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Article: Active leukocyte detachment and apoptosis/necrosis on PEG hydrogels and the implication in the host inflammatory response

TitleActive leukocyte detachment and apoptosis/necrosis on PEG hydrogels and the implication in the host inflammatory response
Authors
KeywordsCell adhesion
Apoptosis
Monocyte
Hydrogel
Cell culture
Issue Date2012
Citation
Biomaterials, 2012, v. 33, n. 1, p. 29-37 How to Cite?
AbstractMonocytes/Macrophages have long been recognized as key players in inflammation and wound healing and are often employed in vitro to gain an understanding of the inflammatory response to biomaterials. Previous work has demonstrated a drastic decrease in primary monocyte adherent density on biomaterial surfaces coupled with a change in monocyte behavior over time. However, the mechanism responsible for this decrease remains unclear. In this study, we explored active detachment and cellular death as possible regulating factors. Specifically, extracellular TNF-α and ROS production were analyzed as potential endogenous stimulators of cell death. MMPs, but not calpains, were found to play a key role in active monocyte detachment. Monocyte death was found to peak at 24 h and occur by both apoptosis and necrosis as opposed to polymorphonuclear leukocyte death which mainly occurred through apoptosis. Finally, TNF-α and ROS production were not found to have a causal relationship with monocyte death on TCPS or PEG surfaces. The occurrence of primary monocyte apoptosis/necrosis as well as active detachment from a material surface has implications not only in in vitro study, but also in the translation of the in vitro inflammatory response of these cells to in vivo applications. © 2011 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/216214
ISSN
2015 Impact Factor: 8.387
2015 SCImago Journal Rankings: 3.565

 

DC FieldValueLanguage
dc.contributor.authorWaldeck, Heather-
dc.contributor.authorWang, Xintong-
dc.contributor.authorJoyce, Evan-
dc.contributor.authorKao, Weiyuan John-
dc.date.accessioned2015-08-25T10:22:30Z-
dc.date.available2015-08-25T10:22:30Z-
dc.date.issued2012-
dc.identifier.citationBiomaterials, 2012, v. 33, n. 1, p. 29-37-
dc.identifier.issn0142-9612-
dc.identifier.urihttp://hdl.handle.net/10722/216214-
dc.description.abstractMonocytes/Macrophages have long been recognized as key players in inflammation and wound healing and are often employed in vitro to gain an understanding of the inflammatory response to biomaterials. Previous work has demonstrated a drastic decrease in primary monocyte adherent density on biomaterial surfaces coupled with a change in monocyte behavior over time. However, the mechanism responsible for this decrease remains unclear. In this study, we explored active detachment and cellular death as possible regulating factors. Specifically, extracellular TNF-α and ROS production were analyzed as potential endogenous stimulators of cell death. MMPs, but not calpains, were found to play a key role in active monocyte detachment. Monocyte death was found to peak at 24 h and occur by both apoptosis and necrosis as opposed to polymorphonuclear leukocyte death which mainly occurred through apoptosis. Finally, TNF-α and ROS production were not found to have a causal relationship with monocyte death on TCPS or PEG surfaces. The occurrence of primary monocyte apoptosis/necrosis as well as active detachment from a material surface has implications not only in in vitro study, but also in the translation of the in vitro inflammatory response of these cells to in vivo applications. © 2011 Elsevier Ltd.-
dc.languageeng-
dc.relation.ispartofBiomaterials-
dc.subjectCell adhesion-
dc.subjectApoptosis-
dc.subjectMonocyte-
dc.subjectHydrogel-
dc.subjectCell culture-
dc.titleActive leukocyte detachment and apoptosis/necrosis on PEG hydrogels and the implication in the host inflammatory response-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.biomaterials.2011.09.044-
dc.identifier.pmid21963150-
dc.identifier.scopuseid_2-s2.0-82855175148-
dc.identifier.volume33-
dc.identifier.issue1-
dc.identifier.spage29-
dc.identifier.epage37-
dc.identifier.eissn1878-5905-

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