SETD2-mediated epigenetic regulation of noncanonical Wnt5A during osteoclastogenesis

Deb, Moonmoon; Laha, Dipranjan; Maity, Jyotirindra; Das, Hiranmoy

doi:10.1186/s13148-021-01125-2

Cited by 8 publications

(6 citation statements)

References 56 publications

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“…6A ). In our previous work, we showed an increased level of SETD2, an epigenetic regulator is involved in the regulation of OC differentiation [ 26 ]. Therefore, in this study, we also determined the effect of EGCG on the mRNA expression and protein level of SETD2 and found that the EGCG inhibited both the mRNA expression and protein level of the SETD2 molecule (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Epigallocatechin-3-gallate inhibits osteoclastic differentiation by modulating mitophagy and mitochondrial functions

et al. 2022

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A natural plant product, epigallocatechin-3-gallate (EGCG), was evaluated for its effectiveness in the regulation of osteoclastogenesis. We found that EGCG inhibited the osteoclast (OC) differentiation in vitro, and in primary bone marrow cells in a dose-dependent manner. Quantitative RT-PCR studies showed that the EGCG reduced the expression of OC differentiation markers. DCFDA, MitoSOX, and JC-1 staining revealed that the EGCG attenuated the reactive oxygen species (ROS), and mitochondrial membrane potential; and flux analysis corroborated the effect of EGCG. We further found that the EGCG inhibited mRNA and protein expressions of mitophagy-related molecules. We confirmed that the OC differentiation was inhibited by EGCG by modulating mitophagy through AKT and p38MAPK pathways. Furthermore, in silico analysis revealed that the binding of RANK and RANKL was blocked by EGCG. Overall, we defined the mechanisms of osteoclastogenesis during arthritis for developing a new therapy using a natural compound besides the existing therapeutics.

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Section: Resultsmentioning

confidence: 99%

“…6A ). In our previous research, we showed that the SETD2, an epigenetic regulator is upregulated during OC differentiation and after induction of arthritis and SETD2’s regulatory mechanisms [ 26 ]. In this study, we found that the EGCG inhibited the mRNA and protein expressions of SETD2 (Fig.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits osteoclastic differentiation by modulating mitophagy and mitochondrial functions

et al. 2022

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“…In addition, the NF-κB pathway was confirmed to be involved in the expression of Wnt5a. During RANKL-induced osteoclast differentiation, upregulated NF-κB expression was found to lead to the recruitment of histone acetyl transferases to the Wnt5a gene, leading to Wnt5a transcription (Deb et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

AdipoAI suppresses osteoclastogenesis by activating AdipoR1/APPL1: An in vivo experimental study in diabetes‐associated peri‐implantitis

Qiu

Chen

Wang

et al. 2023

Clinical Oral Implants Res

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Aim Diabetics experience severe peri‐implant inflammatory bone damage. We aimed to provide powerful evidence supporting the novel adiponectin receptor agonist AdipoAI in treating diabetes‐associated peri‐implantitis. Materials and Methods Twenty‐four ZDF‐Leprfa/Crl rats were randomly allocated to three groups (N = 8). After feeding with a high‐fat diet to establish diabetic rats, experimental peri‐implantitis was induced by implanting titanium rods (1.5 mm diameter and 20 mm length) contaminated with Staphylococcus aureus into the femurs. Radiographic evaluation, microCT, histological analyses and qRT–PCR were used to detect inflammatory infiltration and bone destruction. In vitro, the inhibition by AdipoAI of osteoclastogenesis, including the number and function of osteoclasts, was investigated by TRAP staining, immunofluorescence, qRT–PCR and Western blotting. Immunofluorescence, qRT–PCR and Western blotting were also utilized to explore AdipoR1, APPL1, NF‐κB and Wnt5a‐Ror2 signalling molecules in this process. One‐way ANOVA with Tukey's post hoc test was used to compare the data. Results AdipoAI reduced inflammation and bone destruction caused by peri‐implantitis in diabetic rats, which were manifested by a reduction in F4/80‐positive macrophage infiltration by 72%, the number of osteoclasts by 58% and the levels of cytokines (p < .05) in disease group. In vitro, 1 μM AdipoAI decreased the number of osteoclasts to 51%, inhibited F‐actin ring formation and reduced the levels of related markers (p < .05). Mechanistically, AdipoAI activated AdipoR1/APPL1 and conversely suppressed the phosphorylation of IκB‐α, nuclear translocation of P65 and the Wnt5a‐Ror2 signalling pathway (p < .05). Conclusions AdipoAI suppressed osteoclastogenesis in diabetes‐associated peri‐implantitis by inhibiting the NF‐κB and Wnt5a‐Ror2 pathways via the AdipoR1/APPL1 axis.

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“…The pre-cooled RIPA buffer comprising the protease and phosphatase inhibitors was used to extract the protein from each group of cells by following the method used previously [ 31 ] . The quantification of total cell protein concentration was done with a precision red advanced protein assay kit.…”

Section: Methodsmentioning

confidence: 99%

Secretome of Dental Pulp-Derived Stem Cells Reduces Inflammation and Proliferation of Glioblastoma Cells by Deactivating Mapk-Akt Pathway

Prateeksha¹,

Howlader²,

Hansda³

et al. 2023

jbyyj

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Background: Dental pulp-derived stem cells (DPSC) is a promising therapy as they modulate the immune response, so we evaluated the inhibitory effect of DPSC secretome (DPSC ℗ ) on the proliferation and inflammation in human glioblastoma (GBM) cells (U-87 MG) and elucidated the concomitant mechanisms involved. Methods: The U87-MG cells were cultured with DPSC ℗ for 24 h and assessed the expression of inflammatory molecules using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), generation of reactive oxygen species (ROS), and mitochondrial functionality using a seahorse flux analyzer. MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay and cell cycle analysis were performed to evaluate the proliferation and cell cycle. Finally, the protein levels were determined by western blot. Results: DPSC ℗ reduced the inflammation and proliferation of U-87 MG cells by down-regulating the pro-inflammatory markers and up-regulating anti-inflammatory markers expressions through ROS-mediated signaling. Moreover, DPSC ℗ significantly reduced the mitochondrial membrane potential (MMP) in the cells. The cellular bioenergetics revealed that all the parameters of oxygen consumption rate (OCAR) and the extracellular acidification rate (ECAR) were significantly decreased in the GBM cells after the addition of DPSC ℗ . Additionally, DPSC ℗ decreased the GBM cell proliferation by arresting the cell cycle at the G1 phase through activation (phosphorylation) of checkpoint molecule CHK1. Furthermore, mechanistically, we found that the DPSC ℗ impedes the phosphorylation of the mitogen-activated protein kinases (P38 MAPK) and protein kinase B (AKT) pathway. Conclusion: Our findings lend the first evidence of the inhibitory effects of DPSC ℗ on proliferation and inflammation in GBM cells by altering the P38 MAPK-AKT pathway.

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SETD2-mediated epigenetic regulation of noncanonical Wnt5A during osteoclastogenesis

Cited by 8 publications

References 56 publications

Epigallocatechin-3-gallate inhibits osteoclastic differentiation by modulating mitophagy and mitochondrial functions

Epigallocatechin-3-gallate inhibits osteoclastic differentiation by modulating mitophagy and mitochondrial functions

AdipoAI suppresses osteoclastogenesis by activating AdipoR1/APPL1: An in vivo experimental study in diabetes‐associated peri‐implantitis

Secretome of Dental Pulp-Derived Stem Cells Reduces Inflammation and Proliferation of Glioblastoma Cells by Deactivating Mapk-Akt Pathway

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