scholarly journals Violations of cell-molecular mechanisms of bone remodeling under influence of glucocorticoids

2018 ◽  
Vol 9 (1) ◽  
pp. 124-129
Author(s):  
S. B. Pavlov ◽  
N. M. Babenko ◽  
M. V. Kumetchko ◽  
O. B. Litvinova
Keyword(s):  
Bone Tissue ◽  
Bone Remodeling ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Tissue Remodeling ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Interleukin 17 ◽  
Mineral Density ◽  
Bone Tissue Remodeling

The fact is disturbance of the processes of bone tissue remodeling leads to a change in the balance between synthesis and resorption of bone and the development of osteoporosis. The most common cause of secondary osteoporosis is the use of glucocorticoid therapy. The aim of this study is to investigate the cellular-molecular mechanisms of disturbance of the processes of bone remodeling regulation, reflected by hormones and intercellular mediators (for example parathyroid hormone, calcitonin, RANKL, osteoprotegerin, P-selectin, interleukin-17, transforming growth factor-β1, adiponectin and visfatin) on the background experimental glucocorticoid osteoporosis. The experimental study carried out in two groups of white female rats. Disturbance of bone tissue remodeling was verified by histological examination of the femoral head, vertebrae of the thoracic and lumbar spine of rats and the measurement of bone density. The study of the levels of hormones and intercellular mediators in the blood serum of animals was carried out by the method of enzyme immunoassay. The bone mineral density of the experimental group was reduced compared to the bone mineral density of the control group. The study of the histostructure of the femoral head and vertebrae in rats of the experimental group in comparison with the animals of the control group revealed changes in the structural organization of bone tissue, confirmed by histomorphometry, indicating inhibition of the processes of osteosynthesis. The article analyzes the nature of the involvement of hormones and cytokines in pathogenetic mechanisms of development of bone tissue disorders. The levels of cytokines RANKL, osteoprotegerin, interleukin-17 and calcitonin in the blood serum of animals of the group with the violation of bone tissue remodeling by glucocorticoids were higher than in intact animals. Serum levels of P-selectin, parathyroid hormone, transforming growth factor-β1, adiponectin and visfatin were lower than similar levels in animals from the control group. The use of glucocorticoids increases the expression of RANKL and inhibits the synthesis of osteoprotegerin, resulting in stimulation of bone resorption. The effect of glucocorticoids in the experimental model is realized by changing the production of the studied hormones, cytokines and adhesion molecules. These changes stimulate the apoptosis of osteoblasts and inhibit their proliferation and differentiation, which is another mechanism of bone loss. Correlations found during the study reflect the relationship in the system of regulation of bone tissue remodeling under the influence of glucocorticoids. A complex system for regulating bone remodeling, which includes many regulatory pathways and their interactions, requires further study.

Refraction Introscopy at Synchronized Radiation: Expansion of Possibilities for Visualization of Bone Tissue Remodeling

2010 ◽  
Vol 17 (2) ◽  
pp. 78-82
Author(s):  
D K Pogorelyi ◽  
A N Torgashin ◽  
K M Podurets ◽  
S S Rodionova
Keyword(s):  
Bone Tissue ◽  
Bone Remodeling ◽  
Tissue Remodeling ◽  
Laboratory Animals ◽  
Experimental Animals ◽  
Rat Tibia ◽  
Bone Structures ◽  
Bone Tissue Remodeling

Method of refraction introscopy at synchronized radiation for visualization of bone structures and allografts in laboratory animals was described. The aim of study was adaptation of method for the study of alloigrafts in bones of laboratory anomals. Method was approved at 150 samples of rat tibia. It was shown that use of refraction introscopy at synchronized radiation enabled properly to visualize the borders of allografts and own bone tissue of rat. Method may be recommended for the study of bone remodeling dynamics in experimental animals during long term after operation.

scholarly journals Effect of Collagen Hydrolysates from Silver Carp Skin (Hypophthalmichthys molitrix) on Osteoporosis in Chronologically Aged Mice: Increasing Bone Remodeling

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1434 ◽  
Author(s):  
Ling Zhang ◽  
Siqi Zhang ◽  
Hongdong Song ◽  
Bo Li
Keyword(s):  
Body Weight ◽  
Bone Remodeling ◽  
Transforming Growth Factor ◽  
Silver Carp ◽  
Daily Intake ◽  
Transforming Growth Factor Β1 ◽  
Tartrate Resistant Acid Phosphatase ◽  
Hypophthalmichthys Molitrix ◽  
Mineral Density ◽  
Collagen Hydrolysates

Osteoporosis is a common skeletal disorder in humans and gelatin hydrolysates from mammals have been reported to improve osteoporosis. In this study, 13-month-old mice were used to evaluate the effects of collagen hydrolysates (CHs) from silver carp skin on osteoporosis. No significant differences were observed in mice body weight, spleen or thymus indices after daily intake of antioxidant collagen hydrolysates (ACH; 200 mg/kg body weight (bw) (LACH), 400 mg/kg bw (MACH), 800 mg/kg bw (HACH)), collagenase hydrolyzed collagen hydrolysates (CCH) or proline (400 mg/kg body weight) for eight weeks, respectively. ACH tended to improve bone mineral density, increase bone hydroxyproline content, enhance alkaline phosphatase (ALP) level and reduce tartrate-resistant acid phosphatase 5b (TRAP-5b) activity in serum, with significant differences observed between the MACH and model groups (p < 0.05). ACH exerted a better effect on osteoporosis than CCH at the identical dose, whereas proline had no significant effect on repairing osteoporosis compared to the model group. Western blotting results demonstrated that CHs mainly increased bone remodeling by stimulating the transforming growth factor β1 (TGF-β1)/Smad signaling pathway and improving the interaction between collagen and α2β1 integrin. The results indicated that CHs from fish could be applied to alleviate osteoporosis or treat bone loss.

scholarly journals Long-term resveratrol treatment prevents ovariectomy-induced osteopenia in rats without hyperplastic effects on the uterus

2013 ◽  
Vol 111 (5) ◽  
pp. 836-846 ◽  
Author(s):  
Haifeng Zhao ◽  
Xuemin Li ◽  
Na Li ◽  
Tiantian Liu ◽  
Juan Liu ◽  
...  
Keyword(s):  
Dose Response ◽  
Transforming Growth Factor ◽  
Biological Activities ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Mineral Density ◽  
Trabecular Microarchitecture ◽  
Protein Ratio ◽  
Ovx Rats

Resveratrol (Res), a polyphenol that is abundant in many medicinal plants and is a selective oestrogen receptor modulator, exhibits multiple biological activities. In the present study, we determined whether Res prevents oestrogen deficiency-induced osteopenia and whether Res administration decreases pathological changes in the endometrium and lumen of the uterus compared with oestradiol replacement therapy (ERT). A total of sixty 3–4-month-old female Wistar rats were randomly divided into a sham-operated group (Sham) and five ovariectomy (OVX) subgroups, i.e. OVX rats as a control group (OVX); OVX rats receiving oestradiol valerate (ERT, 0·8 mg/kg); and OVX rats receiving Res 20, 40 and 80 mg/kg. Daily oral administration was initiated at week 2 after OVX for 12 weeks. A dose–response difference was observed in the effects of Res on bone mineral density (BMD) and trabecular microarchitecture. Only at the highest dose, bone loss was almost equivalent to that observed in the ERT group. The dose–response effects of Res on the biochemical parameters (alkaline phosphatase, IL-6, TNF-α and transforming growth factor-β1 concentrations in the serum as well as urinary Ca and P excretion) and the expressions of receptor activator of nuclear factor κB ligand (RANKL) and the RANKL:osteoprotegerin protein ratio in the femur were also observed. Furthermore, the thickening of the endometrium and the infiltration of lymphocytes were prevented in all the three Res-treated groups compared with the ERT group. In conclusion, Res treatment not only improves BMD and trabecular microarchitecture but also does not affect the uterus and Res might be a potential remedy for the treatment of postmenopausal osteoporosis.

MACROPHAGE SUBSETS AND MESENCHYMAL STEM CELLS IN REGULATION OF BONE TISSUE REMODELING

Tsitologiya ◽  
2018 ◽  
Vol 6o (4) ◽  
pp. 252-261 ◽  
Author(s):  
E.E. Ivanyuk ◽  
◽  
S.V. Nadezhdin ◽  
L.A. Pokrovskaya ◽  
V.V. Shupletsova ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Tissue ◽  
Tissue Remodeling ◽  
Bone Tissue Remodeling ◽  
Macrophage Subsets

scholarly journals Genes associated with inflammation and bone remodeling are highly expressed in the bone of patients with the early-stage cam-type femoroacetabular impingement

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Guanying Gao ◽  
Ruiqi Wu ◽  
Rongge Liu ◽  
Jianquan Wang ◽  
Yingfang Ao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Tissue ◽  
Bone Remodeling ◽  
Femoroacetabular Impingement ◽  
Early Stage ◽  
Control Group ◽  
Tissue Samples ◽  
Expression Levels ◽  
Normal Bone ◽  
Impingement Zone

Abstract Background Recent studies have shown high expression levels of certain inflammatory, anabolic, and catabolic genes in the articular cartilage from the impingement zone of the hips with femoroacetabular impingement (FAI), representing an increased metabolic state. Nevertheless, little is known about the molecular properties of bone tissue from the impingement zone of hips with FAI. Methods Bone tissue samples from patients with early-stage cam-type FAI were collected during hip arthroscopy for treatment of cam-type FAI. Control bone tissue samples were collected from six patients who underwent total hip replacement because of a femoral neck fracture. Quantitative real-time polymerase chain reaction (PCR) was performed to determine the gene expression associated with inflammation and bone remodeling. The differences in the gene expression in bone tissues from the patients with early-stage cam-type FAI were also evaluated based on clinical parameters. Results In all, 12 patients with early-stage cam-type FAI and six patients in the control group were included in this study. Compared to the control samples, the bone tissue samples from patients with FAI showed higher expression levels of interleukin-6 (IL-6), alkaline phosphatase (ALP), receptor activator of nuclear factor-kB ligand (RANKL), and osteoprotegerin (OPG) (P < 0.05). IL-1 expression was detected only in the control group. On the other hand, there was no significant difference in IL-8 expression between the patients with FAI and the control group. The patients with FAI having a body mass index (BMI) of >24 kg/m2 showed higher ALP expression (P < 0.05). Further, the expression of IL-6 and ALP was higher in the patients with FAI in whom the lateral center-edge angle was >30° (P < 0.05). Conclusions Our results indicated the metabolic condition of bone tissues in patients with early-stage cam-type FAI differed from that of normal bone in the femoral head-neck junction. The expression levels of the genes associated with inflammation and bone remodeling were higher in the bone tissue of patients with early-stage cam-type FAI than in the patients with normal bone tissue.

scholarly journals A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation

2021 ◽  
Vol 10 (19) ◽  
pp. 4430
Author(s):  
Grażyna Sygitowicz ◽  
Agata Maciejak-Jastrzębska ◽  
Dariusz Sitkiewicz
Keyword(s):  
Atrial Fibrillation ◽  
Molecular Mechanisms ◽  
Cardiac Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Signalling Pathways ◽  
Ang Ii ◽  
Atrial Fibrosis ◽  
Genes Encoding ◽  
Tgf Β1

The cellular and molecular mechanism involved in the pathogenesis of atrial fibrosis are highly complex. We have reviewed the literature that covers the effectors, signal transduction and physiopathogenesis concerning extracellular matrix (ECM) dysregulation and atrial fibrosis in atrial fibrillation (AF). At the molecular level: angiotensin II, transforming growth factor-β1, inflammation, and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodelling in AF. We conclude that the Ang-II-MAPK and TGF-β1-Smad signalling pathways play a major, central role in regulating atrial fibrotic remodelling in AF. The above signalling pathways induce the expression of genes encoding profibrotic molecules (MMP, CTGF, TGF-β1). An important mechanism is also the generation of reactive oxygen species. This pathway induced by the interaction of Ang II with the AT2R receptor and the activation of NADPH oxidase. Additionally, the interplay between cardiac MMPs and their endogenous tissue inhibitors of MMPs, is thought to be critical in atrial ECM metabolism and fibrosis. We also review recent evidence about the role of changes in the miRNAs expression in AF pathophysiology and their potential as therapeutic targets. Furthermore, keeping the balance between miRNA molecules exerting anti-/profibrotic effects is of key importance for the control of atrial fibrosis in AF.

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