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Article: Molecular and Cellular Crosstalk between Bone and Brain: Accessing Bidirectional Neural and Musculoskeletal Signaling during Aging and Disease.

Schurman, Charles A / Burton, Jordan B / Rose, Jacob / Ellerby, Lisa M / Alliston, Tamara / Schilling, Birgit

2023 Volume 30, Issue 1, Page(s) 1–29

Abstract: Molecular omics technologies, including proteomics, have enabled the elucidation of key signaling pathways that mediate bidirectional communication between the brain and bone tissues. Here we provide a brief summary of the clinical and molecular evidence ...

Abstract	Molecular omics technologies, including proteomics, have enabled the elucidation of key signaling pathways that mediate bidirectional communication between the brain and bone tissues. Here we provide a brief summary of the clinical and molecular evidence of the need to study the bone-brain axis of cross-tissue cellular communication. Clear clinical and molecular evidence suggests biological interactions and similarities between bone and brain cells. Here we review the current mass spectrometric techniques for studying brain and bone diseases with an emphasis on neurodegenerative diseases and osteoarthritis/osteoporosis, respectively. Further study of the bone-brain axis on a molecular level and evaluation of the role of proteins, neuropeptides, osteokines, and hormones in molecular pathways linked to bone and brain diseases is critically needed. The use of mass spectrometry and other omics technologies to analyze these cross-tissue signaling events and interactions will help us better understand disease progression and comorbidities and potentially identify new pathways and targets for therapeutic interventions. Proteomic measurements are particularly favorable for investigating the role of signaling and secreted and circulating analytes and identifying molecular and metabolic pathways implicated in age-related diseases.
Language	English
Publishing date	2023-02-28
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2765291-9
ISSN	2287-7029 ; 2287-6375
ISSN (online)	2287-7029
ISSN	2287-6375
DOI	10.11005/jbm.2023.30.1.1
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Article ; Online: Disrupted osteocyte connectivity and pericellular fluid flow in bone with aging and defective TGF-β signaling.

Schurman, Charles A / Verbruggen, Stefaan W / Alliston, Tamara

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 25

Abstract: Skeletal fragility in the elderly does not simply result from a loss of bone mass. However, the mechanisms underlying the concurrent decline in bone mass, quality, and mechanosensitivity with age remain unclear. The important role of osteocytes in these ... ...

Abstract	Skeletal fragility in the elderly does not simply result from a loss of bone mass. However, the mechanisms underlying the concurrent decline in bone mass, quality, and mechanosensitivity with age remain unclear. The important role of osteocytes in these processes and the age-related degeneration of the intricate lacunocanalicular network (LCN) in which osteocytes reside point to a primary role for osteocytes in bone aging. Since LCN complexity severely limits experimental dissection of these mechanisms in vivo, we used two in silico approaches to test the hypothesis that LCN degeneration, due to aging or an osteocyte-intrinsic defect in transforming growth factor beta (TGF-β) signaling (TβRII
MeSH term(s)	Aging/physiology ; Animals ; Bone and Bones/physiology ; Finite Element Analysis ; Hydrodynamics ; Male ; Mice, Inbred C57BL ; Models, Biological ; Osteocytes/physiology ; Protein Transport ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction ; Stress, Mechanical ; Transforming Growth Factor beta/metabolism ; Mice
Chemical Substances	Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta
Language	English
Publishing date	2021-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2023999118
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Article: Deep learning models to map osteocyte networks can successfully distinguish between young and aged bone.

Vetter, Simon D / Schurman, Charles A / Alliston, Tamara / Slabaugh, Gregory G / Verbruggen, Stefaan W

bioRxiv : the preprint server for biology

2023

Abstract: Osteocytes, the most abundant and mechanosensitive cells in bone tissue, play a pivotal role in bone homeostasis and mechano-responsiveness, orchestrating the intricate balance between bone formation and resorption under daily activity. Studying ... ...

Abstract	Osteocytes, the most abundant and mechanosensitive cells in bone tissue, play a pivotal role in bone homeostasis and mechano-responsiveness, orchestrating the intricate balance between bone formation and resorption under daily activity. Studying osteocyte connectivity and understanding their intricate arrangement within the lacunar canalicular network (LCN) is essential for unraveling bone physiology. This is particularly true as our bones age, which is associated with decreased integrity of the osteocyte network, disrupted mass transport, and lower sensitivity to the mechanical stimuli that allow the skeleton to adapt to changing demands. Much work has been carried out to investigate this relationship, often involving high resolution microscopy of discrete fragments of this network, alongside advanced computational modelling of individual cells. However, traditional methods of segmenting and measuring osteocyte connectomics are time-consuming and labour-intensive, often hindered by human subjectivity and limited throughput. In this study, we explore the application of deep learning and computer vision techniques to automate the segmentation and measurement of osteocyte connectomics, enabling more efficient and accurate analysis. We compare several state-of-the-art computer vision models (U-Nets and Vision Transformers) to successfully segment the LCN, finding that an Attention U-Net model can accurately segment and measure 81.8% of osteocytes and 42.1% of dendritic processes, when compared to manual labelling. While further development is required, we demonstrate that this degree of accuracy is already sufficient to distinguish between bones of young (2 month old) and aged (36 month old) mice, as well as capturing the degeneration induced by genetic modification of osteocytes. By harnessing the power of these advanced technologies, further developments can unravel the complexities of osteocyte networks in unprecedented detail, revolutionising our understanding of bone health and disease.
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.20.572567
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Article: Bone-cartilage crosstalk informed by aging mouse bone transcriptomics and human osteoarthritis genome-wide association studies.

Kaya, Serra / Bailey, Karsyn N / Schurman, Charles A / Evans, Daniel S / Alliston, Tamara

Bone reports

2022 Volume 18, Page(s) 101647

Abstract: Subchondral bone participates in crosstalk with articular cartilage to maintain joint homeostasis, and disruption of either tissue results in overall joint degeneration. Among the subchondral bone changes observed in osteoarthritis (OA), subchondral bone ...

Abstract	Subchondral bone participates in crosstalk with articular cartilage to maintain joint homeostasis, and disruption of either tissue results in overall joint degeneration. Among the subchondral bone changes observed in osteoarthritis (OA), subchondral bone plate (SBP) thickening has a time-dependent relationship with cartilage degeneration and has recently been shown to be regulated by osteocytes. Here, we evaluate the effect of age on SBP thickness and cartilage degeneration in aging mice. We find that SBP thickness significantly increases by 18-months of age, corresponding temporally with increased cartilage degeneration. To identify factors in subchondral bone that may participate in bone cartilage crosstalk or OA, we leveraged mouse transcriptomic data from one joint tissue compartment - osteocyte-enriched bone - to search for enrichment with human OA in UK Biobank and Arthritis Research UK Osteoarthritis Genetics (arcOGEN) GWAS using the mouse2human (M2H, www.mouse2human.org) strategy. Genes differentially expressed in aging mouse bone are significantly enriched for human OA, showing joint site-specific (knee vs. hip) relationships, exhibit temporal associations with age, and unique gene clusters are implicated in each type of OA. Application of M2H identifies genes with known and unknown functions in osteocytes and OA development that are clinically associated with human OA. Altogether, this work prioritizes genes with a potential role in bone/cartilage crosstalk for further mechanistic study based on their association with human OA in GWAS.
Language	English
Publishing date	2022-12-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821774-3
ISSN	2352-1872
ISSN	2352-1872
DOI	10.1016/j.bonr.2022.101647
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Article ; Online: Prioritization of Genes Relevant to Bone Fragility Through the Unbiased Integration of Aging Mouse Bone Transcriptomics and Human GWAS Analyses.

Kaya, Serra / Schurman, Charles A / Dole, Neha S / Evans, Daniel S / Alliston, Tamara

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2022 Volume 37, Issue 4, Page(s) 804–817

Abstract: Identifying new genetic determinants of bone mineral density (BMD) and fracture promises to yield improved diagnostics and therapies for bone fragility. However, prioritizing candidate genes from genome-wide screens can be challenging. To overcome this ... ...

Abstract	Identifying new genetic determinants of bone mineral density (BMD) and fracture promises to yield improved diagnostics and therapies for bone fragility. However, prioritizing candidate genes from genome-wide screens can be challenging. To overcome this challenge, we prioritized mouse genes that are differentially expressed in aging mouse bone based on whether their human homolog is associated with human BMD and/or fracture. Unbiased RNA-seq analysis of young and old male C57BL/6 mouse cortical bone identified 1499, 1685, and 5525 differentially expressed genes (DEGs) in 1, 2, and 2.5-year-old bone, relative to 2-month-old bone, respectively. Gene-based scores for heel ultrasound bone mineral density (eBMD) and fracture were estimated using published genome-wide association studies (GWAS) results of these traits in the UK Biobank. Enrichment analysis showed that mouse bone DEG sets for all three age groups, relative to young bone, are significantly enriched for eBMD, but only the oldest two DEG sets are enriched for fracture. Using gene-based scores, this approach prioritizes among thousands of DEGs by a factor of 5- to 100-fold, yielding 10 and 21 genes significantly associated with fracture in the two oldest groups of mouse DEGs. Though these genes were not the most differentially expressed, they included Sost, Lrp5, and others with well-established functions in bone. Several others have, as yet, unknown roles in the skeleton. Therefore, this study accelerates identification of new genetic determinants of bone fragility by prioritizing a clinically relevant and experimentally tractable number of candidate genes for functional analysis. Finally, we provide a website (www.mouse2human.org) to enable other researchers to easily apply our strategy. © 2022 American Society for Bone and Mineral Research (ASBMR).
MeSH term(s)	Aging/genetics ; Animals ; Bone Density/genetics ; Fractures, Bone/genetics ; Genome-Wide Association Study ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Polymorphism, Single Nucleotide ; Transcriptome/genetics
Language	English
Publishing date	2022-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.4516
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Article: Aging impairs the osteocytic regulation of collagen integrity and bone quality.

Schurman, Charles A / Kaya, Serra / Dole, Neha / Luna, Nadja M Maldonado / Castillo, Natalia / Potter, Ryan / Rose, Jacob P / Bons, Joanna / King, Christina D / Burton, Jordan B / Schilling, Birgit / Melov, Simon / Tang, Simon / Schaible, Eric / Alliston, Tamara

Bone research

2024 Volume 12, Issue 1, Page(s) 13

Abstract: Poor bone quality is a major factor in skeletal fragility in elderly individuals. The molecular mechanisms that establish and maintain bone quality, independent of bone mass, are unknown but are thought to be primarily determined by osteocytes. We ... ...

Abstract	Poor bone quality is a major factor in skeletal fragility in elderly individuals. The molecular mechanisms that establish and maintain bone quality, independent of bone mass, are unknown but are thought to be primarily determined by osteocytes. We hypothesize that the age-related decline in bone quality results from the suppression of osteocyte perilacunar/canalicular remodeling (PLR), which maintains bone material properties. We examined bones from young and aged mice with osteocyte-intrinsic repression of TGFβ signaling (TβRII
MeSH term(s)	Humans ; Aged ; Male ; Animals ; Mice ; Osteocytes ; Bone Remodeling/physiology ; Collagen/pharmacology ; Aging ; Transforming Growth Factor beta/pharmacology
Chemical Substances	Collagen (9007-34-5) ; Transforming Growth Factor beta
Language	English
Publishing date	2024-02-26
Publishing country	China
Document type	Journal Article
ZDB-ID	2803313-9
ISSN	2095-6231 ; 2095-4700
ISSN (online)	2095-6231
ISSN	2095-4700
DOI	10.1038/s41413-023-00303-7
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Article ; Online: Investigating Osteocytic Perilacunar/Canalicular Remodeling.

Yee, Cristal S / Schurman, Charles A / White, Carter R / Alliston, Tamara

Current osteoporosis reports

2019 Volume 17, Issue 4, Page(s) 157–168

Abstract: Purpose of review: In perilacunar/canalicular remodeling (PLR), osteocytes dynamically resorb, and then replace, the organic and mineral components of the pericellular extracellular matrix. Given the enormous surface area of the osteocyte lacuna- ... ...

Abstract	Purpose of review: In perilacunar/canalicular remodeling (PLR), osteocytes dynamically resorb, and then replace, the organic and mineral components of the pericellular extracellular matrix. Given the enormous surface area of the osteocyte lacuna-canalicular network (LCN), PLR is important for maintaining homeostasis of the skeleton. The goal of this review is to examine the motivations and critical considerations for the analysis of PLR, in both in vitro and in vivo systems. Recent findings: Morphological approaches alone are insufficient to elucidate the complex mechanisms regulating PLR in the healthy skeleton and in disease. Understanding the role and regulation of PLR will require the incorporation of standardized PLR outcomes as a routine part of skeletal phenotyping, as well as the development of improved molecular and cellular outcomes. Current PLR outcomes assess PLR enzyme expression, the LCN, and bone matrix composition and organization, among others. Here, we discuss current PLR outcomes and how they have been applied to study PLR induction and suppression in vitro and in vivo. Given the role of PLR in skeletal health and disease, integrated analysis of PLR has potential to elucidate new mechanisms by which osteocytes participate in skeletal health and disease.
MeSH term(s)	Bone Matrix/metabolism ; Bone Matrix/ultrastructure ; Bone Remodeling/physiology ; Carbonic Anhydrases/metabolism ; Cathepsin K/metabolism ; Cell Line ; Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Imaging, Three-Dimensional ; Matrix Metalloproteinases/metabolism ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Osteocytes/enzymology ; Osteocytes/metabolism ; Osteocytes/ultrastructure ; Proton-Translocating ATPases/metabolism ; X-Ray Microtomography
Chemical Substances	Cathepsin K (EC 3.4.22.38) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Proton-Translocating ATPases (EC 3.6.3.14) ; Carbonic Anhydrases (EC 4.2.1.1)
Language	English
Publishing date	2019-05-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-019-00514-0
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Article ; Online: Deep coverage and quantification of the bone proteome provides enhanced opportunities for new discoveries in skeletal biology and disease.

Rose, Jacob P / Schurman, Charles A / King, Christina D / Bons, Joanna / Patel, Sandip K / Burton, Jordan B / O'Broin, Amy / Alliston, Tamara / Schilling, Birgit

PloS one

2023 Volume 18, Issue 10, Page(s) e0292268

Abstract: Dysregulation of cell signaling in chondrocytes and in bone cells, such as osteocytes, osteoblasts, osteoclasts, and an elevated burden of senescent cells in cartilage and bone, are implicated in osteoarthritis (OA). Mass spectrometric analyses provides ... ...

Abstract	Dysregulation of cell signaling in chondrocytes and in bone cells, such as osteocytes, osteoblasts, osteoclasts, and an elevated burden of senescent cells in cartilage and bone, are implicated in osteoarthritis (OA). Mass spectrometric analyses provides a crucial molecular tool-kit to understand complex signaling relationships in age-related diseases, such as OA. Here we introduce a novel mass spectrometric workflow to promote proteomic studies of bone. This workflow uses highly specialized steps, including extensive overnight demineralization, pulverization, and incubation for 72 h in 6 M guanidine hydrochloride and EDTA, followed by proteolytic digestion. Analysis on a high-resolution Orbitrap Eclipse and Orbitrap Exploris 480 mass spectrometer using Data-Independent Acquisition (DIA) provides deep coverage of the bone proteome, and preserves post-translational modifications, such as hydroxyproline. A spectral library-free quantification strategy, directDIA, identified and quantified over 2,000 protein groups (with ≥ 2 unique peptides) from calcium-rich bone matrices. Key components identified were proteins of the extracellular matrix (ECM), bone-specific proteins (e.g., secreted protein acidic and cysteine rich, SPARC, and bone sialoprotein 2, IBSP), and signaling proteins (e.g., transforming growth factor beta-2, TGFB2), and lysyl oxidase homolog 2 (LOXL2), an important protein in collagen crosslinking. Post-translational modifications (PTMs) were identified without the need for specific enrichment. This includes collagen hydroxyproline modifications, chemical modifications for collagen self-assembly and network formation. Multiple senescence factors were identified, such as complement component 3 (C3) protein of the complement system and many matrix metalloproteinases, that might be monitored during age-related bone disease progression. Our innovative workflow yields in-depth protein coverage and quantification strategies to discover underlying biological mechanisms of bone aging and to provide tools to monitor therapeutic interventions. These novel tools to monitor the bone proteome open novel horizons to investigate bone-specific diseases, many of which are age-related.
MeSH term(s)	Humans ; Proteome/analysis ; Proteomics/methods ; Hydroxyproline ; Bone and Bones/metabolism ; Osteoarthritis/metabolism ; Collagen
Chemical Substances	Proteome ; Hydroxyproline (RMB44WO89X) ; Collagen (9007-34-5)
Language	English
Publishing date	2023-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0292268
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Article ; Online: Assessment of Osteocytes: Techniques for Studying Morphological and Molecular Changes Associated with Perilacunar/Canalicular Remodeling of the Bone Matrix.

Dole, Neha S / Yee, Cristal S / Schurman, Charles A / Dallas, Sarah L / Alliston, Tamara

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2230, Page(s) 303–323

Abstract: Recent advances have revived interest in the concept of osteocyte perilacunar/canalicular remodeling (PLR) and have motivated efforts to identify the mechanisms regulating this process in bone in the context of normal physiology and pathological ... ...

Abstract	Recent advances have revived interest in the concept of osteocyte perilacunar/canalicular remodeling (PLR) and have motivated efforts to identify the mechanisms regulating this process in bone in the context of normal physiology and pathological conditions. Here, we describe several methods that are evaluating morphological changes associated with PLR function of osteocytes.
MeSH term(s)	Animals ; Bone Matrix/ultrastructure ; Bone Remodeling/physiology ; Cell Culture Techniques/methods ; Humans ; Osteocytes/ultrastructure
Language	English
Publishing date	2020-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1028-2_17
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Article ; Online: Fluid shear stress generates a unique signaling response by activating multiple TGFβ family type I receptors in osteocytes.

Monteiro, David A / Dole, Neha S / Campos, J Luke / Kaya, Serra / Schurman, Charles A / Belair, Cassandra D / Alliston, Tamara

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2021 Volume 35, Issue 3, Page(s) e21263

Abstract: Bone is a dynamic tissue that constantly adapts to changing mechanical demands. The transforming growth factor beta (TGFβ) signaling pathway plays several important roles in maintaining skeletal homeostasis by both coupling the bone-forming and bone- ... ...

Abstract	Bone is a dynamic tissue that constantly adapts to changing mechanical demands. The transforming growth factor beta (TGFβ) signaling pathway plays several important roles in maintaining skeletal homeostasis by both coupling the bone-forming and bone-resorbing activities of osteoblasts and osteoclasts and by playing a causal role in the anabolic response of bone to applied loads. However, the extent to which the TGFβ signaling pathway in osteocytes is directly regulated by fluid shear stress (FSS) is unknown, despite work suggesting that fluid flow along canaliculi is a dominant physical cue sensed by osteocytes following bone compression. To investigate the effects of FSS on TGFβ signaling in osteocytes, we stimulated osteocytic OCY454 cells cultured within a microfluidic platform with FSS. We find that FSS rapidly upregulates Smad2/3 phosphorylation and TGFβ target gene expression, even in the absence of added TGFβ. Indeed, relative to treatment with TGFβ, FSS induced a larger increase in levels of pSmad2/3 and Serpine1 that persisted even in the presence of a TGFβ receptor type I inhibitor. Our results show that FSS stimulation rapidly induces phosphorylation of multiple TGFβ family R-Smads by stimulating multimerization and concurrently activating several TGFβ and BMP type I receptors, in a manner that requires the activity of the corresponding ligand. While the individual roles of the TGFβ and BMP signaling pathways in bone mechanotransduction remain unclear, these results implicate that FSS activates both pathways to generate a downstream response that differs from that achieved by either ligand alone.
MeSH term(s)	Activin Receptors, Type II/physiology ; Animals ; Cells, Cultured ; Lab-On-A-Chip Devices ; Mice ; Osteocytes/physiology ; Protein Multimerization ; Receptor, Transforming Growth Factor-beta Type I/chemistry ; Receptor, Transforming Growth Factor-beta Type I/physiology ; Sequence Analysis, RNA ; Signal Transduction/physiology ; Smad2 Protein/physiology ; Smad3 Protein/physiology ; Stress, Mechanical
Chemical Substances	Smad2 Protein ; Smad3 Protein ; Activin Receptors, Type II (EC 2.7.11.30) ; Acvrl1 protein, mouse (EC 2.7.11.30) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30)
Language	English
Publishing date	2021-02-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202001998R
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