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Abstract
BackgroundBone Marrow (BM) progenitor cells can target the site of myocardial injury, contributing to tissue repair by neovascolarization and/or by a possible direct paracrine effect on the inflammatory cascade. Angiotensin Converting Enzyme inhibitors (ACE-I) are effective in reducing mortality and preventing left ventricular (LV) function deterioration after myocardial infarction.MethodsWe investigated the short term effects of BM mononuclear cells (BMMNCs) therapy on the pro-inflammatory cytokines (pro-CKs) and on LV remodelling and compared these effects over a standard ACE-I therapy in a rat model of myocardial cryodamage.Forty two adult inbread Fisher-F344 rats were randomized into three groups: untreated (UT; n = 12), pharmacological therapy (ACE-I; n = 14, receiving quinapril), and cellular therapy (BMMNCs; n = 16, receiving BMMNCs infusion). Rats underwent to a standard echocardiogram in the acute setting and 14 days after the damage, before the sacrifice. Pro-CKs analysis (interleukin (IL)1β, IL-6, tumor necrosis factor (TNF)α was performed (multiplex proteome arrays) on blood samples obtained by direct aorta puncture before the sacrifice; a control group of 6 rats was considered as reference.ResultsConcerning the extension of the infarcted area as well as the LV dimensions, no differences were observed among the animal groups; treated rats had lower left atrial diameters and higher indexes of LV function. Pro-Cks were increased in infarcted-UT rats if compared with controls, and significantly reduced by BMMNCs and ACE-I ; TNFα inversely correlated with LV fractional shortening.ConclusionAfter myocardial infarction, both BMMNCs and ACE-I reduce the pattern of pro-Ck response, probably contributing to prevent the deterioration of LV function observed in UT rats.
Highlights
Bone Marrow (BM) progenitor cells can target the site of myocardial injury, contributing to tissue repair by neovascolarization and/or by a possible direct paracrine effect on the inflammatory cascade
The animals were randomized into three groups: untreated group receiving no treatment (UT; n = 12), pharmacological therapy group treated with quinapril (ACE-I; n = 14), and cellular therapy group treated with BM mononuclear cells (BMMNCs) infusion (BMMNCs; n = 16) (Figure 1)
In the hypothesis that the efficacy of BM mononuclear cells (BMMNCs) after myocardial infarction is mediated by a paracrine mechanism, in this study we investigated the short term effects of BMMNC therapy on the proinflammatory cytokine signaling pathways and on left ventricular (LV) remodelling markers and compared these effects over a standard Angiotensin Converting Enzyme inhibitors (ACE-I) pharmacological therapy in a rat model of myocardial cryodamage
Summary
Bone Marrow (BM) progenitor cells can target the site of myocardial injury, contributing to tissue repair by neovascolarization and/or by a possible direct paracrine effect on the inflammatory cascade. Experimental animal studies have provided evidence that bone marrow (BM) progenitor cells are capable to selectively target the site of myocardial injury [2] and contribute to tissue repair [3]. Other possible explanations have been proposed in order to clarify the mechanisms underlying the positive results observed in animals models and humans In this context, a possible mechanism of the BM cell therapy benefit could derive either by new vessels formation [7,8] at the infarct site and/or by a direct paracrine effect on the inflammatory cascade [9]
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