Effect of Gold Nanorod Surface Chemistry on Cellular Response

Gold nanorods (GNRs) stabilized with cetyltrimethylammonium bromide (CTAB) and GNR functionalized via a ligand exchange method with either thiolated polyethylene glycol (PEG5000) or mercaptohexadecanoic acid (MHDA) were investigated for their stability in biological media and subsequent toxicological effects to HaCaT cells. GNR-PEG and GNR-MHDA exhibited minimal effects on cell proliferation, whereas GNR-CTAB reduced cell proliferation significantly due to the inherent toxicity of the cationic surfactant to cells. Cell uptake studies indicated relatively low uptake for GNR-PEG and high uptake for GNR-MHDA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that GNR-PEG induced less significant and unique changes in the transcription levels of 84 genes related to stress and toxicity compared to GNR-MHDA. The results demonstrate that, although cell proliferation was not affected by both particles, there is a significant difference in gene expression in GNR-MHDA exposed cells, suggesting long-term implications for chronic exposure.Oak Ridge Institute for Science and EducationNational Science Foundation (U.S.) (NSF DMR # 0906838

Transcriptome analysis reveals new insights into the modulation of endometrial stromal cell receptive phenotype by embryo-derived signals interleukin-1 and human chorionic gonadotropin: possible involvement in early embryo implantation.

The presence of the conceptus in uterine cavity necessitates an elaborate network of interactions between the implanting embryo and a receptive endometrial tissue. We believe that embryo-derived signals play an important role in the remodeling and the extension of endometrial receptivity period. Our previous studies provided original evidence that human Chorionic Gonadotropin (hCG) modulates and potentiates endometrial epithelial as well as stromal cell responsiveness to interleukin 1 (IL1), one of the earliest embryonic signals, which may represent a novel pathway by which the embryo favors its own implantation and growth within the maternal endometrial host. The present study was designed to gain a broader understanding of hCG impact on the modulation of endometrial cell receptivity, and in particular, cell responsiveness to IL1 and the acquisition of growth-promoting phenotype capable of receiving, sustaining, and promoting early and crucial steps of embryonic development. Our results showed significant changes in the expression of genes involved in cell proliferation, immune modulation, tissue remodeling, apoptotic and angiogenic processes. This points to a relevant impact of these embryonic signals on the receptivity of the maternal endometrium, its adaptation to the implanting embryo and the creation of an environment that is favorable for the implantation and the growth of this latter within a new and likely hostile host tissue. Interestingly our data further identified a complex interaction between IL1 and hCG, which, despite a synergistic action on several significant endometrial target genes, may encompass a tight control of endogenous IL1 and extends to other IL1 family members