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Molecular Biology of Osteoporosis
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Molecular Biology of Osteoporosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 2917

Special Issue Editor

Dr. Harish K. Datta

E-Mail Website
Guest Editor
Blood Sciences, South Tees Hospitals NHS Foundation Trust, Middlesbrough TS4 3BW, UK
Interests: osteoporosis; bone cells; molecular; cell signalling; therapies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Osteoporosis is one of the most common metabolic bone diseases. Osteoporotic fractures, which represent a growing economic burden on global healthcare systems, impair quality of life and increase morbidity and mortality. In health, bone homeostasis encompasses coordinated dynamic equilibrium between bone-forming cells (osteoblasts) and bone-resorbing cells (osteoclasts). Mechanical stress is crucial for bone homeostasis and decreased mechanical loading is an established cause of bone loss and osteoporosis. Osteocytes, the most abundant and long-lived bone cells, are terminally differentiated osteoblasts that have a mechanosensory role and have emerged as a master regular of bone homeostasis. Osteocytes produce endocrine and paracrine factors, and this activity is regulated by mechanical stress as well as osteotropic factors such as, oestrogen, vitamin D and parathyroid hormone. This Special Issue explores intricate intra- and intercellular molecular signalling in bone cells in health and osteoporosis.

Dr. Harish K. Datta
Guest Editor

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Keywords

  • osteoporosis
  • bone
  • signalling
  • molecular
  • fractures
  • endocrine
  • paracrine

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Published Papers (2 papers)

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Research

14 pages, 1944 KiB  
Article
The DLEU2–miR-15a–16-1 Cluster Is a Determinant of Bone Microarchitecture and Strength in Postmenopausal Women and Mice
by Sjur Reppe, Janne Elin Reseland, Vid Prijatelj, Michael Prediger, Liebert Parreiras Nogueira, Tor Paaske Utheim, Fernando Rivadeneira, Kaare M. Gautvik and Harish Kumar Datta
Int. J. Mol. Sci. 2024, 25(23), 12724; https://doi.org/10.3390/ijms252312724 - 27 Nov 2024
Viewed by 807
Abstract
This study explores how select microRNAs (miRNAs) influence bone structure in humans and in transgenic mice. In trabecular bone biopsies from 84 postmenopausal women (healthy, osteopenic, and osteoporotic), we demonstrate that DLEU2 (deleted in lymphocytic leukemia 2)-encoded miR-15a-5p is strongly positively associated with [...] Read more.
This study explores how select microRNAs (miRNAs) influence bone structure in humans and in transgenic mice. In trabecular bone biopsies from 84 postmenopausal women (healthy, osteopenic, and osteoporotic), we demonstrate that DLEU2 (deleted in lymphocytic leukemia 2)-encoded miR-15a-5p is strongly positively associated with bone mineral density (BMD) at different skeletal sites. In bone transcriptome analyses, miR-15a-5p levels correlated positively with the osteocyte characteristic transcripts SOST (encoding sclerostin) and MEPE (Matrix Extracellular Phosphoglycoprotein), while the related miR-15b-5p showed a negative association with BMD and osteoblast markers. The data imply that these miRNAs have opposite roles in bone remodeling with distinct actions on bone cells. Expression quantitative trait loci (eQTL) variants confirmed earlier DLEU2 associations. Furthermore, a novel variant (rs12585295) showed high localization with transcriptionally active chromatin states in osteoblast primary cell cultures. The supposition that DLEU2-encoded miRNAs have an important regulatory role in bone remodeling was further confirmed in a transgenic mice model showing that miR-15a/16-1-deleted mice had significantly higher percentage bone volume and trabecular number than the wild type, possibly due to prenatal actions. However, the three-point mechanical break force test of mice femurs showed a positive correlation between strength and miR-15a-5p/miR-16-5p levels, indicating differential effects on cortical and trabecular bone. Moreover, these miRNAs appear to have distinct and complex actions in mice prenatally and in adult humans, impacting BMD and microstructure by regulating bone cell transcription. However, detailed interactions between these miRNAs and their downstream mechanisms in health and disease need further clarification. Full article
(This article belongs to the Special Issue Molecular Biology of Osteoporosis)
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15 pages, 1820 KiB  
Article
Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease
by Sjur Reppe, Sveinung Gundersen, Geir K. Sandve, Yunpeng Wang, Ole A. Andreassen, Carolina Medina-Gomez, Fernando Rivadeneira, Tor P. Utheim, Eivind Hovig and Kaare M. Gautvik
Int. J. Mol. Sci. 2024, 25(10), 5554; https://doi.org/10.3390/ijms25105554 - 20 May 2024
Cited by 2 | Viewed by 1642
Abstract
Epidemiological evidence suggests existing comorbidity between postmenopausal osteoporosis (OP) and cardiovascular disease (CVD), but identification of possible shared genes is lacking. The skeletal global transcriptomes were analyzed in trans-iliac bone biopsies (n = 84) from clinically well-characterized postmenopausal women (50 to 86 years) [...] Read more.
Epidemiological evidence suggests existing comorbidity between postmenopausal osteoporosis (OP) and cardiovascular disease (CVD), but identification of possible shared genes is lacking. The skeletal global transcriptomes were analyzed in trans-iliac bone biopsies (n = 84) from clinically well-characterized postmenopausal women (50 to 86 years) without clinical CVD using microchips and RNA sequencing. One thousand transcripts highly correlated with areal bone mineral density (aBMD) were further analyzed using bioinformatics, and common genes overlapping with CVD and associated biological mechanisms, pathways and functions were identified. Fifty genes (45 mRNAs, 5 miRNAs) were discovered with established roles in oxidative stress, inflammatory response, endothelial function, fibrosis, dyslipidemia and osteoblastogenesis/calcification. These pleiotropic genes with possible CVD comorbidity functions were also present in transcriptomes of microvascular endothelial cells and cardiomyocytes and were differentially expressed between healthy and osteoporotic women with fragility fractures. The results were supported by a genetic pleiotropy-informed conditional False Discovery Rate approach identifying any overlap in single nucleotide polymorphisms (SNPs) within several genes encoding aBMD- and CVD-associated transcripts. The study provides transcriptional and genomic evidence for genes of importance for both BMD regulation and CVD risk in a large collection of postmenopausal bone biopsies. Most of the transcripts identified in the CVD risk categories have no previously recognized roles in OP pathogenesis and provide novel avenues for exploring the mechanistic basis for the biological association between CVD and OP. Full article
(This article belongs to the Special Issue Molecular Biology of Osteoporosis)
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