RESUMEN
When a wound forms due to any injuries, it should be covered with a functional wound dressing for accelerating wound healing and reducing infection. In this study, crosslinked ulvan/chitosan complex films were prepared with or without the addition of glycerol and chlorophyll, and their wound healing properties were evaluated for potential application in wound dressing. The results showed that the tensile strength and elongation at break of the prepared ulvan/chitosan complex films were 2.23-2.48 MPa and 83.8-108.5%, respectively. Moreover, their water vapor transmission rates (WVTRs) were in the range of 1791-2029 g/m2-day, providing suitable environment for wound healing. Particularly, these complex films could release ulvan in situ in a short time, and the film with chlorophyll added had the highest release rate, reaching 62.8% after 20 min of releasing. In vitro studies showed that they were biocompatible toward NIH 3T3 and HaCaT cells, and promoted the migration of NIH 3T3 cells. These complex films could protect HaCaT cells from oxidative damage and reduce the production of reactive oxygen species (ROS); the addition of chlorophyll also effectively reduced the inflammatory response induced by LPS as found in the reduction in both NO and IL-6. Animal models showed that the complex films added with glycerol and chlorophyll could promote wound healing in the early stage, while accelerating the regeneration of dermal glands and collagen production. Briefly, these ulvan/chitosan complex films had good physiochemical properties and biological activity, and could accelerate wound healing both in vitro and in vivo.
RESUMEN
Chromatin assembly factor 1 (CAF1) consisting of p150, p60 and p48 is known to assemble histones onto newly synthesized DNA and thus maintain the chromatin structure. Here, we show that CAF1 expression was induced in human cytomegalovirus (HCMV)-infected cells, concomitantly with global chromatin decondensation. This apparent conflict was thought to result, in part, from CAF1 mislocalization to compartments of HCMV DNA synthesis through binding of its largest subunit p150 to viral immediate-early protein 2 (IE2). p150 interaction with p60 and IE2 facilitated HCMV DNA synthesis. The IE2Q548R mutation, previously reported to result in impaired HCMV growth with unknown mechanism, disrupted IE2/p150 and IE2/histones association in our study. Moreover, IE2 interaction with histones partly depends on p150, and the HCMV-induced chromatin decondensation was reduced in cells ectopically expressing the p150 mutant defective in IE2 binding. These results not only indicate that CAF1 was hijacked by IE2 to facilitate the replication of the HCMV genome, suggesting chromatin assembly plays an important role in herpesviral DNA synthesis, but also provide a model of the virus-induced chromatin instability through CAF1.
