Indexed by:期刊论文

Date of Publication:2017-12-01

Journal:JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A

Included Journals:Scopus、SCIE、EI

Volume:105

Issue:12

Page Number:3242-3250

ISSN No.:1549-3296

Key Words:cell-material interaction; nanoparticles; hydrogel; neural interfaces; foreign body reaction; inflammatory response

Abstract:Central nervous system (CNS) neural device functionality hinges on effective communication with surrounding neurons. This depends on both the permissiveness of the device material to promote neuron integration and the ability of the device to avoid a chronic inflammatory response. Previously our lab developed a method using surface adsorbed hydrogel particles (HPs) to promote neuron integration onto typically non-neural-permissive substrates. However, little information is known regarding CNS inflammatory cell type responses towards the modified HP surface. In vitro adhesion, proliferation, and activation studies were implemented using NIH 3T3, RAW 264.7, and A172 cell lines to model fibroblast, macrophages and activated microglia, and astrocytes, respectively. For all cell types, the HP modified substrates elicited cell adhesion and sustained cell metabolic activity during a 3-day culture. RAW 264.7 cell activation was evaluated using a tumor necrosis factor-alpha (TNF-) enzyme-linked immunosorbent assay and scanning electron microscope (SEM) imaging. Quantified TNF- levels from the LbL/HP cells were greater than the control substrate, however, investigation with SEM suggested these cells' morphology was different from a typical activated state. A172 cell activation was evaluated by fluorescent staining of glial fibrillary acidic protein (GFAP) and SEM imaging, which revealed similarly low GFAP levels on both bare and HP modified substrates. A172 cell morphology showed mainly an undifferentiated and non-activated state. These results help lay the groundwork to design the HP system for future in vitro and in vivo investigations to ultimately realize stable long-term neural device communication. (c) 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 3242-3250, 2017.