scholarly journals 4-Hexylresorcinol Administration Increases Dental Hard Tissue Formation and Incisor Eruption Rate in Rats

2020 ◽  
Vol 10 (16) ◽  
pp. 5511 ◽  
Author(s):  
Ji-Hwan Kim ◽  
Dae-Won Kim ◽  
Seong-Gon Kim ◽  
Tae-Woo Kim

Dental hard tissue formation and bone turnover are required for tooth eruption. 4-Hexylresorcinol (4HR) accelerates tooth movement by increasing bone turnover in orthodontic treatment. This study aimed to evaluate the following: (1) the effect of 4HR application on the expression of proteins associated with tooth formation, and (2) the effect of 4HR application on mandibular incisor eruption rate in a rat model. Primary cultured pulp cells received either 4HR (1 to 100 µM) or solvent only; western blotting was performed for transforming growth factor-beta 1 (TGF-β1), bone morphogenic protein-2/4 (BMP-2/4), runt-related transcription factor 2 (Runx2), osterix (OSX), dentin sialophosphoprotein (DSPP), and parathyroid hormone-related protein receptor (PTHrP-R). In in vivo study, rats (15 males and 15 females) received either solvent or 0.128 mg/kg or 12.8 mg/kg of 4HR via subcutaneous injection; mandibular incisor eruption rate was subsequently recorded. Immunohistochemical staining and western blotting for TGF-β1, BMP-2/4, Runx2, OSX, DSPP, and PTHrP-R were performed in the mandibular tissue samples. 4HR administration was found to increase TGF-β1, BMP-2/4, Runx2, OSX, DSPP, and PTHrP-R expression in both cell culture and tissue samples. Immunohistochemical staining of some markers showed site-specific expression, thereby indicating programmed differentiation of odontoblasts and ameloblasts. The eruption rate was significantly higher in the 12.8 mg/kg 4HR-administered group than in the untreated control (p = 0.001 and 0.010 for males and females, respectively). Collectively, 4HR administration increased the expression of markers related to dental hard tissue formation and accelerated the eruption rate of incisors in rats.

1976 ◽  
Vol 22 (S1) ◽  
pp. 454-457 ◽  
Author(s):  
M. Joostlarsen ◽  
O. Fejerskov ◽  
K. Josephsen ◽  
L. Hammarström

2021 ◽  
Vol 8 ◽  
Author(s):  
Claire S. Luke Krishnan ◽  
Helen D. Brasch ◽  
Josie Patel ◽  
Nicholas Bockett ◽  
Erin Paterson ◽  
...  

Objectives: Arteriovenous malformation (AVM) consists of a nidus with poorly formed low-resistance vessels in place of a functional capillary network. The role of somatic mutations in embryonic stem cells (ESCs) and vascular anomalies and the presence of primitive populations in vascular anomalies led us to investigate the presence of a primitive population in extracranial AVM.Methods: Extracranial AVM tissue samples from 12 patients were stained for stemness-associated markers OCT4, SOX2, NANOG, KLF4, and c-MYC using immunohistochemical staining. In situ hybridization (ISH) was performed on six tissue samples to determine transcript expression. Western blotting and RT-qPCR were performed on two AVM-derived primary cell lines to determine protein and transcript expression of these markers, respectively. Immunofluorescence staining was performed on two tissue samples to investigate marker co-localization.Results: Immunohistochemical staining demonstrated the expression of OCT4, SOX2, KLF4, and c-MYC on the endothelium and media of lesional vessels and cells within the stroma of the nidus in all 12 AVM tissue samples. ISH and RT-qPCR confirmed transcript expression of all five markers. Western blotting showed protein expression of all markers except NANOG. Immunofluorescence staining demonstrated an OCT4+/SOX2+/KLF4+/c-MYC+ population within the endothelium and media of the lesional vessels and cells within the stroma of the AVM nidus.Conclusions: Our findings may suggest the presence of a primitive population within the AVM nidus. Further investigation may lead to novel therapeutic targeting of this population.


2010 ◽  
Vol 85 (8) ◽  
pp. 953-963 ◽  
Author(s):  
Eija Salmela ◽  
Pirjo-Liisa Lukinmaa ◽  
Anna-Maija Partanen ◽  
Carin Sahlberg ◽  
Satu Alaluusua

2001 ◽  
Vol 26 (3) ◽  
pp. 137-142 ◽  
Author(s):  
Ali Riza Alpöz ◽  
Necip Tosun ◽  
Cemal Eronat ◽  
Nafiz Delen ◽  
Bilge Hakan Şen

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199651
Author(s):  
Jie Yang ◽  
Enzi Feng ◽  
Yanxin Ren ◽  
Shun Qiu ◽  
Liufang Zhao ◽  
...  

Objectives To identify key long non-coding (lnc)RNAs responsible for the epithelial–mesenchymal transition (EMT) of CNE1 nasopharyngeal carcinoma cells and to investigate possible regulatory mechanisms in EMT. Methods CNE1 cells were divided into transforming growth factor (TGF)-β1-induced EMT and control groups. The mRNA and protein expression of EMT markers was determined by real-time quantitative PCR and western blotting. Differentially expressed genes (DEGs) between the two groups were identified by RNA sequencing analysis, and DEG functions were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. EMT marker expression was re-evaluated by western blotting after knockdown of a selected lncRNA. Results TGF-β1-induced EMT was characterized by decreased E-cadherin and increased vimentin, N-cadherin, and Twist expression at both mRNA and protein levels. Sixty lncRNA genes were clustered in a heatmap, and mRNA expression of 14 dysregulated lncRNAs was consistent with RNA sequencing. Knockdown of lnc-PNRC2-1 increased expression of its antisense gene MYOM3 and reduced expression of EMT markers, resembling treatment with the TGF-β1 receptor inhibitor LY2109761. Conclusion Various lncRNAs participated indirectly in the TGF-β1-induced EMT of CNE1 cells. Lnc-PNRC2-1 may be a key regulator of this and is a potential target to alleviate CNE1 cell EMT.


Author(s):  
Valerie G.A. Suter ◽  
Peter A. Reichart ◽  
Dieter D. Bosshardt ◽  
Michael M. Bornstein
Keyword(s):  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jinyuan Zhu ◽  
Faxuan Wang ◽  
Xueyan Feng ◽  
Beibei Li ◽  
Liqiong Ma ◽  
...  

Abstract Background To explore the role of family with sequence similarity 13 member A (FAM13A) in TGF-β1-induced EMT in the small airway epithelium of patients with chronic obstructive pulmonary disease (COPD). Methods Small airway wall thickness and protein levels of airway remodeling markers, EMT markers, TGF-β1, and FAM13A were measured in lung tissue samples from COPD and non-COPD patients. The correlations of FAM13A expression with COPD severity and EMT marker expression were evaluated. Gain- and loss-of-function assays were performed to explore the functions of FAM13A in cell proliferation, motility, and TGF-β1-induced EMT marker alterations in human bronchial epithelial cell line BEAS-2B. Results Independent of smoking status, lung tissue samples from COPD patients exhibited significantly increased small airway thickness and collagen fiber deposition, along with enhanced protein levels of remodeling markers (collagen I, fibronectin, and MMP-9), mesenchymal markers (α-SMA, vimentin, and N-cadherin), TGF-β1, and FAM13A, compared with those from non-COPD patients. FAM13A expression negatively correlated with FEV1% and PO2 in COPD patients. In small airway epithelium, FAM13A expression negatively correlated with E-cadherin protein levels and positively correlated with vimentin protein levels. In BEAS-2B cells, TGF-β1 dose-dependently upregulated FAM13A protein levels. FAM13A overexpression significantly promoted cell proliferation and motility in BEAS-2B cells, whereas FAM13A silencing showed contrasting results. Furthermore, FAM13A knockdown partially reversed TGF-β1-induced EMT marker protein alterations in BEAS-2B cells. Conclusions FAM13A upregulation is associated with TGF-β1-induced EMT in the small airway epithelium of COPD patients independent of smoking status, serving as a potential therapeutic target for anti-EMT therapy in COPD.


Development ◽  
1977 ◽  
Vol 41 (1) ◽  
pp. 279-287
Author(s):  
J. A. Sofaer

The semidominant gene ‘crooked’ (Cd) in the mouse produces anomalies of the axial skeleton (resulting in a crooked tail), microphthalmia and dental abnormalities, including small molars with simplified cusp patterns that are equivalent to patterns passed through during normal morphodifferentiation. A series of embryonic litters from Cd/ + × Cd / + matings was used to investigate the embryological basis for the dental abnormalities. Microphthalmic embryos were classed as Cd/Cd, and their most normal litter mates were selected as controls (+ / + or Cd / +). An additional set of control embryos came from the inbred strain CBA/Cam (+ / +). Serial sagittal sections of the heads of these embryos were examined microscopically, and the maximum anteroposterior diameters of the developing upper and lower first molars were measured. Reduction in the rates of growth and morphodifferentiation of Cd/Cd first molars, relative to those of litter mate controls, was associated with the appearance of an adjacent abnormal proliferation of the dental lamina. Some proliferations in older embryos showed signs of early tooth germ formation, but many were seen to have regressed and no examples of supernumerary teeth have been found in Cd/Cd adults. Small size of Cd/Cd molars may therefore result from competitive inhibition of molar growth by a transient abnormal laminal proliferation, and Cd/Cd cusp patterns from the relatively premature onset of hard tissue formation during normal but retarded sequences of morphodifferentiation.


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