Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites

Martino Introna, Victor Vidal Alles, Marina Castellano, Giuseppina Picardi, Luca De Gioia, Barbara Bottazzi, Giuseppe Peri, Ferruccio Breviario, Mario Salmona, Laura De Gregorio, Tommaso A. Dragani, Narayanaswamy Srinivasan, Tom L. Blundell, Thomas A. Hamilton, Alberto Mantovani

Research output: Contribution to journalArticle

Abstract

Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences, the third (203 aa) for a domain related to classical pentraxins, which contains the 'pentraxin family signature.' Analysis of the N terminal portion predicts a predominantly α helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1β (IL-1β) and tumor necrosis factor (TNF)α. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.

Original languageEnglish
Pages (from-to)1862-1872
Number of pages11
JournalBlood
Volume87
Issue number5
Publication statusPublished - Mar 1 1996

Fingerprint

Serum Amyloid P-Component
Cloning
Organism Cloning
Exons
Genes
Acute-Phase Proteins
Endothelial cells
Pathology
Fibroblasts
Chromosomes
Protein Sorting Signals
Interleukin-1
C-Reactive Protein
Lipopolysaccharides
Muscle
Proteins
Complementary DNA
Tumor Necrosis Factor-alpha
Messenger RNA
Chromosomes, Human, Pair 3

ASJC Scopus subject areas

  • Hematology

Cite this

Introna, M., Vidal Alles, V., Castellano, M., Picardi, G., De Gioia, L., Bottazzi, B., ... Mantovani, A. (1996). Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites. Blood, 87(5), 1862-1872.

Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites. / Introna, Martino; Vidal Alles, Victor; Castellano, Marina; Picardi, Giuseppina; De Gioia, Luca; Bottazzi, Barbara; Peri, Giuseppe; Breviario, Ferruccio; Salmona, Mario; De Gregorio, Laura; Dragani, Tommaso A.; Srinivasan, Narayanaswamy; Blundell, Tom L.; Hamilton, Thomas A.; Mantovani, Alberto.

In: Blood, Vol. 87, No. 5, 01.03.1996, p. 1862-1872.

Research output: Contribution to journalArticle

Introna, M, Vidal Alles, V, Castellano, M, Picardi, G, De Gioia, L, Bottazzi, B, Peri, G, Breviario, F, Salmona, M, De Gregorio, L, Dragani, TA, Srinivasan, N, Blundell, TL, Hamilton, TA & Mantovani, A 1996, 'Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites', Blood, vol. 87, no. 5, pp. 1862-1872.
Introna M, Vidal Alles V, Castellano M, Picardi G, De Gioia L, Bottazzi B et al. Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites. Blood. 1996 Mar 1;87(5):1862-1872.
Introna, Martino ; Vidal Alles, Victor ; Castellano, Marina ; Picardi, Giuseppina ; De Gioia, Luca ; Bottazzi, Barbara ; Peri, Giuseppe ; Breviario, Ferruccio ; Salmona, Mario ; De Gregorio, Laura ; Dragani, Tommaso A. ; Srinivasan, Narayanaswamy ; Blundell, Tom L. ; Hamilton, Thomas A. ; Mantovani, Alberto. / Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites. In: Blood. 1996 ; Vol. 87, No. 5. pp. 1862-1872.
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