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1,111 results on '"Smith, Charles E."'

8. Dental enamel cells express functional SOCE channels

Author

Nurbaeva, Meerim K, Eckstein, Miriam, Concepcion, Axel R, Smith, Charles E, Srikanth, Sonal, Paine, Michael L, Gwack, Yousang, Hubbard, Michael J, Feske, Stefan, and Lacruz, Rodrigo S

Subjects
Dental/Oral and Craniofacial Disease, Underpinning research, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Oral and gastrointestinal, Ameloblasts, Animals, Calcium Channel Blockers, Calcium Channels, Calcium Signaling, Calcium-Binding Proteins, Cells, Cultured, Dental Enamel, Fura-2, Humans, Inositol 1, 4, 5-Trisphosphate Receptors, Male, Membrane Glycoproteins, Membrane Proteins, Mice, Mice, Inbred C57BL, ORAI1 Protein, Rats, Rats, Sprague-Dawley, Ryanodine Receptor Calcium Release Channel, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Stromal Interaction Molecule 1, Stromal Interaction Molecule 2, Thapsigargin
Abstract

Dental enamel formation requires large quantities of Ca(2+) yet the mechanisms mediating Ca(2+) dynamics in enamel cells are unclear. Store-operated Ca(2+) entry (SOCE) channels are important Ca(2+) influx mechanisms in many cells. SOCE involves release of Ca(2+) from intracellular pools followed by Ca(2+) entry. The best-characterized SOCE channels are the Ca(2+) release-activated Ca(2+) (CRAC) channels. As patients with mutations in the CRAC channel genes STIM1 and ORAI1 show abnormal enamel mineralization, we hypothesized that CRAC channels might be an important Ca(2+) uptake mechanism in enamel cells. Investigating primary murine enamel cells, we found that key components of CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were expressed and most abundant during the maturation stage of enamel development. Furthermore, inositol 1,4,5-trisphosphate receptor (IP3R) but not ryanodine receptor (RyR) expression was high in enamel cells suggesting that IP3Rs are the main ER Ca(2+) release mechanism. Passive depletion of ER Ca(2+) stores with thapsigargin resulted in a significant raise in [Ca(2+)]i consistent with SOCE. In cells pre-treated with the CRAC channel blocker Synta-66 Ca(2+) entry was significantly inhibited. These data demonstrate that enamel cells have SOCE mediated by CRAC channels and implicate them as a mechanism for Ca(2+) uptake in enamel formation.

Published
2015

11. Expressions for frictional and conservative force combinations within the dissipative Lagrange-Hamilton formalism

Author

Smith, Charles E.

Subjects
Physics - Classical Physics, Physics - General Physics
Abstract

Dissipative Lagrangians and Hamiltonians having Coulomb, viscous and quadratic damping,together with gravitational and elastic terms are presented for a formalism that preserves the Hamiltonian as a constant of the motion. Their derivations are also shown. The resulting L's and H's may prove useful in exploring new types of damped quantum systems., Comment: 7 pages LaTEX file

Published
2006

20. Handheld Antennas

Author

Elsherbeni, Atef Z., primary, Huang, Chun-Wen Paul, additional, and Smith, Charles E., additional

Published
2018
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23. Pseudo-classical Nonseparability and Mass Politics in Two-Party Systems

Author

Zorn, Christopher, Smith, Charles E., Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, Song, Dawei, editor, Melucci, Massimo, editor, Frommholz, Ingo, editor, Zhang, Peng, editor, Wang, Lei, editor, and Arafat, Sachi, editor

Published
2011
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33. Dentin defects caused by a Dspp−1 frameshift mutation are associated with the activation of autophagy.

Author

Liang, Tian, Smith, Charles E., Hu, Yuanyuan, Zhang, Hong, Zhang, Chuhua, Xu, Qian, Lu, Yongbo, Qi, Ling, Hu, Jan C.-C., and Simmer, James P.

Subjects
*FRAMESHIFT mutation, *DENTIN, *AMELOBLASTS, *DENTINAL tubules, *AUTOPHAGY, *ODONTOBLASTS, *UBIQUITINATION
Abstract

Dentin sialophosphoprotein (DSPP) is primarily expressed by differentiated odontoblasts (dentin-forming cells), and transiently expressed by presecretory ameloblasts (enamel-forming cells). Disease-causing DSPP mutations predominantly fall into two categories: 5' mutations affecting targeting and trafficking, and 3' − 1 frameshift mutations converting the repetitive, hydrophilic, acidic C-terminal domain into a hydrophobic one. We characterized the dental phenotypes and investigated the pathological mechanisms of DsppP19L and Dspp−1fs mice that replicate the two categories of human DSPP mutations. In DsppP19L mice, dentin is less mineralized but contains dentinal tubules. Enamel mineral density is reduced. Intracellular accumulation and ER retention of DSPP is observed in odontoblasts and ameloblasts. In Dspp−1fs mice, a thin layer of reparative dentin lacking dentinal tubules is deposited. Odontoblasts show severe pathosis, including intracellular accumulation and ER retention of DSPP, strong ubiquitin and autophagy activity, ER-phagy, and sporadic apoptosis. Ultrastructurally, odontoblasts show extensive autophagic vacuoles, some of which contain fragmented ER. Enamel formation is comparable to wild type. These findings distinguish molecular mechanisms underlying the dental phenotypes of DsppP19L and Dspp−1fs mice and support the recently revised Shields classification of dentinogenesis imperfecta caused by DSPP mutations in humans. The Dspp−1fs mice may be valuable for the study of autophagy and ER-phagy. [ABSTRACT FROM AUTHOR]

Published
2023
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