The　role　of　microRNA-21　(miRNA-21,　miR-21)　in　cardiac　fibrosis　remains　controversial,　while　the　role　of　microRNA-224　(miRNA-224,　miR-224)　in　cardiac　fibroblasts　has　not　been　reported.　Angiotensin　II　(Ang　II)　is　known　to　play　a　pivotal　role　in　the　pathogenesis　of　cardiac　fibrosis.　The　aim　of　this　study　was　to　confirm　whether　the　expression　of　miR-21　and　miR-224　is　regulated　by　Ang　II　in　adult　rat　cardiac　fibroblasts.　Semi-quantitative　reverse　transcription-polymerase　chain　reaction　(RT-PCR)　and　quantitative　PCR　(qPCR)　were　performed　to　measure　the　levels　of　miR-21　and　miR-224　in　Ang　II-treated　or　untreated　adult　rat　cardiac　fibroblasts.　The　RT-PCR,　qPCR　and　previous　miRNA　array　results　demonstrated　that　treatment　with　Ang　II　(100　nM)　for　24　h　did　not　induce　the　increase　of　miR-21　in　cardiac　fibroblasts,　although　the　level　of　miR-21　in　cardiac　fibroblasts　was　not　considered　as　low.　The　results　of　the　present　study　also　demonstrated　that　Ang　II　significantly　upregulated　the　expression　of　miR-224　in　adult　rat　cardiac　fibroblasts.　Bioinformatic　analysis　revealed　that　the　potential　target　genes　of　miR-224　included　SMAD4,　SMAD5,　cyclin-dependent　kinase　9　and　early　growth　response　1/2.　In　previous　studies,　it　was　reported　that　miR-224　was　upregulated　in　tumors　by　promoting　cell　proliferation　and　targeting　SMAD4.　Those　results　indicated　the　potential　roles　of　miR-224　in　cardiac　fibroblasts　and　cardiac　fibrosis.　In　conclusion,　results　of　the　present　study　demonstrated　that　miR-21　was　not　induced　by　Ang　II,　whereas　Ang　II　upregulated　miR-224　expression　in　adult　rat　cardiac　fibroblasts,　a　finding　that　may　provide　a　starting　point　for　the　investigation　of　the　potential　role　of　miR-224　in　cardiac　fibrosis.