Myocardial
fibrosis after
myocardial infarction (MI) leads to
heart failure, which has become an important global public health issue. One of the most important features of myocardial
fibrosis is the abnormal deposition of extracellular matrix (ECM)
proteins.
Periostin is one of the ECM
proteins.
Cyclic AMP response element-binding protein 1 (CREB) is well known for its involvement in multiple signaling in myocardial
fibrosis. It has been confirmed that CREB could regulate ECM
proteins deposition. However, little is known about the relationship between CREB and
periostin post-MI. This study aims to verify the hypothesis that CREB promotes the expression of
periostin in MI-induced myocardial
fibrosis. To test this hypothesis, primary rat cardiac fibroblasts were cultured and rat model of MI was established. The level of myocardial
fibrosis post-MI was identified by histological staining. The expressions of CREB and
periostin were detected through western blot and reverse transcription quantity polymerase chain reaction. The upregulation and downregulation of CREB and
periostin were established by plasmid, small interfere
RNA (
siRNA), and lentivirus, respectively. High levels of CREB and
periostin were found post-MI in our study. Meanwhile, the expression of
periostin was decreased after CREB downregulation both in vivo and in vitro. Finally, with the treatment of pAV-CREB and si-
periostin, the expressions of
collagen Ⅰ and Ⅲ were attenuated. The expression of
periostin was elevated post-MI and participated in MI-induced myocardial
fibrosis, which was regulated through CREB. This study provides a novel idea and potential intervention target for MI-induced myocardial
fibrosis.