Retraction of 'In vivo and in vitro effects of PTH1‐34 on osteogenic and adipogenic differentiation of human bone marrow‐derived mesenchymal stem cells through regulating microRNA‐155'

Han, Huansheng; Ju, Fang; Geng, Shuo

doi:10.1002/jcb.29823

Cited by 3 publications

(3 citation statements)

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“…Microarray is a powerful tool to study the role of miRNAs and their involvement in a broad spectrum of developmental and physiological mechanisms . Although previous studies have revealed the expression of specific miRNAs in osteoporosis, these studies were limited by sample size or data integrity. Therefore, we recruited microarray and bioinformatics analyses to investigate miRNAs in a larger osteoporotic study group.…”

Section: Discussionmentioning

confidence: 99%

Noncoding RNA miR‐205‐5p mediates osteoporosis pathogenesis and osteoblast differentiation by regulating RUNX2

Huang

Zhou

et al. 2019

J of Cellular Biochemistry

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As a kind of noncoding RNAs, microRNAs (miRNAs) play important roles in disease pathogenesis by regulating gene expression. However, the molecular mechanism of miRNAs in osteoporosis remains largely unknown. In the present study, we aim to explore the genome‐wide miRNAs expression profile and the regulatory mechanism of miR‐205‐5p in osteoporosis. A total of 72 differentially expressed miRNAs were identified in osteoporosis via microarray technology and bioinformatics analysis. We focused on one of the abnormally expressed miRNAs, miR‐205‐5p, which was previously unknown in osteoporosis. Quantitative real‐time polymerase chain reaction (qRT‐PCR) results showed that miR‐205‐5p was upregulated in osteoporosis samples and its expression was gradually decreased during osteogenic differentiation. Besides, miR‐205‐5p overexpression could inhibit the activity of osteoblast markers, including collagen, type I, α 1 (COL1A1) and alkaline phosphatase (ALP) while miR‐205‐5p inhibition showed the opposite results. Moreover, bioinformatics analysis identified the potential targets of miR‐205‐5p, including runt‐related transcription factor 2 (RUNX2), SMAD1 and BCL6, etc. The dual‐luciferase reporter assay confirmed RUNX2 was directly targeted by miR‐205‐5p. Furthermore, the rescue experiments showed that RUNX2 overexpression could significantly weaken the effect of miR‐205‐5p on osteoblast markers, indicating that miR‐205‐5p may inhibit osteogenic differentiation by targeting RUNX2.

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Section: Discussionmentioning

confidence: 99%

Noncoding RNA miR‐205‐5p mediates osteoporosis pathogenesis and osteoblast differentiation by regulating RUNX2

Huang

Zhou

et al. 2019

J of Cellular Biochemistry

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“…This dose of hormone is frequently used in rodents to evaluate PTH bone anabolic action. (52,53) The Indiana University Institutional Animal Care and Use Committee approved all experimental treatments described in this investigation.…”

Section: Osteocyte Outgrowth Culturesmentioning

confidence: 99%

Conditional Loss of Nmp4 in Mesenchymal Stem Progenitor Cells Enhances PTH-Induced Bone Formation

Atkinson

Adaway

Horan

et al. 2020

Journal of Bone and Mineral Research

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Activation of bone anabolic pathways is a fruitful approach for treating severe osteoporosis, yet FDA‐approved osteoanabolics, eg, parathyroid hormone (PTH), have limited efficacy. Improving their potency is a promising strategy for maximizing bone anabolic output. Nmp4 (Nuclear Matrix Protein 4) global knockout mice exhibit enhanced PTH‐induced increases in trabecular bone but display no overt baseline skeletal phenotype. Nmp4 is expressed in all tissues; therefore, to determine which cell type is responsible for driving the beneficial effects of Nmp4 inhibition, we conditionally removed this gene from cells at distinct stages of osteogenic differentiation. Nmp4‐floxed (Nmp4fl/fl) mice were crossed with mice bearing one of three Cre drivers including (i) Prx1Cre+ to remove Nmp4 from mesenchymal stem/progenitor cells (MSPCs) in long bones; (ii) BglapCre+ targeting mature osteoblasts, and (iii) Dmp1Cre+ to disable Nmp4 in osteocytes. Virgin female Cre+ and Cre− mice (10 weeks of age) were sorted into cohorts by weight and genotype. Mice were administered daily injections of either human PTH 1‐34 at 30 μg/kg or vehicle for 4 weeks or 7 weeks. Skeletal response was assessed using dual‐energy X‐ray absorptiometry, micro‐computed tomography, bone histomorphometry, and serum analysis for remodeling markers. Nmp4fl/fl;Prx1Cre+ mice virtually phenocopied the global Nmp4−/− skeleton in the femur, ie, a mild baseline phenotype but significantly enhanced PTH‐induced increase in femur trabecular bone volume/total volume (BV/TV) compared with their Nmp4fl/fl;Prx1Cre− controls. This was not observed in the spine, where Prrx1 is not expressed. Heightened response to PTH was coincident with enhanced bone formation. Conditional loss of Nmp4 from the mature osteoblasts (Nmp4fl/fl;BglapCre+) failed to increase BV/TV or enhance PTH response. However, conditional disabling of Nmp4 in osteocytes (Nmp4fl/fl;Dmp1Cre+) increased BV/TV without boosting response to hormone under our experimental regimen. We conclude that Nmp4−/− Prx1‐expressing MSPCs drive the improved response to PTH therapy and that this gene has stage‐specific effects on osteoanabolism. © 2022 American Society for Bone and Mineral Research (ASBMR).

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“…Microsensor systems are already in use regarding culture stable constants, such as O 2 , pH, glucose, and lactate (Kieninger et al, ; Zhang et al, ). Live‐monitoring of specific cell activity markers would provide unique insights into cellular interactions within a dynamic mechanical and chemical environment (Kieninger et al, ), such as osteoblast, osteocyte, osteoclast, or adipocyte markers (e.g., alkaline phosphatase, osteocalcin, sclerostin, Trap5b, adiponectin, and FABP4; Daniele et al, ; Han, Ju, & Geng, ; Wedrychowicz, Sztefko, & Starzyk, ; Zhu et al, ). Among other approaches, organic electrochemical transistor (OECT) technology appears to be a strong candidate for this application (Inal et al, ; Khodagholy et al, ; Rivnay et al, ; Rivnay et al, ).…”

Section: Future Challenges and Strategymentioning

confidence: 99%

Strategy for achieving standardized bone models

Hadida

Marchat

2019

Biotech & Bioengineering

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Reliably producing functional in vitro organ models, such as organ‐on‐chip systems, has the potential to considerably advance biology research, drug development time, and resource efficiency. However, despite the ongoing major progress in the field, three‐dimensional bone tissue models remain elusive. In this review, we specifically investigate the control of perfusion flow effects as the missing link between isolated culture systems and scientifically exploitable bone models and propose a roadmap toward this goal.

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Retraction of 'In vivo and in vitro effects of PTH1‐34 on osteogenic and adipogenic differentiation of human bone marrow‐derived mesenchymal stem cells through regulating microRNA‐155'

Cited by 3 publications

References 0 publications

Noncoding RNA miR‐205‐5p mediates osteoporosis pathogenesis and osteoblast differentiation by regulating RUNX2

Noncoding RNA miR‐205‐5p mediates osteoporosis pathogenesis and osteoblast differentiation by regulating RUNX2

Conditional Loss of Nmp4 in Mesenchymal Stem Progenitor Cells Enhances PTH-Induced Bone Formation

Strategy for achieving standardized bone models

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