905
Views
64
CrossRef citations to date
0
Altmetric
Research Article

Long pentraxin 3 (PTX3) in the light of its structure, mechanism of action and clinical implications

&
Pages 119-128 | Received 06 Mar 2011, Accepted 04 Aug 2011, Published online: 11 Oct 2011
 

Abstract

Pentraxins are a group of evolutionarily conserved ancient proteins. Depending on their structure, pentraxins are divided into short and long pentraxin families. Pentraxin 3 (PTX3) is the prototype of the long pentraxin group. PTX3 synthesis is stimulated by a variety of molecules involved in the inflammatory process. The inflammatory mediator is typically produced at inflammatory sites; however, it can also be released at the sites remote from the original inflammatory insult. Although mainly expressed by vascular endothelium and smooth muscle cells, PTX3 is also synthesized by myeloid dendritic cells, mononuclear macrophages/phagocytes, vascular endothelial and smooth muscle cells, fibroblasts, adipocytes, cumulus oophorus cells mesangial cells, synovial cells and chondrocytes. PTX3 binds to several ligands including complement component C1q, factor H, ficolin-1 (M-ficolin), mannose-binding lectin, fibroblast growth factor 2, P-selectin, matrix protein TSG6 and Klebsiella pneumoniae; it is also known to play a role in humoral innate immunity as well as in degenerated and apoptotic cells clearance. PTX3 acts as a modulator of inflammatory processes, modifies angiogenesis and atherosclerotic lesion development, and participates in extracellular matrix formation. Due to the fact of PTX3 being primarily produced and released by vascular wall cells, it might be used as a sensitive and independent inflammatory marker.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.