Vignacyanidin Polyphenols Isolated from Vigna Angularis Bean Promote Osteoblast Differentiation

Rojasawasthien, Thira; Shirakawa, Tomohiko; Washio, Ayako; Tsujisawa, Toshiyuki; Matsubara, Takuma; Inoue, Asako; Takahama, Umeo; Nakashima, Keisuke; Kokabu, Shoichiro

doi:10.21873/invivo.12328

Cited by 9 publications

(7 citation statements)

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“…Therefore, VAE can effectively suppress the increase in the thickness of the epidermis and dermis and the expression of inflammatory cytokines by suppressing the inflammation-related signaling pathway. V. angularis contains several compounds, and these compounds have been reported to exert various pharmacological effects [ 23 , 24 , 25 , 26 ]. However, hemiphloin, a new indicator component, is isolated from 70% EtOH extract of V. angularis .…”

Section: Discussionmentioning

confidence: 99%

Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

Bak¹,

Lim²,

Park³

et al. 2023

Heliyon

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Section: Discussionmentioning

confidence: 99%

Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

Bak¹,

Lim²,

Park³

et al. 2023

Heliyon

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“…Cells were plated at a density of 5000 cells/well in 96-well plates. For direct viable cell counts by the trypan blue pigment exclusion method, cells were plated at a density of 2.5 × 10 4 cells/well in 24-well plates [ 34 ]. Three days later, cells were detached with trypsin (Fujifilm Wako) mixed with Trypan Blue counted with a TC20 Automated Cell Counter (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

Plectin promotes tumor formation by B16 mouse melanoma cells via regulation of Rous sarcoma oncogene activity

et al. 2022

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Background Melanoma is a malignant tumor characterized by high proliferation and aggressive metastasis. To address the molecular mechanisms of the proto-oncogene, Rous sarcoma oncogene (Src), which is highly activated and promotes cell proliferation, migration, adhesion, and metastasis in melanoma. Plectin, a cytoskeletal protein, has recently been identified as a Src-binding protein that regulates Src activity in osteoclasts. Plectin is a candidate biomarker of certain tumors because of its high expression and the target of anti-tumor reagents such as ruthenium pyridinecarbothioamide. The molecular mechanisms by which plectin affects melanoma is still unclear. In this study, we examined the role of plectin in melanoma tumor formation. Methods We used CRISPR/Cas9 gene editing to knock-out plectin in B16 mouse melanoma cells. Protein levels of plectin and Src activity were examined by western blotting analysis. In vivo tumor formation was assessed by subcutaneous injection of B16 cells into nude mice and histological analysis performed after 2 weeks by Hematoxylin-Eosin (H&E) staining. Cell proliferation was evaluated by direct cell count, cell counting kit-8 assays, cyclin D1 mRNA expression and Ki-67 immunostaining. Cell aggregation and adhesion were examined by spheroid formation, dispase-based dissociation assay and cell adhesion assays. Results In in vivo tumor formation assays, depletion of plectin resulted in low-density tumors with large intercellular spaces. In vitro experiments revealed that plectin-deficient B16 cells exhibit reduced cell proliferation and reduced cell-to-cell adhesion. Since Src activity is reduced in plectin-deficient melanomas, we examined the relationship between plectin and Src signaling. Src overexpression in plectin knockout B16 cells rescued cell proliferation and improved cell-to-cell adhesion and cell to extracellular matrix adhesion. Conclusion These results suggest that plectin plays critical roles in tumor formation by promoting cell proliferation and cell-to-cell adhesion through Src signaling activity in melanoma cells.

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“…The mouse calvaria osteoblast cell line MC3T3‐E1 cells from Riken BioResource Center (Tsukuba, Japan) were cultured. Cells were maintained in a 5% CO 2 , 37°C with α‐minimal essential medium (MEM‐α) (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan) supplemented with 10% fetal bovine serum (Nichirei Biosciences Inc., Tokyo, Japan), 100 U/ml penicillin–streptomycin (Fujifilm Wako Pure Chemical Corporation) 20 . Primary calvaria osteoblasts (POBs) were isolated from 3‐day‐old C57BL/6 mice.…”

Section: Methodsmentioning

confidence: 99%

“…Cells were maintained in a 5% CO 2 , 37°C with α‐minimal essential medium (MEM‐α) (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan) supplemented with 10% fetal bovine serum (Nichirei Biosciences Inc., Tokyo, Japan), 100 U/ml penicillin–streptomycin (Fujifilm Wako Pure Chemical Corporation). 20 Primary calvaria osteoblasts (POBs) were isolated from 3‐day‐old C57BL/6 mice. They were dissected and removed under general anesthesia using isoflurane, and soft tissue Calvariae were incubated at 37°C for 15 min in digestion medium (1 mg/ml Collagenase I [WAKO], Dispase 10 mg/ml [WAKO] αMEM [WAKO]).…”

Section: Methodsmentioning

confidence: 99%

Nobiletin, a NF‐κB signaling antagonist, promotes BMP ‐induced bone formation

et al. 2022

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The NF‐κB family of transcription factors plays an important role in skeletal development and bone homeostasis. In osteoblast cells, NF‐κB signaling has been shown to suppress survival, proliferation, and differentiation. Furthermore, pharmacological suppression of NF‐κB enhances osteoblast differentiation and bone formation. Thus, NF‐κB antagonists are promising candidates as anabolic agents for enhancing bone mass. In this study, we describe the mechanism by which nobiletin, an inhibitor of NF‐κB activity, regulates osteoblast differentiation and mineralization. We found that in MC3T3‐E1 osteoblast cells, nobiletin inhibited a TNF‐α responsive NF‐κB luciferase reporter and also decreased the induction of classical NF‐κB target genes by TNF‐α. Consistent with this, nobiletin prevented TNF‐α ‐mediated suppression of osteogenesis and potently enhanced the differentiation and mineralization of MC3T3‐E1 cells. Likewise, in an in vivo BMP2‐induced ectopic bone formation assay, nobiletin markedly enhanced ossicle bone volume. Western blotting and SMAD‐responsive luciferase assays also demonstrated that NF‐κB suppression of BMP signaling could be inhibited by nobiletin. Thus, our data suggest that mechanistically, nobiletin prevents the endogenous repression of BMP signaling by TNF‐α, thereby enhancing osteoblast activity. In conclusion, nobiletin is a novel NF‐κB antagonist that may be a useful anabolic agent for bone formation.

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Vignacyanidin Polyphenols Isolated from Vigna Angularis Bean Promote Osteoblast Differentiation

Cited by 9 publications

References 0 publications

Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

Plectin promotes tumor formation by B16 mouse melanoma cells via regulation of Rous sarcoma oncogene activity

Nobiletin, a NF‐κB signaling antagonist, promotes BMP ‐induced bone formation

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