Literature DB >> 7494542

Importance of monocytes/macrophages and fibroblasts for healing of micronecroses in porcine myocardium.

D Weihrauch1, M Arras, R Zimmermann, J Schaper.   

Abstract

In porcine heart, embolization of small coronary arteries with microspheres in 25 microns in diameter induces collateral capillary vessel growth by angiogenesis in and around focal necrosis. By histological analysis the inflammatory infiltrates in this porcine tissue were characterized by numerous monocytes/macrophages and fibroblasts as well as neutrophils and numerous capillaries, some in mitosis. The aim of the present study, therefore, was to clarify the role of monocytes/macrophages and fibroblasts in angiogenesis and in repair in ischemic porcine myocardium. Using a human acidic fibroblast growth factor (aFGF) cDNA probe for in situ hybridisation labeling for aFGF mRNA was seen in monocytes and macrophages only, beginning at day 1, with a maximum at 3 and 7 days, and minimal labeling at 4 weeks. We have also shown, with a specific antibody and fluorescence microscopy, that tumur necrosis factor alpha (TNF alpha) follows the same time sequence and that it is produced by monocytes/macrophages. The number of capillaries in infiltrates at 3 and 7 days as revealed by the lectin Dolichus Biflorus Agglutinin was high and declined at 4 weeks. In situ hybridisation using a rat cDNA probe for fibronectin showed the increased production of fibronectin mRNA in fibroblasts. To describe the expression of fibronectin and the collagens I, III, VI immunohistochemistry was used. A comparison showed that fibroblasts produced fibronectin mRNA starting at day 3, but the protein was only maximally expressed at day 7 and 4 weeks. Collagen I, III, VI expression was highest at 1-4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1995        PMID: 7494542     DOI: 10.1007/bf00944778

Source DB:  PubMed          Journal:  Mol Cell Biochem        ISSN: 0300-8177            Impact factor:   3.396


  17 in total

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Authors:  D Ingber; J Folkman
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  9 in total

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6.  Inflammation and ischemia: macrophages activated by fibronectin fragments enhance the survival of injured cardiac myocytes.

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7.  Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarction.

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8.  Modulation of mononuclear phagocyte inflammatory response by liposome-encapsulated voltage gated sodium channel inhibitor ameliorates myocardial ischemia/reperfusion injury in rats.

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9.  Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction.

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  9 in total

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