Dependence of macrophage superoxide release on the pulse amplitude of an applied pressure regime: A potential factor at the soft tissue-implant interface

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Dependence of macrophage superoxide release on the pulse amplitude of an applied pressure regime : A potential factor at the soft tissue-implant interface. / Shin, Hainsworth Y.; Frechette, Danielle M.; Rohner, Nathan; Zhang, Xiaoyan; Puleo, David A.; Bjursten, Lars M.

I: Journal of Tissue Engineering and Regenerative Medicine, Vol. 10, Nr. 3, 01.03.2016, s. E227-E238.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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TY - JOUR

T1 - Dependence of macrophage superoxide release on the pulse amplitude of an applied pressure regime

T2 - Journal of Tissue Engineering and Regenerative Medicine

AU - Shin, Hainsworth Y.

AU - Frechette, Danielle M.

AU - Rohner, Nathan

AU - Zhang, Xiaoyan

AU - Puleo, David A.

AU - Bjursten, Lars M.

PY - 2016/3/1

Y1 - 2016/3/1

N2 - Failure of soft tissue implants has been largely attributed to the influence of biomaterial surface properties on the foreign body response, but some implant complications, e.g. macrophage accumulation and necrosis, are still not effectively addressed with surface treatments to minimize deleterious biomaterial effects. We explored an alternative explanation for implant failure, linking biocompatibility with implant micromotion-induced pressure fluctuations at the tissue-biomaterial interface. For this purpose, we used a custom in vitro system to characterize the effects of pressure fluctuations on the activity of macrophages, the predominant cells at a healing implant site. Initially, we quantified superoxide production by HL60-derived macrophage-like cells under several different pressure regimes with means of 5-40 mmHg, amplitudes of 0-15 mmHg and frequencies of 0-1.5 Hz. All pressure regimes tested elicited significantly (p2=0.74; p

AB - Failure of soft tissue implants has been largely attributed to the influence of biomaterial surface properties on the foreign body response, but some implant complications, e.g. macrophage accumulation and necrosis, are still not effectively addressed with surface treatments to minimize deleterious biomaterial effects. We explored an alternative explanation for implant failure, linking biocompatibility with implant micromotion-induced pressure fluctuations at the tissue-biomaterial interface. For this purpose, we used a custom in vitro system to characterize the effects of pressure fluctuations on the activity of macrophages, the predominant cells at a healing implant site. Initially, we quantified superoxide production by HL60-derived macrophage-like cells under several different pressure regimes with means of 5-40 mmHg, amplitudes of 0-15 mmHg and frequencies of 0-1.5 Hz. All pressure regimes tested elicited significantly (p2=0.74; p

KW - Cell adhesion

KW - Macrophage

KW - Mechanotransduction

KW - Pressure

KW - Superoxide

KW - Tissue-implant interface

UR - http://www.scopus.com/inward/record.url?scp=84961207254&partnerID=8YFLogxK

U2 - 10.1002/term.1789

DO - 10.1002/term.1789

M3 - Article

VL - 10

SP - E227-E238

JO - Journal of Tissue Engineering and Regenerative Medicine

JF - Journal of Tissue Engineering and Regenerative Medicine

SN - 1932-6254

IS - 3

ER -