Distinction Between Cell Proliferation and Apoptosis Signals Regulated by Brain-Derived Neurotrophic Factor in Human Periodontal Ligament Cells and Gingival Epithelial Cells

2015 ◽  
Vol 117 (7) ◽  
pp. 1543-1555 ◽  
Author(s):  
Kei Kashiwai ◽  
Mikihito Kajiya ◽  
Shinji Matsuda ◽  
Kazuhisa Ouhara ◽  
Katsuhiro Takeda ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Neurotrophic Factor ◽  
Periodontal Ligament ◽  
Brain Derived Neurotrophic Factor ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Gingival Epithelial Cells ◽  
Proliferation And Apoptosis

LncRNA TUG1 mediates lipopolysaccharide-induced proliferative inhibition and apoptosis of human periodontal ligament cells by sponging miR-132

2019 ◽  
Author(s):  
Ying Han ◽  
Fang Wang ◽  
Longquan Shao ◽  
Peidi Huang ◽  
Yue Xu
Keyword(s):  
Cell Proliferation ◽  
Periodontal Ligament ◽  
Noncoding Rna ◽  
Biological Properties ◽  
Periodontal Ligament Cells ◽  
Inhibition Of Proliferation ◽  
Inflammatory Reactions ◽  
Inflammatory Conditions ◽  
Human Periodontal Ligament Cells ◽  
Proliferation And Apoptosis

Abstract Emerging evidence shows that the long noncoding RNA taurine-upregulated gene 1 (TUG1) plays pivotal roles in regulating biological properties and functions of parenchyma cells in various types of disease processes. However, the mechanism underlying the effects of TUG1 on cell proliferation and apoptosis of human periodontal ligament cells (PDLCs) in periodontitis is undefined. In this study, we explored the functions of TUG1 and its underlying mechanisms in the inflammatory process induced by Porphyromonas gingivalis–derived lipopolysaccharide (LPS) in PDLCs. Our results showed that TUG1 had a decreased expression in both periodontal ligament (PDL) tissues with periodontitis and PDLCs under a LPS-induced inflammatory condition, and TUG1 expression was negatively correlated with miR-132 expression in periodontitis-affected PDL tissues. Furthermore, we found that TUG1 overexpression in PDLCs alleviated LPS-induced proliferative inhibition and apoptosis promotion, while TUG1 knockdown had the opposite effect. In addition, miR-132 inhibitor alleviated TUG1 knockdown-induced inhibition of proliferation and increase of apoptosis in PDLCs under inflammatory conditions induced by LPS. These findings indicated that TUG1 has an enormous potential in regulating cell proliferation and apoptosis of PDLCs during periodontitis and may provide an effective therapeutic target for periodontitis to reduce the damage caused by inflammatory reactions.

Glial Cell–Derived Neurotrophic Factor Expression in Normal Human Lung and Congenital Cystic Adenomatoid Malformation

2002 ◽  
Vol 126 (4) ◽  
pp. 432-436
Author(s):  
Gaelle Fromont-Hankard ◽  
Pascale Philippe-Chomette ◽  
Anne-Lise Delezoide ◽  
Catherine Nessmann ◽  
Yves Aigrain ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Glial Cell ◽  
Neurotrophic Factor ◽  
Fetal Lung ◽  
Congenital Cystic Adenomatoid Malformation ◽  
Apoptotic Bodies ◽  
Developmental Factors ◽  
Cystic Adenomatoid Malformation ◽  
Proliferation And Apoptosis

Abstract Context.—It has been recently suggested that dysregulation of developmental factors and disruption of cell turnover could play a role in the pathogenesis of congenital cystic adenomatoid malformation of the lung (CCAM). The glial cell–derived neurotrophic factor (GDNF) is a growth factor involved in organogenesis, and the temporal pattern of GDNF expression suggests that this factor may play a role in lung development. Design.—We studied GDNF expression by immunohistochemistry in postnatally resected CCAM of the lung (n = 10), normal fetal lung (n = 5), and normal postnatal lung (n = 5). We also studied the association between GDNF expression and both cell proliferation and apoptosis. Results.—GDNF was expressed in both epithelial and endothelial compartments of normal fetal lung, whereas no expression was found in normal postnatal lung. In contrast, in CCAM tissue, there was strong GDNF immunostaining that was restricted to epithelial cells. The percentage of proliferating epithelial cells was higher in CCAM tissue than in normal postnatal lung (6.3% vs 1.7%, P < .005). Apoptotic bodies were found in the mesenchyme of both normal fetal lung and CCAM tissue, whereas virtually no apoptotic bodies were detected in normal postnatal lung. Conclusions.—Abnormal GDNF expression in CCAM suggests a dysregulation of the GDNF signaling pathway and argues in favor of a focal arrest in maturation during development. GDNF expression in lung tissue seems to be correlated with cell proliferation, suggesting that this factor could play a role in the growth of both fetal lung and CCAM.

The effect of iloprost on cell proliferation and angiogenesis-related gene expression in human periodontal ligament cells

Odontology ◽  
2017 ◽  
Vol 106 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Thanomsuk Jearanaiphaisarn ◽  
Teeranuch Sanharati ◽  
Prasit Pavasant ◽  
Chalida Nakalekha Limjeerajarus
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Related Gene ◽  
Human Periodontal Ligament Cells ◽  
Angiogenesis Related Gene

GDNF From Human Periodontal Ligament Cells Treated With Pro-Inflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells

2016 ◽  
Vol 118 (4) ◽  
pp. 699-708
Author(s):  
Shinichiro Yoshida ◽  
Naohide Yamamoto ◽  
Naohisa Wada ◽  
Atsushi Tomokiyo ◽  
Daigaku Hasegawa ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Pro Inflammatory Cytokines
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