TY - GEN
T1 - In vitro model to mimic aggrecan fragmentation profiles after spinal cord injury
AU - McCrary, Michaela W.
AU - Song, Young Hye
AU - Porvasnik, Stacy L.
AU - Wachs, Rebecca
AU - Fosang, Amanda
AU - Schmidt, Christine E.
N1 - Publisher Copyright:
© 2019 Omnipress - All rights reserved.
PY - 2019
Y1 - 2019
N2 - Statement of Purpose: Spinal cord injury (SCI) is a devastating and complex condition whose mechanistic underpinnings are not entirely understood. One way to study these mechanisms is by using in vitro models. Unfortunately, current in vitro models for SCI lack physiological relevance as most are two dimensional, do not provide a dynamic microenvironment, or utilize materials that do not occur in spinal cord extracellular matrix (ECM) in relevant concentrations.1 Spinal cord ECM is primarily composed of hyaluronan, tenascin-R, and chondroitin sulfate proteoglycans (CSPGs).2 After injury, however, dynamic changes occur in the microenvironment that ultimately lead to excessive deposition of CSPGs to form an inhibitory glial scar.2 Although most CSPG subtypes are upregulated after injury, one type of CSPG called aggrecan is down-regulated and pre-existing protein is actively removed from the ECM.3,4 This fragmentation phenomenon has been linked to disease and injury progression in other contexts including epilepsy and osteoarthritis.5,6 However, the role of aggrecan fragmentation on SCI progression and glial scar response is relatively unknown. The aim of this study is to establish the spatiotemporal profiles of aggrecan fragmentation after SCI then recapitulate these profiles in a novel in vitro model to observe the effect of this phenomenon on native glial cells.
AB - Statement of Purpose: Spinal cord injury (SCI) is a devastating and complex condition whose mechanistic underpinnings are not entirely understood. One way to study these mechanisms is by using in vitro models. Unfortunately, current in vitro models for SCI lack physiological relevance as most are two dimensional, do not provide a dynamic microenvironment, or utilize materials that do not occur in spinal cord extracellular matrix (ECM) in relevant concentrations.1 Spinal cord ECM is primarily composed of hyaluronan, tenascin-R, and chondroitin sulfate proteoglycans (CSPGs).2 After injury, however, dynamic changes occur in the microenvironment that ultimately lead to excessive deposition of CSPGs to form an inhibitory glial scar.2 Although most CSPG subtypes are upregulated after injury, one type of CSPG called aggrecan is down-regulated and pre-existing protein is actively removed from the ECM.3,4 This fragmentation phenomenon has been linked to disease and injury progression in other contexts including epilepsy and osteoarthritis.5,6 However, the role of aggrecan fragmentation on SCI progression and glial scar response is relatively unknown. The aim of this study is to establish the spatiotemporal profiles of aggrecan fragmentation after SCI then recapitulate these profiles in a novel in vitro model to observe the effect of this phenomenon on native glial cells.
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M3 - Conference contribution
AN - SCOPUS:85065443227
T3 - Transactions of the Annual Meeting of the Society for Biomaterials and the Annual International Biomaterials Symposium
SP - 119
BT - Society for Biomaterials Annual Meeting and Exposition 2019
PB - Society for Biomaterials
T2 - 42nd Society for Biomaterials Annual Meeting and Exposition 2019: The Pinnacle of Biomaterials Innovation and Excellence
Y2 - 3 April 2019 through 6 April 2019
ER -