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Berlin Brandenburg

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  • 1
    Language: English
    In: Journal of Surgical Research, August 2013, Vol.183(2), pp.612-619
    Description: This study investigated the site-specific effects of extracorporeal shockwave therapy (ESWT) in osteoarthritis of the knee in rats. Sixty SD rats were divided into five groups. Group I was the control and received sham surgery without anterior cruciate ligament transection (ACLT) and medial meniscectomy (MM) and no ESWT. Group II received ACLT + MM, but no ESWT. Group III received ACLT + MM and ESWT at distal femur. Group IV received ACLT + MM and ESWT at proximal tibia. Group V received ACLT + MM and ESWT at distal femur and proximal tibia. Each ESWT session consisted of 800 impulses at 14 kV (= 0.219 mJ/mm energy flux density). The evaluations included radiograph, bone mineral density (BMD), histomorphologic examination, and immunohistochemical analysis. Radiographic appearance: Group II showed progressive osteoarthritis of the knee at 12 and 24 wk, whereas only subtle changes were noted in Groups I, III, VI, and V. BMD results: Group II showed significant decreases of BMD at 12 and 24 wk. The BMDs of Groups III, IV, and V were comparable to Group I. Cartilage degradation: Group II showed significant increases of Mankin score, Safranin O stain, and matrix metalloproteinase 13 and decrease of collagen II at 12 and 24 wk. The changes of Mankin score, Safranin O stain, matrix metalloproteinase 13, and collagen II in Groups III, IV, and V were comparable to Group I. Subchondral bone remodeling: Group II showed significant decreases of vascular endothelial growth factor, bone morphogenetic protein 2, and osteocalcin at 12 and 24 wk as compared to Group I. The changes of vascular endothelial growth factor, bone morphogenetic protein 2, and osteocalcin in Groups III, IV, and V were comparable to Group I. ESWT shows site-specific effects at distal femur and proximal tibia in osteoarthritis of the knee in rats. The effects of ESWT are consistent at distal femur and proximal tibia, with no additive effects when both areas were simultaneously treated.
    Keywords: Shockwave ; Site-Specific ; Osteoarthritis ; Knee ; Rats
    ISSN: 0022-4804
    E-ISSN: 1095-8673
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  • 2
    Language: English
    In: Arthritis & Rheumatism, October 2012, Vol.64(10), pp.3267-3277
    Description: Objective Synovial hypervascularity is a prominent pathologic feature in osteoarthritic (OA) joints. Wnt inhibitor Dkk-1 contributes to joint remodeling. We undertook this study to investigate whether Dkk-1 regulates cartilage destruction activities in OA synovial fibroblasts. Methods Synovial tissues were harvested from knees of patients with OA and from injured knees of non-OA patients who underwent arthroscopy. Expression of Dkk-1, angiogenic factors (stromal cell-derived factor 1 and colony-stimulating factor 1), and cartilage proteinases (ADAMTS-5 and matrix metalloproteinase 3 [MMP-3]) as well as vascularity in synovium and synovial fluid were quantified using enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and histomorphometry. Synovial fibroblasts were treated with interleukin-1[beta] (IL-1[beta]), anti-Dkk-1 antibody, and RNA interference to characterize their angiogenic activity. Rats with OA knees were administered Dkk-1 antisense oligonucleotide to verify synovial angiogenesis and cartilage integrity. Results OA synovium exhibited increased vascularity and expression of angiogenic factors and proteinases in association with up-regulated Dkk-1 levels. Neutralizing Dkk-1 reduced the inhibitory effects of OA synovial fluid on aggrecan expression in chondrocyte cultures. IL-1[beta] induction of Dkk-1 increased expression of hypoxia-inducible factor 1[alpha] (HIF-1[alpha]), angiogenic factors, ADAMTS-5, and MMP-3 in synovial fibroblasts and promoted angiogenesis in vascular endothelial cells. Knockdown of HIF-1[alpha] decreased Dkk-1 enhancement of angiogenic factor expression. Stabilization of glycogen synthase kinase 3[beta] phosphorylated at Ser super(9), [beta]-catenin, T cell factor 4, and ERK signaling attenuated Dkk-1 up-regulation of angiogenic factor and proteinase expression in synovial fibroblasts. In vivo, Dkk-1 interference reduced the expression of angiogenic factors and proteinases and ameliorated synovial vascularity and cartilage deterioration in knees of rats with OA. Conclusion Dkk-1 promoted angiogenic and cartilage degradation activities in synovial fibroblasts, which accelerated synovial angiogenesis and cartilage destruction. Dkk-1 blockade has therapeutic potential for reducing OA-induced synovitis and joint deterioration.
    Keywords: Cartilage Diseases ; Stromelysin 1 ; Synovium ; Osteoarthritis ; Angiogenesis ; Joint Diseases ; Chondrocytes ; Matrix Metalloproteinase ; Macrophage Colony-Stimulating Factor ; Fibroblasts ; Endothelial Cells ; Extracellular Signal-Regulated Kinase ; Antisense Oligonucleotides ; Synovial Fluid ; Lymphocytes T ; RNA-Mediated Interference ; Dkk1 Protein ; Aggrecan ; Hypoxia-Inducible Factors ; Cartilage and Cartilage Diseases;
    ISSN: 0004-3591
    E-ISSN: 1529-0131
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  • 3
    Language: English
    In: Arthritis & Rheumatism, May 2010, Vol.62(5), pp.1393-1402
    Description: OBJECTIVE: Perturbation of Wnt signaling components reportedly regulates chondrocyte fate and joint disorders. The Wnt inhibitor Dkk-1 mediates remodeling of various tissue types. We undertook this study to examine whether control of Dkk-1 expression prevents joint deterioration in osteoarthritic (OA) knees.METHODS: Anterior cruciate ligament transection-and collagenase-induced OA in rat knees was treated with end-capped phosphorothioate Dkk-1 antisense oligonucleotide (Dkk-1-AS). Articular cartilage destruction, cartilage degradation markers, bone mineral density (BMD), and subchondral trabecular bone volume of injured knee joints were measured using Mankin scoring, enzyme-linked immunosorbent assay, dual x-ray absorptiometry, and histomorphometry. Dkk-1-responsive molecule expression and apoptotic cells in knee tissue were detected by quantitative reverse transcriptase-polymerase chain reaction, immunoblotting, and TUNEL staining.RESULTS: Up-regulated Dkk-1 expression was associated with increased Mankin score and with increased serum levels of cartilage oligomeric matrix protein and C-telopeptide of type II collagen (CTX-II) during OA development. Dkk-1-AS treatment alleviated OA-associated increases in Dkk-1 expression, Mankin score, cartilage fibrillation, and serum cartilage degradation markers. Dkk-1-AS also alleviated epiphyseal BMD loss and subchondral bone exposure associated with altered serum levels of osteocalcin and CTX-I. The treatment abrogated chondrocyte/osteoblast apoptosis and subchondral trabecular bone remodeling in OA. Dkk-1 knockdown increased levels of nuclear beta-catenin and phosphorylated Ser(473)-Akt but attenuated expression of inflammatory factors (Toll-like receptor 4 [TLR-4], TLR-9, interleukin-1beta, and tumor necrosis factor alpha), the apoptosis regulator Bax, matrix metalloproteinase 3, and RANKL in OA knee joints.CONCLUSION: Interference with the cartilage- and bone-deleterious actions of Dkk-1 provides therapeutic potential for alleviating cartilage destruction and subchondral bone damage in OA knee joints.
    Keywords: Medicine;
    ISSN: 0004-3591
    E-ISSN: 1529-0131
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  • 4
    Language: English
    In: Bone, 2015, Vol.81, p.80(9)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.bone.2015.06.022 Byline: Jih-Yang Ko, Pei-Chin Chuang, Huei-Jin Ke, Yu-Shan Chen, Yi-Chih Sun, Feng-Sheng Wang Abstract: Glucocorticoid treatment reportedly increases the morbidity of osteoporotic or osteonecrotic disorders. Exacerbated bone acquisition and escalated marrow adipogenesis are prominent pathological features of glucocorticoid-mediated skeletal disorders. MicroRNAs reportedly modulate tissue metabolism and remodeling. This study was undertaken to investigate the biological roles of microRNA-29a (miR-29a) in skeletal and fat metabolism in the pathogenesis of glucocorticoid-induced osteoporosis. Transgenic mice overexpressing miR-29a precursor or wild-type mice were given methylprednisolone. Bone mass, microarchitecture and histology were assessed by dual energy X-ray absorptiometry, [mu]CT and histomorphometry. Differential gene expression and signaling components were delineated by quantitative RT-PCR and immunoblotting. Glucocorticoid treatment accelerated bone loss and marrow fat accumulation in association with decreased miR-29a expression. The miR-29a transgenic mice had high bone mineral density, trabecular microarchitecture and cortical thickness. miR-29a overexpression mitigated the glucocorticoid-induced impediment of bone mass, skeletal microstructure integrity and mineralization reaction and attenuated fatty marrow histopathology. Ex vivo, miR-29a increased osteogenic differentiation capacity and alleviated the glucocorticoid-induced promotion of adipocyte formation in primary bone-marrow mesenchymal progenitor cell cultures. Through inhibition of histone deacetylase 4 (HDAC4) expression, miR-29a restored acetylated Runx2 and [beta]-catenin abundances and reduced RANKL, leptin and glucocorticoid receptor expression in glucocorticoid-mediated osteoporosis bone tissues. Taken together, glucocorticoid suppression of miR-29a signaling disturbed the balances between osteogenic and adipogenic activities, and thereby interrupted bone formation and skeletal homeostasis. miR-29a inhibition of HDAC4 stabilized the acetylation state of Runx2 and [beta]-catenin that ameliorated the detrimental effects of glucocorticoid on mineralization and lipogenesis reactions in bone tissue microenvironments. This study highlighted emerging skeletal-anabolic actions of miR-29a signaling in the progression of glucocorticoid-induced bone tissue destruction. Sustaining miR-29a actions is beneficial in protecting against glucocorticoid-mediated osteoporosis. Article History: Received 9 April 2015; Revised 8 June 2015; Accepted 29 June 2015 Article Note: (footnote) [star] Disclosure statement: The authors have nothing to disclose.
    Keywords: Genetic Engineering ; Methylprednisolone ; Leptin ; Osteoporosis ; Glucocorticoids ; Stem Cells ; Bone Density ; Gene Expression ; Steroids (Organic Compounds) ; Microrna
    ISSN: 8756-3282
    Source: Cengage Learning, Inc.
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  • 5
    Language: English
    In: Journal of Molecular Medicine, 2016, Vol.94(7), pp.755-769
    Description: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s00109-016-1422-3 Byline: Jih-Yang Ko (1), Yi-Chih Sun (2,3,4), Wen-Chin Li (2,3,4), Feng-Sheng Wang (2,3,4) Keywords: Osteoarthritis; HSP60; SOX9; Ubiquitination Abstract: Abstract Articular cartilage integrity loss is a prominently deleterious feature of osteoarthritis (OA). The mechanistic underlying the development of OA warrants characterization. Heat shock proteins (HSPs), members of the chaperone family, reportedly orchestrate tissue homeostasis and remodeling in response to detrimental stress. This study was undertaken to characterize the biological role of HSP60 in the pathogenesis of OA knee. Articular specimens from OA knee patients displayed severe articular damage histopathology concomitant with low HSP60 concentrations in cartilage and synovial fluid compared to non-OA patients. In vitro, a gain of HSP60 signaling counteracted the IL-1[beta]-mediated suppression of mitochondrial biogenesis, chondrogenic transcription factor SOX9, and cartilage matrix expression of human chondrocytes cultures. Transgenic mice that overexpressed human HSP60 (TgHSP60) had higher chondrocyte proliferation and thicker articular cartilage than wild-type mice. In collagenase-induced OA knees, analyses of CatWalk, 2-deoxyglucose-probed fluorescence imaging, and [micro]CT revealed that affected knees of TgHSP60 mice showed minor footprint irregularity, joint inflammation, and osteophyte formation. HSP60 overexpression also alleviated the histopathology of cartilage damage, synovial hypervascularization, and macrophage infiltration within joint lesions. Intra-articular administration of exogenous HSP60 ameliorated the pathogenesis of cartilage deterioration, synovitis, and osteophyte accumulation, thereby improving gait profiles of the collagenase-injured knees. HSP60 signaling maintains SOX9 levels by attenuating SOX9 hyper-ubiquitination of affected joints. Taken together, HSP60 deficiency in articular compartments was relevant to OA knee incidence. Sustained HSP60 signaling is favorable to mitigate the progression of OA. This study highlights the joint-anabolic actions of HSP60 and provides perspective on its therapeutic potential for OA. Key messages HSP60 deficiency is relevant to the existence of end-stage knee osteoarthritis. HSP60 overexpression attenuates cartilage matrix loss of inflammatory chondrocytes. HSP60 transgenic mice showed mild articular injury during knee osteoarthritis. HSP60 maintains knee joint homeostasis through reducing SOX9 ubiquitination. Control of cartilage-anabolic regulator HSP60 ameliorates knee osteoarthritis. Author Affiliation: (1) Department of Orthopedic Surgery, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan (2) Core Laboratory for Phenomics and Diagnostics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan (3) Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Kaohsiung, Taiwan (4) Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital, 123 Ta-Pei Road, Niao Sung District, Kaohsiung, 833, Taiwan Article History: Registration Date: 18/04/2016 Received Date: 19/01/2016 Accepted Date: 17/04/2016 Online Date: 27/04/2016 Article note: J.-Y. Ko and Y.-C. Sun contributed equally to this work. Electronic supplementary material The online version of this article (doi: 10.1007/s00109-016-1422-3) contains supplementary material, which is available to authorized users.
    Keywords: Osteoarthritis ; HSP60 ; SOX9 ; Ubiquitination
    ISSN: 0946-2716
    E-ISSN: 1432-1440
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  • 6
    Language: English
    In: Journal of Surgical Research, 2011, Vol.171(1), pp.114-119
    Description: Strong vascular endothelial growth factor (VEGF) expression of osteoprogenitors was found in callus site during fracture healing. The aim of this study was to investigate whether VEGF modulates the angiogenesis and osteogenesis in shockwave-promoted fracture healing in rabbits. Twenty-seven Japanese rabbits were used in the study. A fracture of left tibia with 5 mm gap was created, and the fracture was stabilized with an external fixator. The rabbits were randomly divided into three groups. Group I was the control group and received no shockwave therapy. Group II received shockwave therapy, and group III was pretreated with bevacizumab, a monoclonal antibody against VEGF, before receiving shockwave. Radiographs of the tibia were obtained at 1, 4, and 8 wk. Bone mineral density was performed at 8 wk. The rabbits were euthanized at 8 wk, and the bone specimens were subjected to histomorphological examination and immunohistochemical analysis. At 8 wk, radiographs showed considerably better bone healing and remodeling of the fracture in group II compared with groups I and III, whereas no discernable difference was noted between group I and group III. The BMD values were significantly higher in group II than groups I and III, but no difference noted between group I and group III. In histomorphological examination, significant increases in bone tissue was were noted in group II compared with groups I and III, but no difference was noted between group I and group III. In immunohistochemical analysis, significant increases in VEGF, vWF, PCNA, BMP-2 and osteocalcin, and a decrease in TUNEL expression were observed in group II compared with groups I and III, but no statistical difference was noted between group I and group III. Significant increases in VEGF and angiogenic and osteogenic growth factors were noted in shockwave-promoted bone healing. Pre-treatment with bevacizumab inhibited VEGF and in turn, attenuated the effect of shockwave. It appears that VEGF modulates angiogenesis and osteogenesis in shockwave-promoted bone healing in rabbits.
    Keywords: Vegf ; Angiogenesis ; Osteogenesis ; Fracture ; Shockwave
    ISSN: 0022-4804
    E-ISSN: 1095-8673
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  • 7
    Language: English
    In: BMC Musculoskeletal Disorders, Jan 28, 2013, Vol.14(1)
    Description: Background Extracorporeal shockwave therapy (ESWT) shows chondroprotective effect in osteoarthritis of the rat knees. However, the ideal number of ESWT is unknown. This study investigated the effects of different numbers of ESWT in osteoarthritis of the knee in rats. Methods Forty-five male Sprague-Dawley rats were divided into five groups. Group I underwent sham arthrotomy without anterior cruciate ligament transection (ACLT) or medial meniscectomy (MM) and received no ESWT. Group II underwent ACLT + MM and received no ESWT. Group III underwent ACLT + MM, and received ESWT once a week for one treatment. Group IV underwent ACLT + MM and received ESWT twice a week for 2 treatments. Group V underwent ACLT + MM and received ESWT three times a week for 3 treatments. Each treatment consisted of 800 impulses of shockwave at 14 Kv to the medial tibia condyle. The evaluations included radiographs of the knee, histomorphological examination and immunohistochemical analysis at 12 weeks. Results At 12 weeks, group II and V showed more radiographic arthritis than groups I, III and IV. On histomorphological examination, the Safranin O matrix staining in groups III and IV are significantly better than in groups II and V, and the Mankin scores in groups III and IV are less than groups II and V. Groups III and IV showed significant decreases of Mankin score and increase of Safranin O stain as compared to group I. Group V showed significant increases of Mankin score and a decrease of Safranin O stain as compared to group II. In articular cartilage, group II showed significant increase of MMP13 and decrease of collagen II as compared to group I. Groups III and IV showed significant decrease of MMP13 and increase of collagen II as compared to group I. Group V showed significant increase of MMP13 and decrease of collagen II as compared to group II. In subchondral bone, vWF, VEGF, BMP-2 and osteocalcin significantly decreased in groups II and V, but increased in groups III and IV relative to group I. Conclusions ESWT shows a number of treatment related chondroproctective effect in osteoarthritis of the knee in rats. Keywords: Shockwave, Number of treatment, Chondroprotective, Osteoarthritis, Knee, Rats
    Keywords: Vascular Endothelial Growth Factor ; Lithotripsy ; Osteoarthritis ; Knee Joint ; Articular Cartilage
    ISSN: 1471-2474
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  • 8
    Language: English
    In: Journal of Surgical Research, December 2011, Vol.171(2), pp.601-608
    Description: This study investigated the effects of extracorporeal shockwave technology (ESWT) in osteoarthritis of the knee in rats. Thirty-six Sprague-Dawley rats were randomly divided into three groups with 12 rats in each group. Group I was the control group and received neither anterior cruciate ligament transection (ACLT) nor ESWT. In groups II and III, ACLT was performed in left knee and osteoarthritis (OA) was verified at 12 wk. Group II received no ESWT, and group III received ESWT at 12 wk after ACLT. Radiographs and bone mineral density (BMD) were obtained at 0, 12, and 24 wk. The animals were sacrificed at 24 wk. One half of the animals were subjected to bone strength test, and the other half for histomorphologic examination and immunohistochemical analysis. Radiographs of the left knee showed progressive OA changes at 12 and 24 wk in group II, whereas, very subtle OA changes were noted in group I and group III. BMD and bone strength were significantly lower in group II compared with groups I and III, but no difference was noted between group I and group III. The cartilage degradations were significantly higher in group II compared with groups I and III, but no difference was noted between group I and group III. The subchondral bone remodeling was significantly less pronounced in group II compared with groups I and III, but no difference was noted between group I and group III. Application of ESWT to the subchondral bone of the medial tibia condyle showed regression of osteoarthritis of the knee in rats.
    Keywords: Osteoarthritis ; Knee ; Subchondral Bone ; Shockwave
    ISSN: 0022-4804
    E-ISSN: 1095-8673
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  • 9
    Language: English
    In: Arthroscopy: The Journal of Arthroscopic and Related Surgery, 2010, Vol.26(7), pp.968-976
    Description: This study investigated the effect of plasmid cytomegalovirus (pCMV)–bone morphogenetic protein 2 (BMP-2) gene therapy on the healing of the tendon-bone interface after anterior cruciate ligament (ACL) reconstruction in rabbits. The pCMV–BMP-2 was synthesized from full-length human BMP-2 complementary deoxyribonucleic acid, followed by cloning into pCMV Script vector (Clontech Laboratories, Inc., San Jose, CA), and was delivered by a xenogeneic (rat kidney) cell line. The ACL was reconstructed by the transfer of extensor digital tendon in the proximal tibia. In the study group the pCMV–BMP-2 gene–transfected normal rat kidney cells mixed with calcium alginate gel were placed at the tendon-bone interface, whereas no pCMV–BMP-2 was used in the control group. The evaluations included radiography, bone mineral density, magnetic resonance imaging, biomechanical study, histologic examination, and immunohistochemical analysis. Bone mineral density showed no significant difference between the groups ( 〉 .05). Magnetic resonance imaging showed significantly better contact between tendon and bone in the study group compared with the control group ( 〈 .0001). In the biomechanical study, significantly higher failure load and maximal graft tension were noted in the study group compared with the control group ( = .034). The modes of graft failure were rupture of the tendon proper in 78% and graft pullout from the bone tunnel in 22% of specimens in the study group versus graft rupture in 22% and graft pullout in 78% in the control group ( = .018). On histologic examination, the study group showed significantly better integration between tendon and bone, as well as more bone tissue around the tendon graft, than the control group ( = .0004). On immunohistochemical analysis, the study group showed significantly higher expressions of von Willebrand factor, vascular endothelial growth factor, proliferation cell nuclear antigen, and BMP-2 than the control group ( 〈 .05). The pCMV–BMP-2 gene therapy significantly improved the healing of tendon to bone and promoted angiogenesis and osteogenesis at the tendon-bone interface after ACL reconstruction in the rabbit model. Application of pCMV–BMP-2 gene therapy may be an effective adjunct therapy in ACL reconstruction.
    Keywords: Transfection ; Anterior Cruciate Ligament -- Surgery ; Bone Morphogenetic Protein 2 -- Genetics ; Cytomegalovirus -- Genetics ; Genetic Therapy -- Methods ; Plasmids -- Genetics ; Reconstructive Surgical Procedures -- Methods;
    ISSN: 0749-8063
    E-ISSN: 1526-3231
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  • 10
    Language: English
    In: Bone, December 2015, Vol.81, pp.80-88
    Description: Glucocorticoid treatment reportedly increases the morbidity of osteoporotic or osteonecrotic disorders. Exacerbated bone acquisition and escalated marrow adipogenesis are prominent pathological features of glucocorticoid-mediated skeletal disorders. MicroRNAs reportedly modulate tissue metabolism and remodeling. This study was undertaken to investigate the biological roles of microRNA-29a (miR-29a) in skeletal and fat metabolism in the pathogenesis of glucocorticoid-induced osteoporosis. Transgenic mice overexpressing miR-29a precursor or wild-type mice were given methylprednisolone. Bone mass, microarchitecture and histology were assessed by dual energy X-ray absorptiometry, μCT and histomorphometry. Differential gene expression and signaling components were delineated by quantitative RT-PCR and immunoblotting. Glucocorticoid treatment accelerated bone loss and marrow fat accumulation in association with decreased miR-29a expression. The miR-29a transgenic mice had high bone mineral density, trabecular microarchitecture and cortical thickness. miR-29a overexpression mitigated the glucocorticoid-induced impediment of bone mass, skeletal microstructure integrity and mineralization reaction and attenuated fatty marrow histopathology. Ex vivo, miR-29a increased osteogenic differentiation capacity and alleviated the glucocorticoid-induced promotion of adipocyte formation in primary bone-marrow mesenchymal progenitor cell cultures. Through inhibition of histone deacetylase 4 (HDAC4) expression, miR-29a restored acetylated Runx2 and β-catenin abundances and reduced RANKL, leptin and glucocorticoid receptor expression in glucocorticoid-mediated osteoporosis bone tissues. Taken together, glucocorticoid suppression of miR-29a signaling disturbed the balances between osteogenic and adipogenic activities, and thereby interrupted bone formation and skeletal homeostasis. miR-29a inhibition of HDAC4 stabilized the acetylation state of Runx2 and β-catenin that ameliorated the detrimental effects of glucocorticoid on mineralization and lipogenesis reactions in bone tissue microenvironments. This study highlighted emerging skeletal-anabolic actions of miR-29a signaling in the progression of glucocorticoid-induced bone tissue destruction. Sustaining miR-29a actions is beneficial in protecting against glucocorticoid-mediated osteoporosis.
    Keywords: Mir-29a ; Bone Loss ; Marrow Fat ; Hdac4 ; Runx2 Acetylation ; Medicine ; Anatomy & Physiology
    ISSN: 8756-3282
    E-ISSN: 1873-2763
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