The Journal of Experimental Medicine
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Published online January 21, 2008
doi:10.1084/jem.20071297
The Journal of Experimental Medicine, Vol. 205, No. 2, 295-303
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Shimazaki et al.
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BRIEF DEFINITIVE REPORT

 Periostin is essential for cardiac healingafter acute myocardial infarction

Masashi Shimazaki1, Kazuto Nakamura2, Isao Kii1, Takeshi Kashima3, Norio Amizuka4, Minqi Li4, Mitsuru Saito5, Keiichi Fukuda6, Takashi Nishiyama1, Satoshi Kitajima7, Yumiko Saga8, Masashi Fukayama3, Masataka Sata2, and Akira Kudo1

1 Department of Biological Information, Tokyo Institute of Technology, Yokohama 226-8501, Japan
2 Department of Cardiovascular Medicine and 3 Department of Pathology, Graduate School of Medicine,The University of Tokyo, Tokyo 113-0033, Japan
4 Center for Transdisciplinary Research, Niigata University, Niigata 951-8514, Japan
5 Department of Orthopaedic Surgery, Jikei University School of Medicine, Tokyo 105-8461, Japan
6 Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine,Tokyo 160-8582, Japan
7 Division of Cellular and Molecular Toxicology, National Institute of Health Science, Tokyo 158-8501, Japan
8 Division of Mammalian Development, National Institute of Genetics, Mishima 411-8540, Japan

CORRESPONDENCE Akira Kudo:akudo{at}bio.titech.ac.jp

Acute myocardial infarction (AMI) is a common and lethal heart disease, and the recruitment of fibroblastic cells to the infarct region is essential for the cardiac healing process. Although stiffness of the extracellular matrix in the infarct myocardium is associated with cardiac healing, the molecular mechanism of cardiac healing is not fully understood. We show that periostin, which is a matricellular protein, is important for the cardiac healing process after AMI. The expression of periostin protein was abundant in the infarct border of human and mouse hearts with AMI. We generated periostin–/– mice and found no morphologically abnormal cardiomyocyte phenotypes; however, after AMI, cardiac healing was impaired in these mice, resulting in cardiac rupture as a consequence of reduced myocardial stiffness caused by a reduced number of {alpha} smooth muscle actin–positive cells, impaired collagen fibril formation, and decreased phosphorylation of FAK. These phenotypes were rescued by gene transfer of a spliced form of periostin. Moreover, the inhibition of FAK or {alpha}v-integrin, which blocked the periostin-promoted cell migration, revealed that {alpha}v-integrin, FAK, and Akt are involved in periostin signaling. Our novel findings show the effects of periostin on recruitment of activated fibroblasts through FAK-integrin signaling and on their collagen fibril formation specific to healing after AMI.


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