Protocols for "Shotgun Metagenomics of 361 elderly women reveals gut microbiome change in bone mass loss" v1 (protocols.io.bqwwmxfe)

protocols.io ◽  
2020 ◽  
Author(s):  
Qi Wang ◽  
Qiang Sun ◽  
Xiaoping Li ◽  
Zhefeng Wang ◽  
Haotian Zheng ◽  
...  
Keyword(s):  
Bone Mass ◽  
Mass Loss ◽  
Gut Microbiome ◽  
Elderly Women ◽  
Shotgun Metagenomics ◽  
Bone Mass Loss

scholarly journals Shotgun Metagenomics of 361 elderly women reveals gut microbiome change in bone mass loss

2019 ◽  
Author(s):  
Qi Wang ◽  
Qiang Sun ◽  
Xiaoping Li ◽  
Zhefeng Wang ◽  
Haotian Zheng ◽  
...  
Keyword(s):  
Bone Mass ◽  
Mass Loss ◽  
Gut Microbiome ◽  
Elderly Women ◽  
The Elderly ◽  
Intestinal Microbiome ◽  
Mineral Density ◽  
Shotgun Metagenomics ◽  
Bone Mass Loss ◽  
Microbiome Data

AbstractBone mass loss contributes to the risk of bone fracture in the elderly. Many factors including age, obesity, estrogen and diet, are associated with bone mass loss. Mice studies suggest that the intestinal microbiome might influence the bone mass by regulating the immune system, however there has been little evidence from human studies.We have recruited 361 Chinese elderly women to collect data for a metagenomic-wide association study (MWAS) to investigate the influence of the gut microbiome on bone health. Gut microbiome data were produced using BGISEQ500 sequencing, BMD was calculated using Hologic dual energy X-ray machine, BMI (Body Mass Index) and age were also provided. This therefore data allows exploration of gut microbiome diversity and links to bone mass loss, as well as microbial species and modules as markers for bone mineral density. Making these data potentially useful in studying the role the gut microbiota might play in bone mass loss and offering exploration into the bone mass loss process.

scholarly journals Linking gut microbiome to bone mineral density: a shotgun metagenomic dataset from 361 elderly women

Gigabyte ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Qi Wang ◽  
Qiang Sun ◽  
Xiaoping Li ◽  
Zhefeng Wang ◽  
Haotian Zheng ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Mass ◽  
Mass Loss ◽  
Bone Mineral ◽  
Gut Microbiome ◽  
Elderly Women ◽  
The Elderly ◽  
Sequencing Data ◽  
Mineral Density ◽  
Bone Mass Loss

Bone mass loss contributes to the risk of bone fracture in the elderly. Many factors including age, obesity, estrogen and diet, are associated with bone mass loss. Mice studies suggested that the gut microbiome might affect the bone mass by regulating the immune system. However, there has been little evidence from human studies. Bone loss increases after menopause. Therefore, we have recruited 361 Chinese post-menopausal women to collect their fecal samples and metadata to conduct a metagenome-wide association study (MWAS) to investigate the influence of the gut microbiome on bone health. Gut microbiome sequencing data were produced using the BGISEQ-500 sequencer. Bone mineral density (BMD) was calculated using a Hologic dual energy X-ray machine, and body mass index (BMI) and age were also recorded. This collected data allows exploration of the gut microbial diversity and their links to bone mass loss as well as to microbial markers for bone mineral density. In addition, these data are potentially useful in studying the role that the gut microbiota might play in bone mass loss and in exploring the process of bone mass loss.

Zoledronic acid modulates osteoclast apoptosis through activation of the NF-κB signaling pathway in ovariectomized rats

2021 ◽  
pp. 153537022110110
Author(s):  
Yu-Ting Cheng ◽  
Jian Liao ◽  
Qian Zhou ◽  
Hua Huo ◽  
Lucas Zellmer ◽  
...  
Keyword(s):  
Zoledronic Acid ◽  
Bone Mass ◽  
Mass Loss ◽  
Ovariectomized Rats ◽  
Therapeutic Effects ◽  
Bone Mass Loss ◽  
Cellular Effects ◽  
Protein Levels ◽  
Adverse Factor ◽  
Osteoclast Apoptosis

Bone mass loss (osteoporosis) seen in postmenopausal women is an adverse factor for implant denture. Using an ovariectomized rat model, we studied the mechanism of estrogen-deficiency-caused bone loss and the therapeutic effect of Zoledronic acid. We observed that ovariectomized-caused resorption of bone tissue in the mandible was evident at four weeks and had not fully recovered by 12 weeks post-ovariectomized compared with the sham-operated controls. Further evaluation with a TUNEL assay showed ovariectomized enhanced apoptosis of osteoblasts but inhibited apoptosis of osteoclasts in the mandible. Zoledronic acid given subcutaneously as a single low dose was shown to counteract both of these ovariectomized effects. Immunohistochemical staining showed that ovariectomized induced the protein levels of RANKL and the 65-kD subunit of the NF-κB complex mainly in osteoclasts, as confirmed by staining for TRAP, a marker for osteoclasts, whereas zoledronic acid inhibited these inductions. Western blotting showed that the levels of RANKL, p65, as well as the phosphorylated form of p65, and IκB-α were all higher in the ovariectomized group than in the sham and ovariectomized + zoledronic acid groups at both the 4th- and 12th-week time points in the mandible. These data collectively suggest that ovariectomized causes bone mass loss by enhancing apoptosis of osteoblasts and inhibiting apoptosis of osteoclasts. In osteoclasts, these cellular effects may be achieved by activating RANKL-NF-κB signalling. Moreover, zoledronic acid elicits its therapeutic effects in the mandible by counteracting these cellular and molecular consequences of ovariectomized.

scholarly journals Bromodomain Protein BRD4 Accelerates Glucocorticoid Dysregulation of Bone Mass and Marrow Adiposis by Modulating H3K9 and Foxp1

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1500
Author(s):  
Feng-Sheng Wang ◽  
Yu-Shan Chen ◽  
Jih-Yang Ko ◽  
Chung-Wen Kuo ◽  
Huei-Jing Ke ◽  
...  
Keyword(s):  
Bone Mass ◽  
Mass Loss ◽  
Osteogenic Differentiation ◽  
Progenitor Cells ◽  
Mesenchymal Progenitor Cells ◽  
Marrow Fat ◽  
Bone Mass Loss ◽  
Brd4 Inhibition ◽  
The Cost

Glucocorticoid provokes bone mass loss and fatty marrow, accelerating osteoporosis development. Bromodomain protein BRD4, an acetyl–histone-binding chromatin reader, regulates stem cell and tissue homeostasis. We uncovered that glucocorticoid inhibited acetyl Lys-9 at the histone 3 (H3K9ac)-binding Runx2 promoter and decreased osteogenic differentiation, whereas bromodomain protein 4 (BRD4) and adipocyte formation were upregulated in bone-marrow mesenchymal progenitor cells. BRD4 knockdown improved H3K9ac occupation at the Runx2 promoter and osteogenesis, but attenuated glucocorticoid-mediated adipocyte formation together with the unaffected H3K9ac-binding PPARγ2 promoter. BRD4 regulated epigenome related to fatty acid metabolism and the forkhead box P1 (Foxp1) pathway, which occupied the PPARγ2 promoter to modulate glucocorticoid-induced adipocytic activity. In vivo, BRD4 inhibitor JQ-1 treatment mitigated methylprednisolone-induced suppression of bone mass, trabecular microstructure, mineral acquisition, and osteogenic differentiation. Foxp1 signaling, marrow fat, and adipocyte formation in glucocorticoid-treated skeleton were reversed upon JQ-1 treatment. Taken together, glucocorticoid-induced H3K9 hypoacetylation augmented BRD4 action to Foxp1, which steered mesenchymal progenitor cells toward adipocytes at the cost of osteogenic differentiation in osteoporotic skeletons. BRD4 inhibition slowed bone mass loss and marrow adiposity. Collective investigations convey a new epigenetic insight into acetyl histone reader BRD4 control of osteogenesis and adipogenesis in skeleton, and highlight the remedial effects of the BRD4 inhibitor on glucocorticoid-induced osteoporosis.

Protective effect of myo-inositol hexaphosphate (phytate) on bone mass loss in postmenopausal women

2012 ◽  
Vol 52 (2) ◽  
pp. 717-726 ◽  
Author(s):  
Ángel A. López-González ◽  
Félix Grases ◽  
Nieves Monroy ◽  
Bartolome Marí ◽  
Mª Teófila Vicente-Herrero ◽  
...  
Keyword(s):  
Bone Mass ◽  
Protective Effect ◽  
Mass Loss ◽  
Postmenopausal Women ◽  
Inositol Hexaphosphate ◽  
Bone Mass Loss

Effectiveness and safety of medium- and long-term elcatonin use in the prevention and treatment of bone mass loss

1995 ◽  
Vol 56 (4) ◽  
pp. 385-399 ◽  
Author(s):  
Fernando Escobar Jiménez ◽  
Jose Miguel Aranburu Albizuri ◽  
Jose Maria Almirall Alier ◽  
Jorge Julian Molina Soto ◽  
Alfredo Gracia Canales
Keyword(s):  
Bone Mass ◽  
Mass Loss ◽  
Bone Mass Loss ◽  
Prevention And Treatment
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