High-frequency low-level diode laser irradiation promotes proliferation and migration of primary cultured human gingival epithelial cells

2013 ◽  
Vol 29 (4) ◽  
pp. 1339-1347 ◽  
Author(s):  
Kenichiro Ejiri ◽  
Akira Aoki ◽  
Yoko Yamaguchi ◽  
Mitsuhiro Ohshima ◽  
Yuichi Izumi
Keyword(s):  
Epithelial Cells ◽  
Laser Irradiation ◽  
Diode Laser ◽  
High Frequency ◽  
Low Level ◽  
Gingival Epithelial Cells ◽  
And Migration ◽  
Human Gingival Epithelial Cells ◽  
Proliferation And Migration

Effects of high-frequency near-infrared diode laser irradiation on the proliferation and migration of mouse calvarial osteoblasts

2018 ◽  
Vol 33 (5) ◽  
pp. 959-966 ◽  
Author(s):  
Ryo Kunimatsu ◽  
Hidemi Gunji ◽  
Yuji Tsuka ◽  
Yuki Yoshimi ◽  
Tetsuya Awada ◽  
...  
Keyword(s):  
Laser Irradiation ◽  
Diode Laser ◽  
High Frequency ◽  
Near Infrared ◽  
And Migration ◽  
Proliferation And Migration

In vitroEffect of Mouthrinse Containing Essential Oils on Proliferation and Migration of Gingival Epithelial Cells

2016 ◽  
Vol 30 (7) ◽  
pp. 1113-1118
Author(s):  
Kouki Yoshikawa ◽  
Jin Sekino ◽  
Kentaro Imamura ◽  
Koki Ota ◽  
Daichi Kita ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Essential Oils ◽  
Gingival Epithelial Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Cigarette Smoke Stimulates SARS-CoV-2 Internalization by Activating AhR and Increasing ACE2 Expression in Human Gingival Epithelial Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7669
Author(s):  
Cassio Luiz Coutinho Almeida-da-Silva ◽  
Harmony Matshik Dakafay ◽  
Kaitlyn Liu ◽  
David M. Ojcius
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Cigarette Smoke ◽  
Large Body ◽  
Receptor Expression ◽  
Host Cells ◽  
Dependent Manner ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells ◽  
Oral Cells

A large body of evidence shows the harmful effects of cigarette smoke to oral and systemic health. More recently, a link between smoking and susceptibility to coronavirus disease 2019 (COVID-19) was proposed. COVID-19 is due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which uses the receptor ACE2 and the protease TMPRSS2 for entry into host cells, thereby infecting cells of the respiratory tract and the oral cavity. Here, we examined the effects of cigarette smoke on the expression of SARS-CoV-2 receptors and infection in human gingival epithelial cells (GECs). We found that cigarette smoke condensates (CSC) upregulated ACE2 and TMPRSS2 expression in GECs, and that CSC activated aryl hydrocarbon receptor (AhR) signaling in the oral cells. ACE2 was known to mediate SARS-CoV-2 internalization, and we demonstrate that CSC treatment potentiated the internalization of SARS-CoV-2 pseudovirus in GECs in an AhR-dependent manner. AhR depletion using small interference RNA decreased SARS-CoV-2 pseudovirus internalization in CSC-treated GECs compared with control GECs. Our study reveals that cigarette smoke upregulates SARS-CoV-2 receptor expression and infection in oral cells. Understanding the mechanisms involved in SARS-CoV-2 infection in cells of the oral cavity may suggest therapeutic interventions for preventing viral infection and transmission.

scholarly journals Effect of Slit/Robo signaling on regeneration in lung emphysema

2021 ◽  
Author(s):  
Jin-Soo Park ◽  
RyeonJin Cho ◽  
Eun-Young Kang ◽  
Yeon-Mok Oh
Keyword(s):  
Epithelial Cells ◽  
Mouse Model ◽  
Lung Epithelial Cells ◽  
Mouse Lung ◽  
Chronic Obstructive ◽  
Irreversible Damage ◽  
Lung Epithelial ◽  
And Migration ◽  
Proliferation And Migration

AbstractEmphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.

scholarly journals Effects of bone morphogenetic proteins on epithelial repair

2021 ◽  
pp. 153537022110281
Author(s):  
Yu Hou ◽  
Yu-Xi He ◽  
Jia-Hao Zhang ◽  
Shu-Rong Wang ◽  
Yan Zhang
Keyword(s):  
Growth Factors ◽  
Epithelial Cells ◽  
Bone Morphogenetic Proteins ◽  
Epithelial Tissue ◽  
Epithelial Repair ◽  
Multiple Functions ◽  
Epithelial Damage ◽  
Damage Repair ◽  
And Migration ◽  
Proliferation And Migration

Epithelial tissue has important functions such as protection, secretion, and sensation. Epithelial damage is involved in various pathological processes. Bone morphogenetic proteins (BMPs) are a class of growth factors with multiple functions. They play important roles in epithelial cells, including in differentiation, proliferation, and migration during the repair of the epithelium. This article reviews the functions and mechanisms of the most profoundly studied BMPs in the process of epithelial damage repair and their clinical significance.

scholarly journals Identification of Porphyromonas gingivalis Genes Specifically Expressed in Human Gingival Epithelial Cells by Using Differential Display Reverse Transcription-PCR

2004 ◽  
Vol 72 (7) ◽  
pp. 3752-3758 ◽  
Author(s):  
Yoonsuk Park ◽  
Özlem Yilmaz ◽  
Il-Young Jung ◽  
Richard J. Lamont
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Abc Transporter ◽  
Differential Display ◽  
Molecular Mechanisms ◽  
Gene Products ◽  
Reverse Transcription Pcr ◽  
Gingival Epithelial Cells ◽  
Insertional Inactivation ◽  
Human Gingival Epithelial Cells

ABSTRACT Porphyromonas gingivalis, one of the causative agents of adult periodontitis, can invade and survive within host epithelial cells. The molecular mechanisms by which P. gingivalis induces uptake and adapts to an intracellular environment are not fully understood. In this study, we have investigated the genetic responses of P. gingivalis internalized within human gingival epithelial cells (GECs) in order to identify factors involved in invasion and survival. We compared the differential display of arbitrarily PCR-amplified gene transcripts in P. gingivalis recovered from GECs with the display of transcripts in P. gingivalis control cultures. Over 20 potential differentially expressed transcripts were identified. Among these, pepO, encoding an endopeptidase, and genes encoding an ATP-binding cassette (ABC) transporter and a cation-transporting ATPase were upregulated in GECs. To investigate the functionality of these gene products, mutants were generated by insertional inactivation. Compared to the parental strain, mutants of each gene showed a significant reduction in their invasion capabilities. In addition, GEC cytoskeletal responses to the mutants were distinct from those induced by the parent. In contrast, adhesion of the mutant strains to GECs was not affected by lack of expression of the gene products. These results suggest that PepO, a cation-transporting ATPase, and an ABC transporter are required for the intracellular lifestyle of P. gingivalis.

scholarly journals Response of Human Gingival Epithelial Cells (HGE-15) to Bioactive Glass RKKP

2008 ◽  
Vol 7 (1) ◽  
pp. 5-11
Author(s):  
Hitoshi Oguchi ◽  
Yasuyo Karube ◽  
Kameji Matsumoto ◽  
Mitsuhiko Morito
Keyword(s):  
Epithelial Cells ◽  
Bioactive Glass ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells
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