In situ complement activation by polyethylene wear debris

DeHeer, David H.; Engels, James A.; DeVries, Aaron; Knapp, Robert H.; Beebe, John D.

doi:10.1002/1097-4636(200101)54:1<12::aid-jbm2>3.0.co;2-x

Cited by 56 publications

(43 citation statements)

References 31 publications

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“…This latter process (''tickover'') is mediated by small nucleophiles or water that gain access and react with the internal thioester of C3, rendering it able to form the C3 convertase with factor B (in the presence of factor D), thus initiating C3b formation (20). All told, in addition to pathogens and immune complexes, complement activation can be triggered by stimuli as diverse as oxidatively modified low-density lipoproteins (21,22), amyloid-␤ (23), polyethylene implants (24,25), and carbon nanotubes (26). The structural features that determine whether activation and amplification will occur are not clear, but particle surfaces bearing hydroxyl (-OH) and amine (-NH 2 ) nucleophiles increase the potential for activation (16 -18, 20).…”

mentioning

confidence: 99%

Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium

Zhou¹,

Jang²,

Kim³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

328

240

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Recent studies have implicated local inflammation and activation of complement amongst the processes involved in the pathogenesis of age-related macular degeneration (AMD). Several lines of investigation also indicate that bis-retinoid pigments, such as A2E, that accumulate as lipofuscin in retinal pigment epithelial (RPE) cells, contribute to the disease process. In an investigation of a potential trigger for complement activation in AMD, we explored the notion that the complex mixture of products resulting from photooxidation of A2E might include a range of fragments that could be recognized by the complement system as ''foreign'' and that could serve to activate the complement system, leading to low-grade inflammation. To this end, we established an in vitro assay by using human serum as a source of complement, and we measured products of C3 activation by enzyme immunoassay. Accordingly, we found that the C3 split products inactivated C3b (iC3b) and C3a were elevated in serum, overlying ARPE-19 cells that had accumulated A2E and were irradiated to induce A2E photooxidation. Precoating of microtiter plates with two species of oxidized A2E, peroxy-A2E, and furano-A2E, followed by incubation with serum, also activated complement. We suggest that products of the photooxidation of bis-retinoid lipofuscin pigments in RPE cells could serve as a trigger for the complement system, a trigger than would predispose the macula to disease and that, over time, could contribute to chronic inflammation. These findings link four factors that have been posited as being associated with AMD: inflammation, oxidative damage, drusen, and RPE lipofuscin.inflammation ͉ macular degeneration

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mentioning

confidence: 99%

Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium

Zhou¹,

Jang²,

Kim³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

328

240

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“…Due to this fact, infected tissue with a high number of active cells revealed an increased uptake of FDG, which leads to a positive finding in the PET scan (Stumpe & Strobel, 2006). Furthermore, higher FDG uptake in patients with aseptic loosening of the THR can be explained by wear debris and the development of granulomatous tissue in the periprosthetic membrane around the THR (DeHeer et al, 2001;Kadoya et al, 1998). The criteria for the interpretation of a PET scan differ between different studies .…”

Section: Fdg-petmentioning

confidence: 99%

Current Possibilities for Detection of Loosening of Total Hip Replacements and How Intelligent Implants Could Improve Diagnostic Accuracy

Ruther¹,

Timm²,

Ewald³

et al. 2012

Recent Advances in Arthroplasty

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Section: Chemical Surface Patterning Followed By Protein Adsorptionmentioning

confidence: 99%

“…Disruption of protein conformation most often causes diminished or abolished native function and can trigger undesirable side effects at the implant surface. It is well documented that the typical host response to implanted materials is a coagulation cascade triggered by nonspecific protein adsorption events [72] and complement protein reaction at the implant-host interface [73][74][75].By acquiring an understanding of basic protein interactions with interfaces, it may be possible to more accurately predict how proteins and surfaces can be manipulated for the creation of cell assays or biocompatible materials that mimic native in vivo protein signals. To this end, numerous methods have been developed to produce model surfaces so that in vitro protein interactions at interfaces and resulting cellular responses can be investigated and evaluated as models of in vivo interactions and signaling.…”

mentioning

confidence: 99%

The effects of proteoglycan surface patterning on neuronal pathfinding

Hlady

Hodgkinson

2007

Materialwissenschaft Werkst

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Protein micropatterning techniques are increasingly applied in cell choice assays to investigate fundamental biological phenomena that contribute to the host response to implanted biomaterials, and to explore the effects of protein stability and biological activity on cell behavior for in vitro cell studies. In the area of neuronal regeneration the protein micropatterning and cell choice assays are used to improve our understanding of the mechanisms directing nervous system during development and regenerative failure in the central nervous system (CNS) wound healing environment. In these cell assays, protein micropatterns need to be characterized for protein stability, bioactivity, and spatial distribution and then correlated with observed mammalian cell behavior using appropriate model system for CNS development and repair. This review provides the background on protein micropatterning for cell choice assays and describes some novel patterns that were developed to interrogate neuronal adaptation to inhibitory signals encountered in CNS injuries. Rationale for studying the role of proteoglycans in CNS injuriesNeurons from the central nervous system (CNS) possess a limited capacity to regenerate beyond scar tissue formation barriers in injuries even in the presence of minimal trauma to tissue organization [1,2]. A major culprit in CNS neuronal regenerative failure are the inihibitory proteoglycans (PGs), which are upregulated at the site of CNS injuries. PGs are composed of a core protein with varying numbers of attached glycosaminoglycan (GAG) side chains [3,4]. Proteoglycans are first translated intracellularly into proteins in the endoplasmic reticulum, and then GAG chains are later attached in the Golgi apparatus before secretion into the extracellular space [5][6][7][8]. The study of PGs has particularly been pronounced in the field of neurobiology and development of the nervous system. Numerous studies have concluded that PGs act as barriers that direct the migration of neural crest cells and the outgrowth direction of pathfinding neurons during development [9][10][11][12][13][14][15][16][17]. A number of these studies have additionally shown that cell guidance by PGs is based on an inhibitory signal located within the chondroitin sulfate GAG chains [9,18,19], with the result that the artificial addition of chondroitin sulfate (CS) sugars to the developing nervous system disrupts normal pathfinding [20] as well as does the removal of chondroitin sulfate chains through enzymatic treatment [9,19]. Davies et al. found that chondroitin sulfate proteoglycans (CSPG) are a major constituent of the glial scar and that dorsal root ganglion (DRG) outgrowth termination coincided with an increase in CSPG expression density [21]. Other sources have also shown that CSPGs are upregulated after CNS injuries [22][23][24][25].Interestingly, native adult CNS neurons actually posses the intrinsic ability to regenerate when the wound healing environment is prepared by eliminating inhibitory factors [23,26,27]. In additi...

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In situ complement activation by polyethylene wear debris

Cited by 56 publications

References 31 publications

Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium

Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium

Current Possibilities for Detection of Loosening of Total Hip Replacements and How Intelligent Implants Could Improve Diagnostic Accuracy

The effects of proteoglycan surface patterning on neuronal pathfinding

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