L. CHENG

Sichuan University, Hua-yang, Sichuan, China

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Publications (9)10.04 Total impact

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    ABSTRACT: Objective: Rho is important in the migration of dental pulp cells (DPCs). Rho-associated kinase (ROCK) and mammalian homolog of Drosophila diaphanous 1 (mDia1) are two major effectors of RhoA. However, the relationships between these factors remain unknown. We investigated the effects of mDia1 and ROCK on the behavior of DPCs under two different conditions—low and high levels of GTP–RhoA (activated RhoA). Method: Lysophosphatidic acid (LPA) was used to activate RhoA signaling pathway, and the function of mDia1 and ROCK were inhibited by short interfering RNA and the specific inhibitor Y-27632, respectively. The migration of DPCs was detected by transwell migration and scratch-wound assay. Cytoskeleton and focal adhesions were investigated with immunofluorescent methods by confocal laser scanning microscopy. Cell adhesion and spreading were analyzed by adhesion and spreading assays. The phosphorylations of focal adhesion kinase (FAK) and paxillin were detected by Western blotting. Result: Under normal culture conditions with low-level GTP–RhoA, inhibition of mDia1 and ROCK increased cell migration. Inhibition of ROCK, but not mDia1, dramatically changed cell morphology and cytoskeleton structure. Silence of mDia1 increased cell adhesion and the phosphorylations of FAK and paxillin. When RhoA was activated by LPA, ROCK inhibition still increased cell speed while inhibition of mDia1 decreased cell migration. Inhibition of mDia1 or ROCK suppressed LPA-induced cytoskeleton remodeling. However, inhibition of each alone increased cell adhesion and spreading. Conclusion: It might be concluded that mDia1 and ROCK have dual effects on the migration and adhesion of DPCs. Under the conditions with low-level GTP–RhoA, mDia1 and ROCK limited the cell migration rate. ROCK might be involved in the maintenance of cell morphology and cytoskeleton. Under the conditions with high-level GTP–RhoA, mDia1 promoted cell migration. mDia1 and ROCK might be involved in the reorganization of cell cytoskeleton.
    IADR General Session and Exhibition 2014; 06/2014
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    ABSTRACT: Dental materials with anticaries properties could help inhibit the development of lesions. Objectives: To investigate the antibacterial effects in vitro of incorporating nanoparticles of silver (NAg) and nanoparticles of amorphous calcium phosphate (NACP) into a bonding agent, and to assess the effects of NACP-filled nanocomposite on enamel mineral loss in an in situ model. Methods: For the in vitro study, commercial adhesive and primer were used as control. NAg were incorporated into the primer and adhesive at 0.1% by mass. NACP were mixed into adhesive at 10%, 20%, 30% and 40%. Dentin bond strength and oral microcosm biofilm response were measured. For the in situ study, caries-like lesions were produced in which 25 volunteers wore palatal devices with enamel slabs restored using NACP nanocomposite or control composite. Ca and P ion concentrations were measured in biofilms on the slabs. Enamel demineralization was assessed by transverse microradiography. Results: Bonding agents containing NAg and NACP showed bond strengths ranged from 26 to 34 MPa, with no significant difference (p>0.1). Substantial reductions in bacterial viability were obtained (p<0.05), including metabolic activity (reduced by 60%), CFU for total microorganisms, total streptococci, and mutans streptococci (50-85%), and lactic acid production (65-85%). SEM examination showed NACP infiltration into dentinal tubules. In the in situ study, NACP nanocomposite significantly increased Ca and P ion concentrations in biofilms and substantially reduced mineral loss in enamel (p<0.05). Conclusions: Incorporation of NACP and NAg imparted a great anticaries effect by inhibiting the cariogenic biofilm viability and lactic acid production, as well as promoting remineralization in tooth enamel. The method of combining an antibacterial agent and a remineralizing agent in the adhesive or the composite is promising to inhibit secondary caries, and may have potential for use in a wide range of materials including adhesives, composites, cements, and sealants.
    IADR/AADR/CADR General Session and Exhibition 2013; 03/2013
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    ABSTRACT: Composites are the principal material for tooth cavity restorations due to their esthetics and direct-filling capabilities. However, composites accumulate biofilms in vivo, and secondary caries due to biofilm acids is the main cause of restoration failure. Objectives: (1) Synthesize new antibacterial monomers and (2) Develop nanocomposite containing nanoparticles of amorphous calcium phosphate (NACP) and new antibacterial monomer. Methods: Two new antibacterial monomers were synthesized: dimethylaminohexyl methacrylate (DMAHM) with a carbon chain length of 6, and dimethylaminododecyl methacrylate (DMADM) with a chain length of 12. A spray-drying technique was used to make NACP. DMADM was incorporated into NACP nanocomposite at mass fractions of 0%, 0.75%, 1.5%, 2.25% and 3%. A dental plaque microcosm biofilm model with human saliva as inoculum measured the viability, metabolic activity, and lactic acid production of biofilms on composites. Results: Minimum inhibitory concentration (MIC) and bactericidal concentration (MBC) measurements indicated that DMAHM was more potent than quaternary ammonium dimethacrylate (QADM). MIC and MBC of DMADM were 2-3 orders of magnitude lower than those of DMAHM, and approached those of chlorhexidine control. At each DMADM mass fraction, DMADM-NACP nanocomposites had strengths similar to that of composite control (69±8)MPa (p>0.1). With 3% DMADM in NACP nanocomposite, the metabolic activity of adherent biofilms was (0.11±0.02), which represents a 95% reduction compared to composite control (p<0.05). Lactic acid production by biofilms on NACP nanocomposite containing 3% DMADM was (0.22±0.08)mmol/L, which represents a 99% reduction compared to composite control (p<0.05). Biofilm colony-forming units on NACP nanocomposite with 3% DMADM were reduced by 2-3 orders of magnitude (p<0.05). Conclusions: New antibacterial monomers were synthesized, and the carbon chain length had a strong effect on antibacterial efficacy. The new DMADM-NACP nanocomposite possessed potent anti-biofilm activity without compromising load-bearing properties, and is promising for antibacterial and remineralizing dental restorations to inhibit secondary caries.
    IADR/AADR/CADR General Session and Exhibition 2013; 03/2013
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    ABSTRACT: Antibacterial bonding agents could combat recurrent caries at the tooth-composite margins. The objectives of this study were to develop novel antibacterial dentin primers containing quaternary ammonium dimethacrylate (QADM) and nanoparticles of silver (NAg), and to investigate the effects on dentin bond strength and dental plaque microcosm biofilms for the first time. Scotchbond Multi-Purpose ("SBMP") bonding agent was used. QADM and NAg were incorporated into SBMP primer, yielding 4 primers: SBMP primer (control), control + 10% QADM (mass), control + 0.05% NAg, and control + 10% QADM + 0.05% NAg. Human saliva was collected to grow microcosm biofilms. The NAg particle size (mean ± SD; n = 100) was 2.7 ± 0.6 nm. Dentin shear bond strengths (n = 10) with human third molars were approximately 30 MPa for all groups (p > 0.1). QADM-NAg-containing primer increased the bacteria inhibition zone by 9-fold, compared with control primer (p < 0.05). QADM-NAg-containing primer reduced lactic acid production and colony-forming units of total micro-organisms, total streptococci, and mutans streptococci by an order of magnitude. In conclusion, novel QADM-NAg-containing primers were strongly antibacterial without compromising dentin bond strength, and hence are promising to inhibit biofilms and secondary caries. The processing method of incorporating QADM and NAg together into the same primer produced the strongest antibacterial effect, which could have a wide applicability to other bonding systems.
    Journal of dental research 04/2012; 91(6):598-604. · 3.46 Impact Factor
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    ABSTRACT: Secondary caries is a frequent reason for restoration failure, resulting from acidogenic bacteria and their biofilms. The objectives of this study were to: (1) develop a novel nanocomposite containing nanoparticles of amorphous calcium phosphate (NACP) and quaternary ammonium dimethacrylate (QADM); and (2) investigate its mechanical and antibacterial durability. A spray-drying technique yielded NACP with particle size of 116 nm. The nanocomposite contained NACP and reinforcement glass fillers, with QADM in the resin. Two commercial composites were tested as controls. Composites were inoculated with Streptococcus mutans. After 180-day water-aging, NACP+QADM nanocomposite had flexural strength and elastic modulus matching those of commercial controls (p > 0.1). NACP+QADM nanocomposite reduced the biofilm colony-forming units (CFU) by 3-fold, compared with commercial composites (p < 0.05). Metabolic activity and lactic acid production of biofilms on NACP+QADM were much less than those on commercial composites (p < 0.05). The antibacterial properties of NACP+QADM were maintained after water-aging for 30, 90, and 180 d (p > 0.05). In conclusion, the novel NACP-QADM nanocomposite greatly decreased biofilm metabolic activity, CFU, and lactic acid, while matching the load-bearing capability of commercial composites without antibacterial properties. The NACP-QADM nanocomposite with strong and durable antibacterial properties, together with its previously reported Ca-PO(4) release capability, may render it useful for caries-inhibiting restorations.
    Journal of dental research 03/2012; 91(5):460-6. · 3.46 Impact Factor
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    ABSTRACT: To investigate the effects of lysophosphatidic acid (LPA) and the Rho/Rho-associated kinase (ROCK) pathway on adhesion of dental pulp cells (DPCs). Human DPCs were cultured ex vivo. After treatment of LPA and Y-27632, a specific ROCK inhibitor, changes in focal contacts (FCs) were examined by immunofluorescent staining. Activation of FCs proteins was examined by measuring tyrosine 397 phosphorylation of focal adhesion kinase (FAK) and paxillin using immunoblotting. The data were analysed by Student's t-test. The immunofluorescent staining indicated LPA stimulation induced larger focal adhesion in the cell periphery, compared with the control. Inhibition of ROCK by Y-27632 decreased the formation of FCs markedly, even in the LPA-stimulated cells. LPA also increased the level of tyrosine phosphorylation of paxillin at 30min (P<0.05) and FAK at 5 and 30min (P<0.05). Furthermore, p-paxillin levels declined immediately after Y-27632 treatment and remained low at 5, 30, 60min. Y-27632 also suppressed the effects of LPA on p-paxillin and p-FAK at 5 and 30min (P<0.05). LPA activated Rho and then subsequently activated ROCK, suggesting that LPA influences the FCs of DPCs by modulating tyrosine phosphorylation of FAK and paxillin via the Rho/ROCK pathway.
    International Endodontic Journal 11/2010; 44(1):2-8. · 2.05 Impact Factor
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    ABSTRACT: Lipopolysaccharide exerts many effects on many cell lines, including cytokine secretion, and cell apoptosis and necrosis. We investigated the in vitro effects of lipopolysaccharide on apoptosis of cultured human dental pulp cells and the expression of Bcl-2 and Bax. Dental pulp cells showed morphologies typical of apoptosis after exposure to lipopolysaccharide. Flow cytometry showed that the rate of apoptosis of human dental pulp cells increased with increasing lipopolysaccharide concentration. Compared with controls, lipopolysaccharide promoted pulp cell apoptosis (P < 0.05) from 0.1 to 100 μg/mL but not at 0.01 μg/mL. Cell apoptosis was statistically higher after exposure to lipopolysaccharide for 3 days compared with 1 day, but no difference was observed between 3 and 5 days. Immunohistochemistry showed that expression of Bax and Bcl-2 was enhanced by lipopolysaccharide at high concentrations, but no evident expression was observed at low concentrations (0.01 and 0.1 μg/mL) or in the control groups. In conclusion, lipopolysaccharide induced dental pulp cell apoptosis in a dose-dependent manner, but apoptosis did not increase with treatment duration. The expression of the apoptosis regulatory proteins Bax and Bcl-2 was also up-regulated in pulp cells after exposure to a high concentration of lipopolysaccharide.
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 10/2010; 43(11):1027-33. · 1.08 Impact Factor
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    ABSTRACT: Objectives:To investigate the in vitro effects of lipopolysaccharide (LPS) on apoptosis of dental pulp cells and on the expression of Bcl-2 and Bax. Methods:Dental pulp cells showed morphologies typical of apoptosis after exposure to LPS concentrations of 100g/mL, 10g/mL, 1g/mL, 0.1g/mL or 0.01g/mL for 24h, 72h or 120h. Morphological changes of cell nuclei were observed by a confocal laser scanning microscope. Apoptosis rate was examined by flow cytometry. Expression of Bax and Bcl-2 were tested by immunohistochemistry. Results:After LPS treatment for 24h, 72h or 120h, chromatin condensation, nuclear fragmentation were seen in dental pulp cells. The apoptosis rate of dental pulp cells increased with increasing LPS concentration. Compared with the control, LPS promoted pulp cell apoptosis (P<0.05) in all but the 0.01g/mL group. LPS-induced apoptosis did not exhibit a temporal pattern and no difference was observed between 72h and 120h. LPS also increased the expression of Bax and Bcl-2 in dental pulp cells. Conclusion:LPS induced dental pulp cell apoptosis in a dose-dependent manner, which may be mediated by Bax and Bcl-2. dose-dependent manner, which may be mediated by Bax and Bcl-2.
    IADR General Session 2010; 07/2010
  • T. HU, R. CHENG, M. SHAO, H. YANG, L. CHENG
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    ABSTRACT: Objectives:To investigate the effects of lysophosphatidic acid (LPA) and the Rho/ Rho-associated kinase (ROCK) pathway on adhesion of dental pulp cells. Methods:Human dental pulp cells were cultured in vitro. After treatment of LPA and Y-27632, a specific ROCK inhibitor, changes in focal contacts were examined by immunofluorescent staining. Activation of focal contacts proteins were examined by measuring Tyrosine 397 phosphorylation of focal adhesion kinase (FAK) and paxillin using immunoblotting. Results:Compared with the control, LPA stimulation induced larger focal adhesion, which appeared in the cell periphery. Inhibition of ROCK by Y-27632 decreased the formation of FCs markedly, even in the LPA-stimulated cells. LPA also increased the level of tyrosine phosphorylation of paxillin (p-paxillin) at 30 min (P < 0.05) and FAK (p-FAK) at 5 and 30 min (P < 0.05). Furthermore, p-paxillin level declined immediately after Y-27632 treatment and remained at a low level at 5, 30, 60 min. Y-27632 also suppressed the effects of LPA on p-paxillin and p-FAK at 5 and 30 min (P < 0.05). Conclusion:LPA activated Rho and then subsequently activated ROCK, suggesting that LPA influences the focal contacts of dental pulp cells by modulating tyrosine phosphorylation of FAK and paxillin via the Rho/ROCK pathway.
    IADR General Session 2010; 07/2010

Publication Stats

37 Citations
10.04 Total Impact Points

Institutions

  • 2010–2014
    • Sichuan University
      • • State Key Laboratory of Oral Diseases
      • • West China School of Stomatology
      Hua-yang, Sichuan, China
  • 2012–2013
    • University of Maryland, Baltimore
      • Department of Endodontics, Prosthodontics and Operative Dentistry
      Baltimore, Maryland, United States