Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Ferretti, Marzia; Cavani, Francesco; Rovedatti, L.; Checchi, Marta; Magarò, Maria Sara; Bertacchini, Jessika; Palumbo, Carla

doi:10.3390/ijms20030753

Cited by 10 publications

(12 citation statements)

References 52 publications

(59 reference statements)

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“…Both these evaluations strongly indicate that one of the possible mechanisms controlling TPTD anabolic role, is the WISP-2 up-regulation. This datum is in line with a recent work by Ferretti and coworkers (Ferretti et al, 2019) demonstrating that PTH(1-34) was actively involved in enhancing bone mass recovery, particularly in trabecular bone depleted after calcium deprivation. In the present study, as expected, a consistent decrease (about 25.5%) of osteoblast laminae surface in rats maintained in calcium-free diet occurs; such decrement is partially recovered upon the TPTD administration, in fact we found that the number of osteoblast laminae surface was increased (about 15,15%) following the active bone deposition triggering induced by the drug.…”

Section: Discussionsupporting

confidence: 91%

WISP-2 expression induced by Teriparatide treatment affects in vitro osteoblast differentiation and improves in vivo osteogenesis

Smargiassi

Bertacchini

Checchi

et al. 2020

Molecular and Cellular Endocrinology

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The Osteocyte, recognized as a major orchestrator of osteoblast and osteoclast activity, is the most important key player during bone remodeling processes. Imbalances occurring during bone remodeling, caused by hormone perturbations or by mechanical loading alterations, can induce bone pathologies such as osteoporosis. Recently, the active fraction of parathormone, PTH (1-34) or Teriparatide (TPTD), was chosen as election treatment for osteoporosis. The effect of such therapy is dependent on the temporal manner of administration. The molecular reasons why the type of administration regimen is so critical for the fate of bone remodeling are numerous and not yet well known. Our study attempts to analyze diverse signaling pathways directly activated in osteocytes upon TPTD treatment. By means of gene array analysis, we found many molecules upregulated or downregulated in osteocytes. Later, we paid attention to Wisp-2, a protein involved in the Wnt pathway, that is secreted by MLO-Y4 cells and increases upon TPTD treatment and that is able to positively influence the early phases of osteogenic differentiation. We also confirmed the pro osteogenic property of Wisp-2 during mesenchymal stem cell differentiation into the preliminary osteoblast phenotype. The same results were confirmed with an in vivo approach confirming a remarkable Wisp-2 expression in metaphyseal trabecular bone. These results highlighted the anabolic roles unrolled by osteocytes in controlling the action of neighboring cells, suggesting that the perturbation of certain signaling cascades, such as the Wnt pathway, is crucial for the positive regulation of bone formation.

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Section: Discussionsupporting

confidence: 91%

WISP-2 expression induced by Teriparatide treatment affects in vitro osteoblast differentiation and improves in vivo osteogenesis

Smargiassi

Bertacchini

Checchi

et al. 2020

Molecular and Cellular Endocrinology

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“…The magnitude of the Tb.Th difference between the D-CTR and C-PEP rats (of ~ 0.015 mm) ( Table 3), was the same as that observed in another study [39]. Animals in the C-PEP group also had a higher Cs.Th as well as a lower Tb.Sp than those in the D-CTR group ( Table 3).…”

Section: Discussionsupporting

confidence: 83%

Effects of C-peptide replacement therapy on bone microarchitecture parameters in streptozotocin-diabetic rats

Maurotti

Russo

Musolino

et al. 2020

Preprint

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Pathological pathways involved in the development of diabetic complications are still unclear.Several studies suggested a pathogenic role of C-peptide deficiency in vascular and neuropathic complications. However, to date, the role of C-peptide on diabetes-related bone loss has not been investigated. The objective of this study was to test the effects of a 6-week regimen of rat C-peptide infusion on bone by combining micro-CT imaging with histological testing.Twenty-three, four-month-old male Wistar rats were randomly divided into three groups: Normal control group; Sham diabetic control group; Diabetic plus C-peptide group. Diabetes was induced by injection of streptozotocin. Rat C-peptide was delivered via subcutaneously osmopumps. We assessed several trabecular microarchitectural parameters and cellular and matrix proteins in bone tissue sections.At the end of the study, both the normal control and diabetic plus C-peptide groups had a higher tibia weight than the diabetic control group (p = 0.05 and p = 0.02, respectively). C-peptide levels significantly and positively correlated with the trabecular thickness (r= 0.45, p=0.08) and negatively with structure model index (r= -0.40, p=0.09). Furthermore, it positively correlated with one of the histological assessments (i.e. PLIN1 score; p=0.02). Micro-CT evaluation showed significant intergroup differences in trabecular thickness (p=0.02), trabecular space (p = 0.05) and cross-sectional thickness (p=0.05). Diabetic plus C-peptide group showed a higher trabecular thickness (p<0.001), cross-sectional thickness (p=0.03) and a lower trabecular space (p=0.05) than the normal control group. Both the normal control and diabetic plus C-peptide groups had more Runx-2 and PLIN1 positive cells in comparison to the diabetic control group (p = 0.045 and p = 0.034).For the first time we demonstrated that the diabetic rats receiving rat C-peptide had higher quality of trabecular bone, than diabetic rats not receiving it. C-peptide could have a role in the prevention of diabetes-related bone loss.

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“…Tomographic measurements of isolated femora and tibiae support earlier observations about differentiated sensitivity and intensity of metabolic changes in the cortical and trabecular compartments [33][34][35]. Cortical bone tissue is less sensitive then trabecula, and any changes of vBMD and BMC, as well as differences between particular groups, are less evident and less expressed [36,37].…”

Section: Discussionsupporting

confidence: 76%

Bone losses in obese, ovariectomized rats appear to be independent from sclerostin-induced inhibition of the Wnt/β-catenin pathway

Radzki¹,

Bieńko²,

Filip³

et al. 2020

Ann Agric Environ Med.

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Introduction. Overweight and obesity, as well as a gonadal function, are pivotal factors influencing bone tissue metabolism. Materials and method. The aim of the study was to determine the effect of dietary induced obesity (DIO) on bone tissue metabolism in sham-operated (SHO) or ovariectomized (OVX) adult female Wistar rats. Additionally, the influence of DIO in SHO or OVX on the concentration of sclerostin in the blood serum was analyzed. After SHO or OVX, the rats were placed in groups (n=8) and either received a standard diet (11.5 MJ/kg) (SHO-CON; OVX-CON) or a high-energy diet (17.6 MJ/kg) (SHO-FAT; OVX-FAT). The experiment lasted for 90 days and allowed for the establishment of osteopenia in OVX females and obesity in the rats that had received the high-energy diet. Results. The results of the study demonstrate that obesity or/and ovariectomy increases the resorption of femora and tibiae, hence decreasing the densitometric and mechanical parameters affecting the bone structure in adult females rats. The strongest osteodegenerative effect was seen in the OVX-FAT females. Interestingly, the degree of bone tissue degradation caused exclusively by ovariectomy was similar to that found in the obese sham-operated rats. Conclusions. Bone losses invoked by DIO seem to be independent from the Wnt/β-catenin pathway inhibition induced by sclerostin. While further study is necessary, the obtained results suggest that the usage of sclerostin anti-body in the treatment of osteoporosis can be ineffective, and in obese patients the undertaking of such therapy should be reassessed.

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Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Cited by 10 publications

References 52 publications

WISP-2 expression induced by Teriparatide treatment affects in vitro osteoblast differentiation and improves in vivo osteogenesis

WISP-2 expression induced by Teriparatide treatment affects in vitro osteoblast differentiation and improves in vivo osteogenesis

Effects of C-peptide replacement therapy on bone microarchitecture parameters in streptozotocin-diabetic rats

Bone losses in obese, ovariectomized rats appear to be independent from sclerostin-induced inhibition of the Wnt/β-catenin pathway

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