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Immun Ageing. 2019 Feb 2;16:4. doi: 10.1186/s12979-019-0144-0. eCollection 2019.

PTX3: an inflammatory protein modulating ultrastructure and bioenergetics of human endothelial cells.

Author information

1
1Vascular Pathophysiology Unit, IRCCS Neuromed, 86077 Pozzilli, IS Italy.
2
2Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Naples, Italy.
3
3IRCSS Fondazione Santa Lucia, Rome, Italy.
4
4Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy.
5
5Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II", Naples, Italy.
6
6Cardiovascular Research Unit, IRCCS MultiMedica, 20099 Sesto San Giovanni, MI Italy.
7
7Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University of Rome, Rome, Italy.
8
8Department of Medicine and Surgery, University of Salerno, Via S. Allende, 84081 Baronissi, SA Italy.

Abstract

Background:

Pentraxin 3 (PTX3), an acute-phase inflammation protein produced by several cell types, has long been described as a possible biomarker for age-related cardiovascular and cerebrovascular diseases. Although several mechanisms of action have been identified to date in the vascular and immune systems, the direct effects of PTX3 on isolated endothelial cells at morphological and metabolic levels remain unknown.

Findings:

PTX3 induced cytoplasmic vacuolization and dilution of mitochondrial matrix in isolated, human endothelial cells. Moreover, metabolic assays revealed that PTX3 increases respiratory capacity in support of mitochondrial function, and partially sustains the glycolytic pathway.

Conclusions:

PTX3 has, per se, a direct action on ultrastructural and bioenergetic parameters of isolated endothelial cells. This finding can be associated with our previous demonstration of a deleterious effect of PTX3 on the endothelial layer. More studies are needed to clearly demonstrate any direct correlation between these ultrastructural and bioenergetic changes with endothelial dysfunction, especially with regard to age-related cerebro- and cardio-vascular diseases.

KEYWORDS:

Bioenergetics; Endothelial cells; Mitochondria; Pentraxin 3

Conflict of interest statement

Not applicable.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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