Publications by authors named "M C Capogrossi"

Aging per se is a major risk factor for cardiovascular diseases and is associated with progressive changes in cardiac structure and function. Rodent models are commonly used to study cardiac aging, but do not closely mirror differences as they occur in humans. Therefore, we performed a 2D echocardiographic study in non-human primates (NHP) to establish age- and sex-associated differences in cardiac function and morphometry in this animal model.

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Two vascular endothelial growth factor (VEGF) receptors, FLT-1 and KDR, are expressed preferentially in proliferating endothelium. There is increasing evidence that recombinant, soluble VEGF receptor domains interfering with VEGF signaling may inhibit in vivo neoangiogenesis, tumor growth and metastatic spread. We hypothesized that a soluble form of FLT-1 receptor (sFLT-1) could inhibit the growth of pre-established tumors via an anti-angiogenic mechanism.

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We previously showed that genotoxic stress induced an active extracellular release of nucleophosmin (NPM) in human cardiac mesenchymal progenitor cells, and that serum deprivation provokes NPM secretion from human endothelial cells, eliciting inflammation nuclear factor kappa B (NF-kB) transcriptional activation. In this study, we wanted to determine whether NPM was similarly modulated in the skin and plasma of psoriatic patients (Pso). We found that NPM was induced in 6 skin biopsies compared to 6 normal skin biopsies and was markedly increased in lesional (LS) vs.

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Article Synopsis
  • Doxorubicin (Dox) is an effective anti-cancer drug but causes harmful effects on normal cells, particularly leading to the secretion of Nucleophosmin (NPM) in response to DNA damage.
  • NPM is released actively from human cardiac mesenchymal progenitor cells after Dox treatment and is also found increased in the plasma of treated mice, indicating its secretion occurs in vivo.
  • The study reveals that extracellular NPM affects hCmPCs by reducing cell proliferation through activation of Toll-like receptor (TLR)4, causing pro-inflammatory responses via gene expression changes.
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