold increase in reactive oxygen species generation, upregulation of ANG II type 1 (AT 1) receptor, and cardiomyocyte growth. Quantitative PCR analysis of these treated cardiomyocytes confirmed upregulation of many of the genes identified in the in vivo study. This study provides the first set of data on the gene expression profiling of cardiac tissue treated with ANG II and expands on the important role of LOX-1 in cardiac response to ANG II.

Original languageEnglish
Pages (from-to)42-54
Number of pages13
JournalPhysiol Genomics
Issue number1
Publication statusPublished - Jun 2010


  • Cardiac hypertrophy
  • Genomewide gene expression
  • Microarray
  • Oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Genetics


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