Resveratrol can enhance osteogenic differentiation and mitochondrial biogenesis from human periosteum-derived mesenchymal stem cells

Moon, Dong Kyu; Kim, Bo Gyu; Lee, A Ram; Choe, Yeong In; Khan, Imran; Moon, Kyoung Mi; Jeon, Ryoung-Hoon; Byun, June‐Ho; Hwang, Sun‐Chul; Woo, Dong Kyun

doi:10.1186/s13018-020-01684-9

Cited by 31 publications

(19 citation statements)

References 65 publications

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“…In this study, the ALP levels, evaluated after 7 days, were increased after the treatment with 1d at 5 µM compared to the control cells and to cells treated with RSV, while 1h did not influence the level of ALP. The results were in accordance with the study of Moon DK et al that showed enhanced ALP levels between 5 and 10 days in mesenchymal cells after the administration of 5 µM of RSV [ 40 ]. In addition, the enhanced osteoblast activity was confirmed by the analysis on mineralization features.…”

Section: Discussionsupporting

confidence: 92%

Emerging Effects of Resveratrol Derivatives in Cells Involved in Oral Wound Healing: A Preliminary Study

D’Amico

Pierfelice

Amoroso

et al. 2023

IJMS

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Recently, there has been an increasing interest in finding new approaches to manage oral wound healing. Although resveratrol (RSV) exhibited many biological properties, such as antioxidant and anti-inflammatory activities, its use as a drug is limited by unfavorable bioavailability. This study aimed to investigate a series of RSV derivatives (1a–j) with better pharmacokinetic profiles. At first, their cytocompatibility at different concentrations was tested on gingival fibroblasts (HGFs). Among them, derivatives 1d and 1h significantly increased cell viability compared to the reference compound RSV. Thus, 1d and 1h were investigated for cytotoxicity, proliferation, and gene expression in HGFs, endothelial cells (HUVECs), and oral osteoblasts (HOBs), which are the main cells involved in oral wound healing. For HUVECs and HGFs, the morphology was also evaluated, while for HOBs ALP and mineralization were observed. The results showed that both 1d and 1h did not exert negative effects on cell viability, and at a lower concentration (5 µM) both even significantly enhanced the proliferative rate, compared to RSV. The morphology observations pointed out that the density of HUVECs and HGFs was promoted by 1d and 1h (5 µM) and mineralization was promoted in HOBs. Moreover, 1d and 1h (5 µM) induced a higher eNOS mRNA level in HUVECs, higher COL1 mRNA in HGFs, and higher OCN in HOBs, compared to RSV. The appreciable physicochemical properties and good enzymatic and chemical stability of 1d and 1h, along with their promising biological properties, provide the scientific basis for further studies leading to the development of RSV-based agents useful in oral tissue repair.

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Section: Discussionsupporting

confidence: 92%

Emerging Effects of Resveratrol Derivatives in Cells Involved in Oral Wound Healing: A Preliminary Study

D’Amico

Pierfelice

Amoroso

et al. 2023

IJMS

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“…It performs an integral function in the healing of fractures and maintenance of bone tissues. 22 In vitro treatment with Res of primary human bone marrow stromal cells (BMSCs) in elderly patients, which were characterized by high adipocyte and low osteoblast differentiation, remarkably enhanced osteoblast differentiation and reduced adipocyte formation. 23 Res therapy reduced the degrees of NF-κB and β-catenin protein expressions in TNF-α-induced BMSCs, increased the downregulated levels of OCN and Runx2 in TNF-α-induced BMSCs, and increased the differentiation of BMSCS into osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol suppresses lipopolysaccharide-mediated activation of osteoclast precursor RAW 264.7 cells by increasing miR-181a-5p expression

Xue

Liu

Yang

2023

Int J Immunopathol Pharmacol

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Resveratrol (Res) has anti-inflammation and antiosteoporosis functions. We evaluated the effect of Res on osteoclast differentiation by releasing inflammatory cytokines from osteoclast precursor RAW 264.7 cells stimulated by lipopolysaccharide (LPS). In the study, LPS (1 ng/L) was used to induce the Raw 264.7 inflammatory injury model in vitro. A total of 25 ng/mL M-CSF + 30 ng/mL RANKL or plus 1 μg/L LPS was used to induce osteoclastogenesis in the experiments. We utilized the Cell Counting Kit-8 assay to measure the relative cell survival of RAW 264.7 cells. Then, enzyme-linked immunosorbent assays were utilized to measure the abundance of inflammatory markers, such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and IL-6. Subsequently, Western blot analysis was applied to assess the abundance of phosphorylated transforming growth factor beta-activated kinase 1 (P-TAK1) protein, TNF receptor-associated factor 6 (TRAF6), nuclear factor-κB inhibitor protein (IκB), phosphorylated IκB-α (P-IκB-α), and nuclear factor κB65 (NF-κB65). mRNA expression levels of miR-181a-5p, TRAF6, specific gene calcitonin receptor (CTR), activated T nuclear factor 1 (NFATC1), cathepsin K (CTSK), and matrix metalloproteinase (MMP)-9 were determined via a real-time polymerase chain reaction. Osteoclast bone resorption function was determined. Finally, tartrate-resistant acid phosphatase (TRAP) staining was performed.The results found that Compared with the model group, the degrees of expressions of supernatant inflammatory factors TNF-α, IL-1β, and IL-6 were substantially attenuated in the Res treatment group ( p < 0.05). Furthermore, the extent of miR-181a-5p expression in the RAW 264.7 cells significantly increased, whereas P-IκB-α, P-TAK1, NF-κB65, and TRAF6 expressions significantly decreased in the Res treatment group as opposed to the model group ( p < 0.05). The CTR, NFATC1, MMP-9, CTSK, and TRAP mRNA expression levels were substantially reduced during osteoclast differentiation and bone resorption in the Res treatment group.The results suggest that Res can reduce the RAW 264.7 cell differentiation into osteoclasts and relieve LPS-stimulated osteoporosis, and the underlying mechanism may be associated with the Res-inhibited activity of the TRAF6/TAK1 pathway through the increased miR-181a-5p expression.

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“…Mitochondrial mass can be increased with osteogenic differentiation, resveratrol has been shown to enhance mtDNA content and mitochondrial quality in a time-dose dependent manner ( 27 ). Therefore, as a SIRT1 activator ( 28 ), resveratrol can promote mitochondrial biogenesis during osteogenic differentiation.…”

Section: The Pathological Role Of Mitochondria In Osteoporosismentioning

confidence: 99%

“…Ma ( 67 ) found that sodium hydrosulfide (NaHS) could reverse dexamethasone-induced mitochondrial dysfunction by upregulating the expression of SIRT1 and its downstream effector PGC-1α, and SIRT1 silencing abolished the protective effect of NaHS on mitochondrial dysfunction in osteoblasts. In addition, resveratrol can protect osteoblasts in osteoporosis rats by activating SIRT1 target to enhance mitochondrial biogenesis and mitophagy ( 27 , 63 ) 75 . Li ( 68 ) found that iristein decreased mitochondrial membrane potential, intracellular ROS level, mitochondrial O 2 · − state, ATP production, complex I and IV activity through SIRT3 pathway, indicating that iristein regulated mitophagy and mitochondrial biogenesis in a SIRT3 dependent manner to reverse the AGE induced inhibition of adipocyte stem cell (ASC) osteoblastic differentiation.…”

Section: Potential Therapeutic Targeting Of Mitochondria In Osteoporosismentioning

confidence: 99%

Mitochondrial quality control and its role in osteoporosis

et al. 2023

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Mitochondria are important organelles that provide cellular energy and play a vital role in cell differentiation and apoptosis. Osteoporosis is a chronic metabolic bone disease mainly caused by an imbalance in osteoblast and osteoclast activity. Under physiological conditions, mitochondria regulate the balance between osteogenesis and osteoclast activity and maintain bone homeostasis. Under pathological conditions, mitochondrial dysfunction alters this balance; this disruption is important in the pathogenesis of osteoporosis. Because of the role of mitochondrial dysfunction in osteoporosis, mitochondrial function can be targeted therapeutically in osteoporosis-related diseases. This article reviews different aspects of the pathological mechanism of mitochondrial dysfunction in osteoporosis, including mitochondrial fusion and fission, mitochondrial biogenesis, and mitophagy, and highlights targeted therapy of mitochondria in osteoporosis (diabetes induced osteoporosis and postmenopausal osteoporosis) to provide novel targets and prevention strategies for the prevention and treatment of osteoporosis and other chronic bone diseases.

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Resveratrol can enhance osteogenic differentiation and mitochondrial biogenesis from human periosteum-derived mesenchymal stem cells

Cited by 31 publications

References 65 publications

Emerging Effects of Resveratrol Derivatives in Cells Involved in Oral Wound Healing: A Preliminary Study

Emerging Effects of Resveratrol Derivatives in Cells Involved in Oral Wound Healing: A Preliminary Study

Resveratrol suppresses lipopolysaccharide-mediated activation of osteoclast precursor RAW 264.7 cells by increasing miR-181a-5p expression

Mitochondrial quality control and its role in osteoporosis

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