Human renal epithelial cells produce the long pentraxin PTX3

Nauta, Alma J.; Haij, Simone de; Bottazzi, Barbara; Mantovani, Alberto; Borrias, Maria C.; Aten, Jan; Rastaldi, Maria Pia; Daha, Mohamed R.; Kooten, Cees van; Roos, Anja

doi:10.1111/j.1523-1755.2005.67111.x

Cited by 112 publications

(84 citation statements)

References 41 publications

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“…It has been reported that renal mesangial and epithelial cells produce PTX3 (61,62). It is possible to hypothesize that a mechanism involving a disturbed interaction of locally produced PTX3 with FH could be involved in the pathogenesis of this condition.…”

Section: ϫ7mentioning

confidence: 99%

Binding of the Long Pentraxin PTX3 to Factor H: Interacting Domains and Function in the Regulation of Complement Activation

Deban

Jarva

Lehtinen

et al. 2008

The Journal of Immunology

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The long pentraxin PTX3 is a multifunctional soluble molecule involved in inflammation and innate immunity. As an acute phase protein, PTX3 binds to the classical pathway complement protein C1q, limits tissue damage in inflammatory conditions by regulating apoptotic cell clearance, and plays a role in the phagocytosis of selected pathogens. This study was designed to investigate the interaction of PTX3 with factor H (FH), the main soluble alternative pathway regulatory protein. We report that PTX3 binds FH with an apparent Kd of 1.1 × 10−7 M, and define two binding sites for PTX3 on FH. The primary binding site is located on FH domains 19–20, which interact with the N-terminal domain of PTX3, while a secondary binding site on domain 7 binds the glycosylated PTX3 pentraxin domain. The FH Y402H polymorphism, which affects binding to the short pentraxin CRP, did not affect binding to PTX3. Surface-bound PTX3 enhances FH recruitment and iC3b deposition and PTX3-bound FH retains its activity as a cofactor for factor I-mediated C3b cleavage. Thus, our findings identify PTX3 as a unique FH ligand in that it can bind both of the two hot-spots of FH, namely SCR7 and SCR19–20 and indicate that PTX3 participates in the localization of functionally active FH.

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Section: ϫ7mentioning

confidence: 99%

Binding of the Long Pentraxin PTX3 to Factor H: Interacting Domains and Function in the Regulation of Complement Activation

Deban

Jarva

Lehtinen

et al. 2008

The Journal of Immunology

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169

219

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“…10 It is present in renal proximal tubular cells, fibroblasts, and mesangial cells and it stimulates opsonization, degradation of apoptotic bodies, and activation of the complement cascade. 11,12 The protein PTX-3 may reflect disease activity directly. The correlation between CRP and PTX-3 may be weak or not significant.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Gürsu

Çelik²,

Öztürk³

et al. 2014

Exp Clin Transplant

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Objectives: There are numerous changes in inflammatory status that occur after a kidney transplant. Pentraxin 3 is a marker of inflammation, but little information is available about pentraxin 3 levels after a kidney transplant. We evaluated the relation between pentraxin 3 and other inflammatory markers including high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α in kidney transplant recipients. Materials and Methods: Adult patients (40 patients; aged, 18-80 y; mean age, 38 ± 10 y) who had a kidney transplant from living-related donors were studied. Patients who had comorbidities associated with chronic inflammation were excluded. Blood samples were obtained before starting immunosuppressive treatment and 2 months after kidney transplant for measurement of pentraxin 3, high sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor α levels. Results: After transplant, mean levels of high sensitivity C-reactive protein and interleukin 6 decreased but levels of pentraxin 3 and tumor necrosis factor α did not change. There were significant correlations between interleukin 6 and high sensitivity C-reactive protein before transplant (r = 0.71; P ≤ .0001) and after transplant (r = 0.45; P ≤ .003). There was no correlation between tumor necrosis factor α and high sensitivity C-reactive protein before transplant, but there was a significant correlation between tumor necrosis factor α and high sensitivity C-reactive protein after transplant (r = 0.36; P ≤ .03). There was no correlation between interleukin 6 and pentraxin 3, tumor necrosis factor α and pentraxin 3, or high sensitivity C-reactive protein and pentraxin 3 before or after transplant. Conclusions: After a kidney transplant, pentraxin 3 may not be useful in determining inflammatory status, and high sensitivity C-reactive protein may be better than pentraxin 3 as a marker of inflammation.

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“…This suggests a low constitutive production of PTX3 by endothelial cells in nonvasculitic inflamed skin and in healthy skin. Constitutive production of PTX3 in vitro has been reported in cultured scleroderma fibroblasts as well as in renal fibroblasts, primary mesangial cells, and primary proximal renal tubular epithelial cells (14,15).…”

Section: Discussionmentioning

confidence: 99%

Abundance of the long pentraxin PTX3 at sites of leukocytoclastic lesions in patients with small‐vessel vasculitis

Rossum

Pas

Fazzini

et al. 2006

Arthritis & Rheumatism

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Objective. The prototypical tissue pentraxin PTX3 inhibits phagocytosis of late apoptotic polymorphonuclear leukocytes (PMNs) by macrophages. Levels of PTX3 parallel disease activity in small-vessel vasculitis. Small-vessel vasculitis is often characterized by leukocytoclasia, a phenomenon of accumulation of nuclear remnants from unscavenged PMNs in or near the vessel wall. We therefore hypothesized that PTX3 accumulates at sites of leukocytoclastic vasculitis and, as such, is a key factor for the induction of leukocytoclasis.Methods. We examined skin biopsy samples from 13 patients with small-vessel vasculitis and from 4 healthy and 3 inflammatory skin disease controls. Biopsy tissues, characterized histopathologically as leukocytoclastic vasculitis, were studied for the presence of PTX3 using rabbit anti-PTX3 polyclonal antibodies. Sections were scored morphometrically for leukocytoclastic infiltrates in conjunction with PTX3 staining. Morphometric scores were expressed as percentages of staining of the total tissue area.Results. Biopsy specimens from patients with leukocytoclastic vasculitis revealed an abundant upregulation of PTX3 at sites of leukocytoclastic infiltrates. Significantly more PTX3 was found in tissues from the 13 patients with vasculitis (mean ؎ SEM 48.9 ؎ 6.1%) than in tissues from the 7 controls (4.5 ؎ 2.7%) (P ‫؍‬ 0.0003). PTX3 was localized around vessels, as well as spread diffusely throughout the tissue.Conclusion. PTX3 is abundantly present at sites of leukocytoclastic infiltrates in patients with smallvessel vasculitis, but not in controls. Since PTX3 inhibits phagocytosis of late apoptotic PMNs by macrophages and is strongly up-regulated at sites of leukocytoclastic infiltration, PTX3 is a candidate factor in the phenomenon of leukocytoclasia in small-vessel vasculitis.

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Human renal epithelial cells produce the long pentraxin PTX3

Abstract: These results indicate that PTX3 is expressed and released by PTECs and that in proinflammatory conditions PTX3 production is up-regulated. Local expression of PTX3 may play a role in the innate immune response and inflammatory reactions in the kidney.

Cited by 112 publications

References 41 publications

Binding of the Long Pentraxin PTX3 to Factor H: Interacting Domains and Function in the Regulation of Complement Activation

Binding of the Long Pentraxin PTX3 to Factor H: Interacting Domains and Function in the Regulation of Complement Activation

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Abundance of the long pentraxin PTX3 at sites of leukocytoclastic lesions in patients with small‐vessel vasculitis

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