Elliott E. Hill
University of Michigan
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Featured researches published by Elliott E. Hill.
Soft Matter | 2008
Rameshwer Shukla; Elliott E. Hill; Xiangyang Shi; Jinkoo Kim; Maria C. Muñiz; Kai Sun; James R. Baker
Monodisperse dendrimer-entrapped gold nanoparticles (diameter = 3.0 nm) were prepared using G5 poly(amidoamine) (PAMAM) dendrimer functionalized with fluorescein isothiocyanate (FI) and Arg-Gly-Asp (RGD) peptide as template; in vitro targeting efficacy to integrin receptor expressing cells was confirmed by flow cytometry, confocal microscopy, and ICP-MS.
Journal of Dental Research | 2010
J. K. Kim; Rameshwer Shukla; Luciano Casagrande; C.M. Sedgley; Jacques E. Nör; James R. Baker; Elliott E. Hill
Traumatic dental injuries are often irreversible, underscoring the need for therapies that protect dental pulp cells and enhance their regeneration. We hypothesized that generation 5 poly amido amine (PAMAM) dendrimers (G5), functionalized with fluorescein isothiocyanate (FL) and αVβ3-specific, cyclic arginine-glycine-aspartic acid (RGD) peptides, will bind to dental pulp cells (DPCs) and modulate their differentiation. Dental pulp cells and mouse odontoblast-like cells (MDPC-23) (±) treated with G5-FL-RGD were analyzed via Western blot, RT-PCR, and quantitative PCR. Transcription of dental differentiation markers was as follows: Dentin matrix protein (DMP-1), dentin sialoprotein (DSPP), and matrix extracellular phosphoglycoprotein (MEPE) as well as vascular endothelial growth factor (VEGF) all increased via the JNK pathway. Long-term G5-RGD treatment of dental pulp cells resulted in enhanced mineralization as examined via Von Kossa assay, suggesting that PAMAM dendrimers conjugated to cyclic RGD peptides can increase the odontogenic potential of these cells.
Journal of Endodontics | 2011
Jin Koo Kim; James R. Baker; Jacques E. Nör; Elliott E. Hill
INTRODUCTION Signaling pathways responsible for dentin regeneration in a dental pulp are not fully understood. In this study, we determined the effects of the mammalian target of rapamycin (mTor) on the differentiation and mineralization of dental pulp stem cells. We hypothesized that the two known mTor complexes Torc1 and Torc 2 play pivotal roles in the differentiation of odontoblasts and that they modulate deposition of a mineralized extracellular matrix. Therefore, we investigated the effects of Torc1 and Torc 2 signaling on the differentiation and mineralization of stem cells from human exfoliated deciduous teeth (SHED). METHODS We used Western blot analysis to examine the expression of markers of dental differentiation in SHED (+/-) inhibition of either Torc1 or Torc 2 complex proteins raptor or rictor, respectively. In addition, the deposition of a mineralized matrix was determined under these conditions via alkaline phosphatase and alizarin red staining. RESULTS Results show that the inhibition of Torc 1, via reduced expression of either raptor or mTor, severely restricts the synthesis of dentin sialoprotein and inhibits deposition of a mineralized matrix. Inhibition of Torc 2, via reduction of rictor, has the opposite effect, enhancing mineralization. This latter effect disappears when both rictor and mTor are inhibited, showing that the Torc 2 effect is Torc 1 dependent. CONCLUSIONS These results strongly suggest an important role for mTor in dental pulp stem cell differentiation and provide evidence that the mechanisms involved in protein synthesis could prove an interesting target for dental pulp tissue engineering.
Journal of Cellular Biochemistry | 2018
Elliott E. Hill; Jin Koo Kim; Younghun Jung; Chris K. Neeley; Kenneth J. Pienta; Russell S. Taichman; Jacques E. Nör; James R. Baker; Paul H. Krebsbach
Therapeutic strategies targeting both cancer cells and associated cells in the tumor microenvironment offer significant promise in cancer therapy. We previously reported that generation 5 (G5) dendrimers conjugated with cyclic‐RGD peptides target cells expressing integrin alpha V beta 3. In this study, we report a novel dendrimer conjugate modified to deliver the mammalian target of rapamycin (mTOR) inhibitor, rapamycin. In vitro analyses demonstrated that this drug conjugate, G5‐FI‐RGD‐rapamycin, binds to prostate cancer (PCa) cells and fibroblasts to inhibit mTOR signaling and VEGF expression. In addition, G5‐FI‐RGD‐rapamycin inhibits mTOR signaling in cancer cells more efficiently under proinflammatory conditions compared to free rapamycin. In vivo studies established that G5‐FI‐RGD‐rapamycin significantly inhibits fibroblast‐mediated PCa progression and metastasis. Thus, our results suggest the potential of new rapamycin‐conjugated multifunctional nanoparticles for PCa therapy.
Tissue Engineering | 2007
Tanyarut Boontheekul; Elliott E. Hill; Hyunjoon Kong; David J. Mooney
Proceedings of the National Academy of Sciences of the United States of America | 2006
Elliott E. Hill; Tanyarut Boontheekul; David J. Mooney
Tissue Engineering | 2006
Elliott E. Hill; Tanyarut Boontheekul; David J. Mooney
Archive | 2006
David J. Mooney; Omar abdel-Rahman Ali; Eduardo A. Silva; Hyunjoon Kong; Elliott E. Hill; Tanyarut Boontheekul
Bioconjugate Chemistry | 2007
Elliott E. Hill; Rameshwer Shukla; Steve S. Park; James R. Baker
Neoplasia | 2013
Jin Koo Kim; Younghun Jung; Jingcheng Wang; Jeena Joseph; Anjali Mishra; Elliott E. Hill; Paul H. Krebsbach; Kenneth J. Pienta; Yusuke Shiozawa; Russell S. Taichman