17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway

Huang, Jia Gu; Xia, Chun; Zheng, Xin; Yi, Ting; Wang, Xiao-Yong; Song, Gang; Zhang, Bing

doi:10.2478/s11658-011-0023-y

Cited by 74 publications

(74 citation statements)

References 51 publications

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“…Therefore, the functional changes of chondrocytes play an important role by contributing to the degradation of the articular cartilage and thus to the pathogenesis of OA (15,16). Several studies have reported that there is a very low proliferative activity in osteoarthritic chondrocytes, which might be an efficient treatment to cure or even delay the progression of OA by promoting chondrocyte proliferation (17,18). Therefore, the present study has focused on chondrocyte proliferation and extends the clinical observations of the potential anti-cartilage degenerative effect of millimeter waves and establishes a scientific foundation for further research.…”

Section: Discussionmentioning

confidence: 99%

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

et al. 2012

Int J Mol Med

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Abstract. Millimeter waves, high-frequency electromagnetic waves, can effectively alleviate the clinical symptoms in osteoarthritis patients, as a non-pharmaceutical and non-invasive physical therapy regimen. However, the molecular mechanisms of the therapeutic effects of millimeter wave treatment are not well understood. In the present study, the effect of millimeter waves on the G 1 /S cell cycle progression in chondrocytes and the underlying mecha nism was investigated. Chondrocytes isolated from the knee of SD rats were cultured and identified using toluidine blue staining. The second generation chondrocytes were collected and stimulated with or without millimeter waves for 48 h. Chondrocyte viability was analyzed using the MTT assay. The cell cycle distribution of chondrocytes was analyzed by flow cytometry. mRNA and protein expression levels of cyclin D1, cyclin-dependent kinases 4 and 6 (CDK4 and CDK6) and p21 were detected using real-time PCR and western blotting, respectively. Millimeter wave stimulation was found to significantly enhance chondrocyte viability. Moreover, the percentage of chondrocytes in the G 0 /G 1 phase was significantly decreased, whereas that in the S phase was significantly increased. In addition, following millimeter wave treatment, cyclin D1, CDK4 and CDK6 expression was significantly upregulated, whereas p21 expression was significantly downregulated. The results indicate that millimeter wave treatment promotes chondrocyte proliferation via cell cycle progression. IntroductionOsteoarthritis (OA), the most frequent arthropathy, is characterized by progressive degradation of hyaline articular cartilage and is associated with aging (1). A complex interplay of mechanical, and functional changes of chondrocytes could precipitate the imbalance between matrix anabolic and catabolic processes in articular cartilage and thus the pathogenesis of OA (2,3). Chondroctyes can rapidly respond to changes in the articular microenvironment and regulate the dynamic equilibrium between the anabolism and catabolism of the extracellular matrix (ECM), which plays a crucial role in the maintenance of the cartilage function (4). Therefore, enhancing chondrocyte function might be an efficient treatment to cure or even delay the progression of OA by promoting chondrocyte proliferation.The cell cycle plays an important role in the influence on chondrocyte function, which takes place in chondrocytes leading to its division and duplication. Cell cycle control is a highly regulated process that involves a complex cascade of events, in which regulation can be realized through a complicated network by cyclins, cyclin-dependent kinases (CDKs) and cyclin dependent kinase inhibitors (CDKI). G 1 /S transition, one of the two main checkpoints, is a rate-limiting step in the cell cycle and regulates cell proliferation (5,6). Cyclin D1 is a key cell cycle regulatory protein, which binds to CDK4 or CDK6 to control cell cycle progression from the G 1 to the S phase (7). Meanwhile, p21 competes with cyclin D1 for bindin...

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Section: Discussionmentioning

confidence: 99%

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

et al. 2012

Int J Mol Med

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“…The apoptosis of chondrocytes is widely considered to play a crucial role in the pathogenesis of OA [8]. Bone marrow-derived mesenchymal stem cells (BMSCs) possess pluripotency during several passages, and are commonly acceptable for differentiation into many cell types, such as chondrocytes and osteoblasts [9-11].…”

Section: Introductionmentioning

confidence: 99%

TGF-β1 is Involved in Vitamin D-Induced Chondrogenic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells by Regulating the ERK/JNK Pathway

Jiang

Huang

Yang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Osteoarthritis (OA) is characterized by degradation of cartilage, sole cell type of which is chondrocytes. Bone marrow-derived mesenchymal stem cells (BMSCs) possess multipotency and can be directionally differentiated into chondrocytes under stimulation. This study was aimed to explore the possible roles of vitamin D and transforming growth factor-β1 (TGF-β1) in the chondrogenic differentiation of BMSCs. Methods: BMSCs were isolated from femurs and tibias of rats and characterized by flow cytometry. After stimulation with vitamin D, BMSC proliferation and migration were measured by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. Chondrogenic differentiation was estimated through expression levels of specific markers by qRT-PCR and Western blot analysis. After stable transfection, the effects of aberrantly expressed TGF-β1 on vitamin D-induced alterations, including BMSC viability, migration and chondrogenic differentiation, were all evaluated utilizing CCK-8 assay, Transwell assay, qRT-PCR and Western blot analysis. Finally, the phosphorylation levels of key kinases in the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways were determined by Western blot analysis. Results: Vitamin D remarkably promoted BMSC viability, migration and chondrogenic differentiation. These alterations of BMSCs induced by vitamin D were reinforced by TGF-β1 overexpression while were reversed by TGF-β1 silencing. Additionally, the phosphorylation levels of ERK, JNK and c-Jun were enhanced by TGF-β1 overexpression but were reduced by TGF-β1 knockdown. Conclusion: Vitamin D promoted BMSC proliferation, migration and chondrogenic differentiation. TGF-β1 might be implicated in the vitamin D-induced alterations of BMSCs through regulating ERK/JNK pathway.

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“…Therefore, the functional changes of chondrocytes play an important role by contributing to the degradation of articular cartilage and thus to the pathogenesis of OA (27,28). Several studies have reported that osteoarthritic chondrocytes have a very low proliferative activity; thus, promoting chondrocyte proliferation may be an efficient treatment strategy to cure or delay the progression of OA (29,30). Therefore, in the present study, we focused on chondrocyte proliferation and the anti-degenerative effects of DHJSD on cartilage.…”

Section: Discussionmentioning

confidence: 99%

Duhuo Jisheng Decoction promotes chondrocyte proliferation through accelerated G1/S transition in osteoarthritis

Chen

Fan

et al. 2013

International Journal of Molecular Medicine

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Abstract. Duhuo Jisheng Decoction (DHJSD), a well known traditional Chinese folk medicine, is used for eliminating stagnation, removing blood stasis, promoting blood circulation and alleviating pain; it is commonly used for the treatment of various diseases, including osteoarthritis (OA). However, the molecular mechanisms behind the therapeutic effects of OA remain unclear. In the present study, the effects of DHJSD on the morphology of articular cartilage and the G1/S cell cycle progression in chondrocytes, as well as the underlying mechanisms, were investigated. A total of 27 two-month-old male Sprague Dawley rats were randomly divided into 3 groups: the control group (no papain-induced OA; received an equivalent amount of saline only), the model group (papain-induced OA; received an equivalent amount of saline only) and the DHJSD group [papain-induced OA; received a clinical oral dose of DHJSD (9.3 g/kg/day)]. After 8 consecutive weeks of treatment, the morphological changes in articular cartilage were observed under an optical microscope and by transmission electron microscopy (TEM) and the mRNA and protein expression levels of cyclin D1, CDK4, CDK6, retinoblastoma protein (Rb) and p16 were measured by RT-PCR and immunohistochemistry, respectively. Treatment with DHJSD significantly improved the arrangement of collagen fibers in the articular cartilage, as well as its structure and reduced cell degeneration compared with the model group. The mRNA and protein expression levels of cyclin D1, CDK4, CDK6 and Rb in the DHJSD-treated group were significantly increased compared with those in the model group, whereas p16 expression was significantly downregulated. Taken together, these results indicate that DHJSD treatment promotes chondrocyte proliferation by promoting the G1/S checkpoint transition in the cell cycle and by upregulating the expression of cyclin D1, CDK4, CDK6 and Rb and downregulating the expression of p16 and this may, in part, explain its clinical efficacy in the treatment of osteoarthritis.

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17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway

Cited by 74 publications

References 51 publications

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

Millimeter wave treatment promotes chondrocyte proliferation via G1/S cell cycle transition

TGF-β1 is Involved in Vitamin D-Induced Chondrogenic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells by Regulating the ERK/JNK Pathway

Duhuo Jisheng Decoction promotes chondrocyte proliferation through accelerated G1/S transition in osteoarthritis

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