Upregulation of relaxin receptors in the PDL by biophysical force

Yang, Sang Yoon; Kim, J. W.; Lee, S. Y.; Kang, Ji-Hyoun; Ulziisaikhan, U.; Yoo, H.I.; Moon, Yea Hwang; Moon, Jung-Sun; Ko, Hyun-Mi; Kim, M. S.; Kim, S. H.

doi:10.1007/s00784-014-1276-4

Cited by 7 publications

(7 citation statements)

References 32 publications

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“…To compare bone destruction, the distance between the first and second molars was measured. The right side was sham operated and used as a control …”

Section: Methodsmentioning

confidence: 99%

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Synergistic alveolar bone resorption by diabetic advanced glycation end products and mechanical forces

Moon

Lee

Kim

et al. 2019

Journal of Periodontology

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Background The association between diabetes mellitus (DM) and bone diseases is acknowledged. However, the mechanistic pathways leading to the alveolar bone (AB) destruction remain unclear. This study aims to elucidate the mechanical forces (MF)‐induced AB destruction in DM and its underlying mechanism. Methods In vivo periodontal tissue responses to MF were evaluated in rats with diabetes. In vitro human periodontal ligament (PDL) cells were either treated with advanced glycation end products (AGEs) alone or with AGEs and MF. Results In vivo, the transcription of VEGF‐A, colony stimulating factor‐1 (CSF‐1), and Ager was upregulated in diabetes, whereas changes in DDOST and Glo1 mRNAs were negligible. DM induced VEGF‐A protein in the vascular cells of the PDL and subsequent angiogenesis, but DM itself did not induce osteoclastogenesis. MF‐induced AB resorption was augmented in DM, and such augmentation was morphologically substantiated by the occasional undermining resorption as well as the frontal resorption of the AB by osteoclasts. The mRNA levels of CSF‐1 and vascular endothelial growth factor (VEGF) during MF application were highly elevated in diabetes, compared with those of the normal counterparts. In vitro, AGEs treatment elevated Glut‐1 and CSF‐1 mRNA levels via the p38 and JNK pathways, whereas OGT and VEGF levels remained unchanged. Compressive MF especially caused upregulation of VEGF, CSF‐1, and Glut‐1 levels, and such upregulation was further enhanced by AGEs treatment. Conclusions Overloaded MF and AGEs metabolites may synergistically aggravate AB destruction by upregulating CSF‐1 and VEGF. Therefore, regulating the compressive overloading of teeth, as well as the levels of diabetic AGEs, may prove to be an effective therapeutic modality for managing DM‐induced AB destruction.

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“…To compare bone destruction, the distance between the first and second molars was measured. The right side was sham operated and used as a control …”

Section: Methodsmentioning

confidence: 99%

“…Cells were plated onto BioFlex culture plates at 3 × 10 5 cells per well and subjected to the strain of maximum 12% elongation at 6 cycles/min. For compression, cells were plated onto 6Φ dishes at a density of 3 × 10 5 cells per dish and subjected to a compression force of 2.5 g/cm 2 by placing cover glasses with titanium discs on them …”

Section: Methodsmentioning

confidence: 99%

Synergistic alveolar bone resorption by diabetic advanced glycation end products and mechanical forces

Moon

Lee

Kim

et al. 2019

Journal of Periodontology

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“…GPCRs have been reported to be involved in the majority of cellular responses like bone remodeling, nerve transmission, inflammation, and homeostasis 32 . Previous reports revealed that CC chemokine receptor 5, relaxin family peptide receptors 1 and 2, known as the GPCRs, controlled PDL tissue remodeling during orthodontic tooth movement 33,34 . Our previous study also demonstrated that mechanical loading regulated the proliferation and osteo/cementblastic differentiation of human PDL stem cells through a kind of GPCRs, AT2 35 .…”

Section: Discussionmentioning

confidence: 81%

“…32 Previous reports revealed that CC chemokine receptor 5, relaxin family peptide receptors 1 and 2, known as the GPCRs, controlled PDL tissue remodeling during orthodontic tooth movement. 33,34 Our previous study also demonstrated that mechanical loading regulated the proliferation and osteo/cementblastic differentiation of human PDL stem cells through a kind F I G U R E 3 Expression of β2-AR in HPDLCs.…”

Section: Discussionmentioning

confidence: 92%

Functions of beta2‐adrenergic receptor in human periodontal ligament cells

Tomokiyo

Hasegawa

Yuda

et al. 2020

J of Cellular Biochemistry

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Adrenergic receptors (ARs) are receptors of noradrenalin and adrenalin, of which there are nine different subtypes. In particular, β2 adrenergic receptor (β2-AR) is known to be related to the restoration and maintenance of homeostasis in bone and cardiac tissues; however, the functional role of signaling through β2-AR in periodontal ligament (PDL) tissue has not been fully examined. In this report, we investigated that β2-AR expression in PDL tissues and their features in PDL cells. β2-AR expressed in rat PDL tissues and human PDL cells (HPDLCs) derived from two different patients (HPDLCs-2G and-3S). Rat PDL tissue with occlusal loading showed high β2-AR expression, while its expression was downregulated in that without loading. In HPDLCs, β2-AR expression was increased exposed to stretch loading. The gene expression of PDL-related molecules was investigated in PDL clone cells (2-23 cells) overexpressing β2-AR. Their gene expression and intracellular cyclic adenosine monophosphate (cAMP) levels were also investigated in HPDLCs treated with a specific β2-AR agonist, fenoterol (FEN). Overexpression of β2-AR significantly promoted the gene expression of PDL-related molecules in 2 to 23 cells. FEN led to an upregulation in the expression of PDL-related molecules and increased intracellular cAMP levels in HPDLCs. In both HPDLCs, inhibition of cAMP signaling by using protein kinase A inhibitor suppressed the FEN-induced gene expression of α-smooth muscle actin. Our findings suggest that the occlusal force is important for β2-AR expression in PDL tissue and β2-AR is involved in fibroblastic differentiation and collagen synthesis of PDL cells. The signaling through β2-AR might be important for restoration and homeostasis of PDL tissue.

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“…Seven‐week‐old male Sprague Dawley rats, weighing 170–190 g, were randomly and evenly divided into the following groups: days 1, 2 and 6 after BTM. The left upper first molar (M1) was moved mesially by applying a coil spring (Supplement 1A) (Lee et al, 2015; Yang et al, 2015).…”

Section: Methodsmentioning

confidence: 99%

SLPI in periodontal Ligament is not sleepy during biophysical force‐induced tooth movement

Lee

Moon

Yang

et al. 2021

J Clinic Periodontology

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Aim:We aimed to identify a key molecule that maintains periodontal tissue homeostasis during biophysical force-induced tooth movement (BTM) by orchestrating alveolar bone (AB) remodelling. Materials and Methods: Differential display-PCR was performed to identify key molecules for BTM in rats. To investigate the localization and expression of the identified molecules, immunofluorescence, real-time RT-PCR and Western blotting were performed in rats and human periodontal ligament (PDL) cells. Functional test and micro-CT analysis were performed to examine the in vivo effects of the identified molecules on BTM. Results: Secretory leucocyte peptidase inhibitor (SLPI) in the PDL was revealed as a key molecule for BTM-induced AB remodelling. SLPI was enhanced in the PDL under both compression and tension, and downregulated by an adenyl cyclases inhibitor. SLPI induced osteoblastogenic genes including runt-related transcription factor 2 (Runx2) and synergistically augmented tension-induced Runx2 expression. SLPI augmented mineralization in PDL cells. SLPI induced osteoclastogenic genes including receptor activator of nuclear factor kappa-Β ligand (RANKL) and synergistically augmented the compression-induced RANKL and macrophage colony-stimulating factor (MCSF) expression. Finally, the in vivo SLPI application into the AB significantly augmented BTM. Conclusions: SLPI or its inhibitors might serve as a biological target molecule for therapeutic interventions to modulate BTM.

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Upregulation of relaxin receptors in the PDL by biophysical force

Abstract: Rln and Rxfps may serve as a PDL turnover molecule complex to control orthodontic tooth movement.

Cited by 7 publications

References 32 publications

Synergistic alveolar bone resorption by diabetic advanced glycation end products and mechanical forces

Synergistic alveolar bone resorption by diabetic advanced glycation end products and mechanical forces

Functions of beta2‐adrenergic receptor in human periodontal ligament cells

SLPI in periodontal Ligament is not sleepy during biophysical force‐induced tooth movement

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