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Expression of type V secretory phospholipase A 2 in myocardial remodelling after infarction
Author(s) -
Ishikawa Y,
Komiyama K,
Masuda S,
Murakami M,
Akasaka Y,
Ito K,
AkishimaFukasawa Y,
Kimura M,
Fujimoto A,
Kudo I,
Ishii T
Publication year - 2005
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2005.02227.x
Subject(s) - fibronectin , myocardial infarction , lesion , granulation tissue , in situ hybridization , phospholipase a2 , immunohistochemistry , pathology , phospholipase , medicine , myocyte , biology , endocrinology , extracellular matrix , messenger rna , wound healing , immunology , microbiology and biotechnology , biochemistry , enzyme , gene
Aims : Secretory phospholipase A 2 is associated with ischaemic injury in the human heart, but the distribution of type V secretory phospholipase A 2 (sPLA2‐V) remains unknown. The significance of sPLA2‐V in myocardial infarction was investigated histopathologically. Methods : Sequential changes in the localization of sPLA2‐V and its mRNA in myocardial tissues obtained from 30 autopsied hearts were examined by immunohistochemistry and in situ hybridization and compared with those of fibronectin, vascular endothelial growth factor (VEGF), interleukin (IL)‐1β, tumour necrosis factor (TNF)‐α, and cyclooxygenase‐2 (COX‐2). Results : No expression of sPLA2‐V was observed in normal heart, but it was promptly expressed in wavy myofibres positive for fibronectin just after the onset of infarction. sPLA2‐V was subsequently expressed in ischaemic cardiomyocytes around the lesion. The expression decreased at the granulation tissue and disappeared at the chronic stage with scar formation. The distribution of the signal for sPLA2‐V mRNA paralleled that of the protein. Ischaemic myocytes around the lesion expressed VEGF, IL‐1β, TNF‐α and COX‐2 at all stages. Conclusions : sPLA2‐V production in myocardium is limited to the acute phase of infarction. sPLA2‐V may play a dual role, acting both to remove degraded cell‐membrane through cooperative activity with COX‐2 in necrotic areas and to attack ischaemic myocytes around the lesion via degradation of membrane phospholipids.