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Article ; Online: A Population of M2 Macrophages Associated With Bone Formation.

Olmsted-Davis, Elizabeth / Mejia, Julio / Salisbury, Elizabeth / Gugala, Zbigniew / Davis, Alan R

2021 Volume 12, Page(s) 686769

Abstract: We previously identified transient brown adipocyte-like cells associated with heterotopic ossification (HO). These ancillary cells support new vessel synthesis essential to bone formation. Recent studies have shown that the M2 macrophage contributes to ... ...

Abstract	We previously identified transient brown adipocyte-like cells associated with heterotopic ossification (HO). These ancillary cells support new vessel synthesis essential to bone formation. Recent studies have shown that the M2 macrophage contributes to tissue regeneration in a similar way. To further define the phenotype of these brown adipocyte-like cells they were isolated and characterized by single-cell RNAseq (scRNAseq). Analysis of the transcriptome and the presence of surface markers specific for macrophages suggest that these cells are M2 macrophages. To validate these findings, clodronate liposomes were delivered to the tissues during HO, and the results showed both a significant reduction in these macrophages as well as bone formation. These cells were isolated and shown in culture to polarize towards either M1 or M2 similar to other macrophages. To confirm that these are M2 macrophages, mice received lipopolysacheride (LPS), which induces proinflammation and M1 macrophages. The results showed a significant decrease in this specific population and bone formation, suggesting an essential role for M2 macrophages in the production of bone. To determine if these macrophages are specific to HO, we isolated these cells using fluorescence-activated cell sorting (FACS) from a bone defect model and subjected them to scRNAseq. Surprisingly, the macrophage populations overlapped between the two groups (HO-derived
MeSH term(s)	Adipocytes, Brown/drug effects ; Adipocytes, Brown/metabolism ; Adipocytes, Brown/pathology ; Animals ; Cell Plasticity ; Cells, Cultured ; Clodronic Acid/pharmacology ; Disease Models, Animal ; Femoral Fractures/genetics ; Femoral Fractures/metabolism ; Femoral Fractures/pathology ; Femur/metabolism ; Femur/pathology ; Lipopolysaccharides/pharmacology ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/pathology ; Mice, Transgenic ; Ossification, Heterotopic/genetics ; Ossification, Heterotopic/metabolism ; Ossification, Heterotopic/pathology ; Osteogenesis ; Phagocytosis ; Phenotype ; Receptors, Adrenergic, beta-3/metabolism ; Transcriptome
Chemical Substances	Adrb3 protein, mouse ; Lipopolysaccharides ; Receptors, Adrenergic, beta-3 ; Clodronic Acid (0813BZ6866)
Language	English
Publishing date	2021-10-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.686769
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Article ; Online: A replicating stem-like cell that contributes to bone morphogenetic protein 2-induced heterotopic bone formation.

Mejia, Julio / Salisbury, Elizabeth / Sonnet, Corinne / Gugala, Zbigniew / Olmsted-Davis, Elizabeth A / Davis, Alan R

Stem cells translational medicine

2020 Volume 10, Issue 4, Page(s) 623–635

Abstract: Bone morphogenetic protein 2 (BMP2)-induced heterotopic bone formation (HBF) starts synchronously from zero upon BMP2 induction, which is advantageous for lineage tracking. The studies reported here in GLAST- ... ...

Abstract	Bone morphogenetic protein 2 (BMP2)-induced heterotopic bone formation (HBF) starts synchronously from zero upon BMP2 induction, which is advantageous for lineage tracking. The studies reported here in GLAST-Cre
MeSH term(s)	Animals ; Bone Morphogenetic Protein 2/pharmacology ; Cell Differentiation ; Mesenchymal Stem Cells ; Mice ; Ossification, Heterotopic ; Osteoblasts ; Stem Cells/cytology
Chemical Substances	Bone Morphogenetic Protein 2
Language	English
Publishing date	2020-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2642270-0
ISSN	2157-6580 ; 2157-6580
ISSN (online)	2157-6580
ISSN	2157-6580
DOI	10.1002/sctm.20-0378
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Article ; Online: The truth about Tamiflu? Data access is matter of trust.

Maryon-Davis, Alan R

BMJ (Clinical research ed.)

2010 Volume 340, Page(s) c134

MeSH term(s)	Access to Information ; Antiviral Agents/therapeutic use ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza, Human/drug therapy ; Oseltamivir/therapeutic use
Chemical Substances	Antiviral Agents ; Oseltamivir (20O93L6F9H)
Language	English
Publishing date	2010-01-13
Publishing country	England
Document type	Letter
ZDB-ID	1362901-3
ISSN	1756-1833 ; 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
ISSN (online)	1756-1833
ISSN	0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
DOI	10.1136/bmj.c134
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Article: TNIK regulation of interferon signaling and endothelial cell response to virus infection.

Chau, Khanh M / Dominic, Abishai / Davis, Eleanor L / Kotla, Sivareddy / Berrios, Estefani Turcios / Fahim, Arsany / Arunesh, Ashwin / Li, Shengyu / Zhao, Dongyu / Chen, Kaifu / Davis, Alan R / Nguyen, Minh T H / Wang, Yongxing / Evans, Scott E / Wang, Guangyu / Cooke, John P / Abe, Jun-Ichi / Huston, David P / Le, Nhat-Tu

Frontiers in cardiovascular medicine

2024 Volume 10, Page(s) 1213428

Abstract: Background: Traf2 and Nck-interacting kinase (TNIK) is known for its regulatory role in various processes within cancer cells. However, its role within endothelial cells (ECs) has remained relatively unexplored.: Methods: Leveraging RNA-seq data and ... ...

Abstract	Background: Traf2 and Nck-interacting kinase (TNIK) is known for its regulatory role in various processes within cancer cells. However, its role within endothelial cells (ECs) has remained relatively unexplored. Methods: Leveraging RNA-seq data and Ingenuity Pathway Analysis (IPA), we probed the potential impact of TNIK depletion on ECs. Results: Examination of RNA-seq data uncovered more than 450 Differentially Expressed Genes (DEGs) in TNIK-depleted ECs, displaying a fold change exceeding 2 with a false discovery rate (FDR) below 0.05. IPA analysis unveiled that TNIK depletion leads to the inhibition of the interferon (IFN) pathway [-log ( Summary: Our findings suggest that TNIK plays a crucial role in regulating the EC response to virus infections through modulation of the IFN pathway.
Language	English
Publishing date	2024-01-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2023.1213428
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Article: Trauma-Induced Heterotopic Ossification Regulates the Blood-Nerve Barrier.

Gugala, Zbigniew / Olmsted-Davis, Elizabeth A / Xiong, Yuqing / Davis, Eleanor L / Davis, Alan R

Frontiers in neurology

2018 Volume 9, Page(s) 408

Abstract: ... De ... ...

Abstract	De novo
Language	English
Publishing date	2018-06-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2018.00408
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Article ; Online: Cell-Based Gene Therapy System for Delivering BMPs.

Dickerson, Austin / Davis, Eleanor L / Sonnet, Corinne / Davis, Alan R / Olmsted-Davis, Elizabeth A

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

2018 Volume 1891, Page(s) 19–28

Abstract: The use of an adenoviral vector to transduce cells allows for certain secreted proteins or growth factors to be generated in vivo in eukaryotic cells with accurate posttranslational processing. The use of transduced cells eliminates viral toxicity, ... ...

Abstract	The use of an adenoviral vector to transduce cells allows for certain secreted proteins or growth factors to be generated in vivo in eukaryotic cells with accurate posttranslational processing. The use of transduced cells eliminates viral toxicity, allows for targeted expression of the secreted factor at a specific site, and ensures that the therapy will be turned off when the cells are cleared by the organism. Here we describe the delivery system which utilizes cells transduced with a non-replicating adenovirus containing bone morphogenetic protein 2 (BMP-2) in the E1 region of the cassette. With this method of delivery, small amounts of the protein can incite de novo bone formation.
MeSH term(s)	Adenoviridae/genetics ; Alkaline Phosphatase ; Animals ; Bone Morphogenetic Proteins/genetics ; Bone Morphogenetic Proteins/metabolism ; Cell Line ; Cell- and Tissue-Based Therapy/methods ; Genetic Therapy/methods ; Genetic Vectors/genetics ; Humans ; Mice ; Rats ; Transduction, Genetic
Chemical Substances	Bone Morphogenetic Proteins ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2018-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8904-1_3
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Article ; Online: Is heterotopic ossification getting nervous?: The role of the peripheral nervous system in heterotopic ossification.

Davis, Eleanor L / Davis, Alan R / Gugala, Zbigniew / Olmsted-Davis, Elizabeth A

Bone

2017 Volume 109, Page(s) 22–27

Abstract: Heterotopic ossification (HO), or de novo bone formation in soft tissue, is often observed following traumatic injury. Recent studies suggest that peripheral nerves may play a key functional role in this process. The results supporting a neurological ... ...

Abstract	Heterotopic ossification (HO), or de novo bone formation in soft tissue, is often observed following traumatic injury. Recent studies suggest that peripheral nerves may play a key functional role in this process. The results supporting a neurological basis for HO are examined in this article. Evidence supports the fact that BMPs released from bone matrix possess the capacity to induce HO. However, the process cannot be recapitulated using recombinant proteins without extremely high doses suggesting other components are required for this process. Study of injuries that increase risk for HO, i.e. amputation, hip replacement, elbow fracture, burn, and CNS injury suggests that a likely candidate is traumatic injury of adjacent peripheral nerves. Recent studies suggest neuroinflammation may play a key functional role, by its ability to open the blood-nerve barrier (BNB). Barrier opening is characterized by a change in permeability and is experimentally assessed by the ability of Evans blue dye to enter the endoneurium of peripheral nerves. A combination of BMP and barrier opening is required to activate bone progenitors in the endoneurial compartment. This process is referred to as "neurogenic HO".
MeSH term(s)	Animals ; Bone Morphogenetic Protein 2/metabolism ; Cell Movement/physiology ; Humans ; Ossification, Heterotopic/pathology ; Peripheral Nervous System/cytology ; Peripheral Nervous System/metabolism ; Stem Cells/pathology ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Bone Morphogenetic Protein 2 ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2017-07-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2017.07.016
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Characterization of neuromas in peripheral nerves and their effects on heterotopic bone formation.

Minarelli, Jordan / Davis, Eleanor L / Dickerson, Austin / Moore, William C / Mejia, Julio A / Gugala, Zbigniew / Olmsted-Davis, Elizabeth A / Davis, Alan R

Molecular pain

2019 Volume 15, Page(s) 1744806919838191

Abstract: The formation of neuromas involves expansion of the cellular components of peripheral nerves. The onset of these disorganized tumors involves activation of sensory nerves and neuroinflammation. Particularly problematic in neuroma is arborization of axons ...

Abstract	The formation of neuromas involves expansion of the cellular components of peripheral nerves. The onset of these disorganized tumors involves activation of sensory nerves and neuroinflammation. Particularly problematic in neuroma is arborization of axons leading to extreme, neuropathic pain. The most common sites for neuroma are the ends of transected nerves following injury; however, this rodent model does not reliably result in neuroma formation. In this study, we established a rodent model of neuroma in which the sciatic nerve was loosely ligated with two chromic gut sutures. This model formed neuromas reliably (∼95%), presumably through activation of the neural inflammatory cascade. Resulting neuromas had a disorganized structure and a significant number of replicating cells. Quantification of changes in perineurial and Schwann cells showed a significant increase in these populations. Immunohistochemical analysis showed the presence of β-tubulin 3 in the rapidly expanding nerve and a decrease in neurofilament heavy chain compared to the normal nerve, suggesting the axons forming a disorganized structure. Measurement of the permeability of the blood-nerve barrier shows that it opened almost immediately and remained open as long as 10 days. Studies using an antagonist of the β3-adrenergic receptor (L-748,337) or cromolyn showed a significant reduction in tumor size and cell expansion as determined by flow cytometry, with an improvement in the animal's gait detected using a Catwalk system. Previous studies in our laboratory have shown that heterotopic ossification is also a result of the activation of neuroinflammation. Since heterotopic ossification and neuroma often occur together in amputees, they were induced in the same limbs of the study animals. More heterotopic bone was formed in animals with neuromas as compared to those without. These data collectively suggest that perturbation of early neuroinflammation with compounds such as L-748,337 and cromolyn may reduce formation of neuromas.
MeSH term(s)	Adrenergic beta-3 Receptor Agonists/therapeutic use ; Animals ; Axons/drug effects ; Axons/metabolism ; Bone Morphogenetic Protein 2/genetics ; Bone Morphogenetic Protein 2/metabolism ; Cell Line ; Flow Cytometry ; Immunohistochemistry ; Mice ; Neuroma/drug therapy ; Neuroma/metabolism ; Rats ; Receptors, Adrenergic, beta-3/metabolism ; Schwann Cells/drug effects ; Schwann Cells/metabolism ; Sciatic Nerve/drug effects ; Sciatic Nerve/metabolism ; Tubulin/metabolism
Chemical Substances	Adrenergic beta-3 Receptor Agonists ; Bone Morphogenetic Protein 2 ; Receptors, Adrenergic, beta-3 ; Tubulin
Language	English
Publishing date	2019-02-27
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2174252-2
ISSN	1744-8069 ; 1744-8069
ISSN (online)	1744-8069
ISSN	1744-8069
DOI	10.1177/1744806919838191
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Article ; Online: Anaplerotic Accumulation of Tricarboxylic Acid Cycle Intermediates as Well as Changes in Other Key Metabolites During Heterotopic Ossification.

Davis, Eleanor L / Salisbury, Elizabeth A / Olmsted-Davis, Elizabeth / Davis, Alan R

Journal of cellular biochemistry

2015 Volume 117, Issue 4, Page(s) 1044–1053

Abstract: Heterotopic ossification (HO) is the de novo formation of bone that occurs in soft tissue, through recruitment, expansion, and differentiation of multiple cells types including transient brown adipocytes, osteoblasts, chondrocytes, mast cells, and ... ...

Abstract	Heterotopic ossification (HO) is the de novo formation of bone that occurs in soft tissue, through recruitment, expansion, and differentiation of multiple cells types including transient brown adipocytes, osteoblasts, chondrocytes, mast cells, and platelets to name a few. Much evidence is accumulating that suggests changes in metabolism may be required to accomplish this bone formation. Recent work using a mouse model of heterotopic bone formation reliant on delivery of adenovirus-transduced cells expressing low levels of BMP2 showed the immediate expansion of a unique brown adipocyte-like cell. These cells are undergoing robust uncoupled oxidative phosphorylation to a level such that oxygen in the microenvironment is dramatically lowered creating areas of hypoxia. It is unclear how these oxygen changes ultimately affect metabolism and bone formation. To identify the processes and changes occurring over the course of bone formation, HO was established in the mice, and tissues isolated at early and late times were subjected to a global metabolomic screen. Results show that there are significant changes in both glucose levels, as well as TCA cycle intermediates. Additionally, metabolites necessary for oxidation of stored lipids were also found to be significantly elevated. The complete results of this screen are presented here, and provide a unique picture of the metabolic changes occurring during heterotopic bone formation.
MeSH term(s)	Adenoviridae/genetics ; Adenoviridae/metabolism ; Animals ; Bone Morphogenetic Protein 2/genetics ; Bone Morphogenetic Protein 2/metabolism ; Cell Differentiation ; Chondrocytes/metabolism ; Chondrocytes/pathology ; Citric Acid Cycle/genetics ; Disease Models, Animal ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression ; Genetic Vectors/chemistry ; Genetic Vectors/metabolism ; Glycolysis/genetics ; Injections, Intramuscular ; Metabolome ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Ossification, Heterotopic/genetics ; Ossification, Heterotopic/metabolism ; Ossification, Heterotopic/pathology ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Oxidative Phosphorylation ; Skin/metabolism ; Skin/pathology ; Transduction, Genetic
Chemical Substances	Bmp2 protein, mouse ; Bone Morphogenetic Protein 2
Language	English
Publishing date	2015-12-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.25454
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Zs.A 1114: Show issues

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Article ; Online: Characterization of Brown Adipose-Like Tissue in Trauma-Induced Heterotopic Ossification in Humans.

Salisbury, Elizabeth A / Dickerson, Austin R / Davis, Thomas A / Forsberg, Jonathan A / Davis, Alan R / Olmsted-Davis, Elizabeth A

The American journal of pathology

2017 Volume 187, Issue 9, Page(s) 2071–2079

Abstract: Heterotopic ossification (HO), the abnormal formation of bone within soft tissues, is a major complication after severe trauma or amputation. Transient brown adipocytes have been shown to be a critical regulator of this process in a mouse model of HO. In ...

Abstract	Heterotopic ossification (HO), the abnormal formation of bone within soft tissues, is a major complication after severe trauma or amputation. Transient brown adipocytes have been shown to be a critical regulator of this process in a mouse model of HO. In this study, we evaluated the presence of brown fat within human HO lesions. Most of the excised tissue samples displayed histological characteristics of bone, fibroproliferative cells, blood vessels, and adipose tissue. Immunohistochemical analysis revealed extensive expression of uncoupling protein 1 (UCP1), a definitive marker of brown adipocytes, within HO-containing tissues but not normal tissues. As seen in the brown adipocytes observed during HO in the mouse, these UCP1
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Humans ; Immunohistochemistry ; Ossification, Heterotopic/etiology ; Ossification, Heterotopic/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Receptors, Adrenergic, beta-3/metabolism ; Uncoupling Protein 1/metabolism ; Wounds and Injuries/complications ; Wounds and Injuries/metabolism
Chemical Substances	ADRB3 protein, human ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Receptors, Adrenergic, beta-3 ; Uncoupling Protein 1
Language	English
Publishing date	2017-07-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2017.05.012
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