Gene expression profile induced by ovariectomy in bone marrow of mice: A functional approach to identify new candidate genes associated to osteoporosis risk in women

Pineda, Begoña; Serna, Eva; Laguna-Fernández, Andrés; Noguera, Inmaculada; Panach, Layla; Hermenegildo, Carlos; Tarı́n, Juan J.; Cano, Antonio; Garcı́a-Pérez, Miguel A.

doi:10.1016/j.bone.2014.05.001

Cited by 22 publications

(16 citation statements)

References 57 publications

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“…IL-17 levels are significantly elevated in postmenopausal osteopenic or osteoporotic women compared with those in premenopausal women and are positively correlated with the sRANK ligand or the ratio of the sRANK ligand to OPG [37]. The RANK/RANKL/OPG axis is also actively regulated by B cells [38]. The surface concentration of RANKL of the marrow cells, characterized as osteoblast lineage, T cells, or B cells, was increased in estrogen-deficient postmenopausal women compared with premenopausal women.…”

Section: Bone Effects Of Estrogen Deficiencymentioning

confidence: 99%

Update on Menopausal Hormone Therapy for Fracture Prevention

Štěpán

Hruskova

Kverka

2019

Curr Osteoporos Rep

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Purpose of Review The goal of the review is to assess the appropriateness of menopausal hormone therapy (MHT) for the primary prevention of bone loss in women at elevated risk in the early years after menopause. Recent Findings Estrogen alone or combined with progestin to protect the uterus from cancer significantly reduces the risk of osteoporosis-related fractures. MHT increases type 1 collagen production and osteoblast survival and maintains the equilibrium between bone resorption and bone formation by modulating osteoblast/osteocyte and T cell regulation of osteoclasts. Estrogens have positive effects on muscle and cartilage. Estrogen, but not antiresorptive therapies, can attenuate the inflammatory bonemicroenvironment associated with estrogen deficiency. However, already on second year of administration, MHT is associated with excess breast cancer risk, increasing steadily with duration of use. Summary MHT should be considered in women with premature estrogen deficiency and increased risk of bone loss and osteoporotic fractures. However, MHT use for the prevention of bone loss is hindered by increase in breast cancer risk even in women younger than 60 years old or who are within 10 years of menopause onset.

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Section: Bone Effects Of Estrogen Deficiencymentioning

confidence: 99%

Update on Menopausal Hormone Therapy for Fracture Prevention

Štěpán

Hruskova

Kverka

2019

Curr Osteoporos Rep

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“…Osteoporosis is a polygenic disease influenced by genetic and environmental factors along with the interaction between these factors . So far, however, the majority of genes associated with osteoporosis pathogenesis remain largely anonymous . Environmental risk factors, such as low calcium intake, vitamin D deficiency, hypogonadism, hormonal inequity, aging, prior diseases, prescription medications for other diseases, and sedentary lifestyle among others, influence osteoporosis pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Novel insights into the complex architecture of osteoporosis molecular genetics

Saad

2019

Annals of the New York Academy of Sciences

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Osteoporosis is a prevalent osteodegenerative disease and silent killer linked to a decrease in bone mass and decline of bone microarchitecture, due to impaired bone matrix mineralization, raising the risk of fracture. Nevertheless, the process of bone matrix mineralization is still an unsolved mystery. Osteoporosis is a polygenic disorder associated with genetic and environmental risk factors; however, the majority of genes associated with osteoporosis remain largely unknown. Several signaling pathways regulate bone mass; therefore, dysregulation of a single signaling pathway leads to metabolic bone disease owing to high or low bone mass. Parathyroid hormone, core‐binding factor α‐1 (Cbfa1), Wnt/β‐catenin, the receptor activator of the nuclear factor kappa‐B (NF‐κB) ligand (RANKL), myostatin, and osteogenic exercise signaling pathways play pivotal roles in the regulation of bone mass. The myostatin signaling pathway increases bone resorption by activating the RANKL signaling pathway, whereas osteogenic exercise inhibits myostatin and sclerostin while inducing irisin that consequentially activates the Cbfa1 and Wnt/β‐catenin bone formation pathways. The aims of this review are to summarize what is known about osteoporosis‐related signaling pathways; define the role of these pathways in osteoporosis drug discovery; focus light on the link between bone, muscle, pancreas, and adipose integrative physiology and osteoporosis; and underline the emerging role of osteogenic exercise in the prevention of, and care for, osteoporosis, obesity, and diabetes.

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“…Genes in these women and the mouse models exhibited similar changes, including many genes related to B cell function and development. These results suggest that some of the pathogenesis of bone loss and osteoporosis diseases may be related to B cell abnormalities [29]. In our study too, we focused on the role of multiple B cell-related pathways in distraction osteogenesis, but the specific mechanisms remain to be further explored.…”

Section: Discussionmentioning

confidence: 95%

Studies on trans-sutural distraction osteogenesis-related genes based on transcriptome sequencing

Wang

Xue

Tong

et al. 2020

Preprint

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Trans-sutural distraction osteogenesis (TSDO) is an important approach to improve mid-face hypoplasia. In recent years, many studies have been carried out on physical mechanisms of TSDO; however, it’s specific cytological and molecular mechanisms are still unclear. In this study, we performed transcriptome sequencing analysis in Sprague Dawley rats at 1 and 2 weeks after suture osteogenesis and compared RNA expression levels between experimental and control groups. At one week, enrichment pathways were mainly up-regulated in muscle- and bone-related pathways. By contrast, pathways of the immune system showed a state of inhibition and down-regulation, especially for B cells; the main immune pathways showed significant down-regulation. However, two weeks later, the experimental group showed positive up-regulation of the pathways related to DNA synthesis and replication, cell cycle, and chromosome replication. At the same time, the immune pathways that were down-regulated in the first week were up-regulated in the second week. In other words, the up-regulated muscle- and bone-related pathways show opposite trends. The expression of bone- and myogenesis-related transcriptome was up-regulated and the immune-related pathways were down-regulated in the experimental group at 1 week. At 2 weeks, the pathways related to bone- and muscle were down-regulated, while those related to cell cycle regulation and DNA replication were up-regulated. These results suggest that musculoskeletal-related molecules may play an important role during suture osteogenesis at 1 week, and immune regulation may be involved in this process; however, at 2 weeks, molecules related to cell proliferation and replication may be a major role.

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Gene expression profile induced by ovariectomy in bone marrow of mice: A functional approach to identify new candidate genes associated to osteoporosis risk in women

Cited by 22 publications

References 57 publications

Update on Menopausal Hormone Therapy for Fracture Prevention

Update on Menopausal Hormone Therapy for Fracture Prevention

Novel insights into the complex architecture of osteoporosis molecular genetics

Studies on trans-sutural distraction osteogenesis-related genes based on transcriptome sequencing

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