Correlating Additives to Deterioration and Assessing the Effectiveness of Acrylic Coatings for the Protection of Rubber

Conservators have long been aware of the problems associated with the preservation of rubber objects due to inherent instability that can be attributed, in part, to the presence of additives. Inorganic additives, such as fillers, accelerators, stabilizers, and special ingredients are necessary in manufacturing to alter the properties of natural rubber. These materials all have different interactions with the rubber, and each other, and differing effects on the ageing process. To date, the most effective and accepted methods to preserve rubber are cold, dark storage of objects, or the use of low oxygen environments. While these methods are effective, they greatly limit access. The application of coatings to the surface of rubber objects can slow deterioration and greatly increase the ability of an institution to handle and display rubber objects. While numerous coatings for preventive and interventive treatment have been tested, none have been so successful to warrant routine use. The first section of this research highlighted the relationship between the inclusion of certain additives in natural rubber objects and the accelerated or slowed down overall degradation. In the second part of this research, the acrylic varnishes Golden Polymer Varnish with UVLS, Lascaux Acrylic Transparent Varnish-UV, Sennelier Matte Lacquer with UV Protection, and Liquitex Soluvar Varnish containing ultraviolet light absorbers or stabilizers were tested as a preventative coating for rubber. Through testing the visual and physical properties of the samples, as well as compound analysis the results of this research suggest that acrylic varnishes do provide protection, each to varying degrees. The results also provided insight into the behavior of rubber and these varnishes with continuing light exposure.

ROLE OF CAVEOLIN-3 IN THE MODULATION OF HERG POTASSIUM CHANNEL

The human ether-a-go-go-related gene (hERG) encodes the pore-forming subunit of the rapidly activating delayed rectifier potassium channel (IKr) that is important for cardiac repolarization. Previously, we have discovered that hERG channels rapidly internalize in low extracellular K+ ([K+]o). In cell culture, this process is driven by the endocytic protein, caveolin-1 (Cav1), which is an integral player in the caveolae-dependant endocytosis pathway. However, in the heart, Caveolin-3 (Cav3) is, in fact, the predominant form in the myocyte, and thus may play a direct role in regulating hERG expression in the heart. Thus, I hypothesize that this reduction of hERG conductance in cardiac myocytes derives from the presence of Cav3, which is integral regulator of hERG homeostasis innately in the heart. To investigate the effect of Cav3 on hERG, I overexpressed Cav3 in human embryonic kidney 293 (HEK-293) cells stably expressing hERG channels. Cav3 overexpression significantly and specifically decreased both the hERG current amplitude and the mature channel expression in normal culture conditions. Co-immunoprecipitation analysis and confocal imaging demonstrated an association between hERG and Cav3 in HEK cells as well as rat and rabbit cardiomyocytes. Mechanistically, I discovered that Cav3 possesses a faster turnover rate compared to Cav1, and can enhance hERG degradation through up-regulating mature channel ubiquitination via the ubiquitin ligase, NEDD4-2. Knockdown of Cav3 in neonatal cardiac myocytes also enhanced hERG expression. My data indicate that Cav3 participates in hERG trafficking, and is an important regulator of hERG channel homeostasis in cardiac myocytes. This information provides a platform for future intervention of the hERG-induced type-2 long QT syndrome (LQTS).