Expression of type V secretory phospholipase A2 in myocardial remodelling after infarction

• Published in: Histopathology Vol. 47; no. 3; pp. 257 - 267
• Main Authors: Ishikawa, Y, Komiyama, K, Masuda, S, Murakami, M, Akasaka, Y, Ito, K, Akishima-Fukasawa, Y, Kimura, M, Fujimoto, A, Kudo, I, Ishii, T
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.09.2005; Blackwell
• Subjects: Biological and medical sciences; Cardiology. Vascular system; Coronary heart disease; cyclooxygenase-2; Heart; immunohistochemistry; in situ hybridization; Investigative techniques, diagnostic techniques (general aspects); Medical sciences; myocardial infarction; myocardial remodelling; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; type V secretory phospholipase A2; Immunohistochemistry; Myocardial infarction; Enzyme; Cyclooxygenase 2; In situ; cyclooxygenase-2; Cardiovascular disease; Esterases; Hybridization; Remodeling; Myocardial disease; Phospholipase A; Carboxylic ester hydrolases; Anatomic pathology; Heart disease; myocardial remodelling; Hydrolases; type V secretory phospholipase A2; Oxidoreductases; in situ hybridization
• ISSN: 0309-0167; 1365-2559
• DOI: 10.1111/j.1365-2559.2005.02227.x

Aims : Secretory phospholipase A2 is associated with ischaemic injury in the human heart, but the distribution of type V secretory phospholipase A2 (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.