Differential development of the distal and proximal femoral epiphysis and physis in mice

Cole, Heather; Yuasa, Masato; Hawley, Gregory D.; Cates, Justin M.; Nyman, Jeffry S.; Schoenecker, Jonathan G.

doi:10.1016/j.bone.2012.10.011

Cited by 41 publications

(52 citation statements)

References 26 publications

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“…Radiographic imaging was performed as described . Briefly, following adequate anesthesia, digital radiographs (Faxitron, Tucson, AZ, USA) were collected at an exposure of 4 s at 35 kV.…”

Section: Methodssupporting

confidence: 89%

Plasmin Prevents Dystrophic Calcification After Muscle Injury

Mignemi

Yuasa

Baker

et al. 2016

Journal of Bone and Mineral Research

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Extensive or persistent calcium phosphate deposition within soft tissues after severe traumatic injury or major orthopedic surgery can result in pain and loss of joint function. The pathophysiology of soft tissue calcification, including dystrophic calcification and heterotopic ossification (HO), is poorly understood; consequently, current treatments are suboptimal. Here, we show that plasmin protease activity prevents dystrophic calcification within injured skeletal muscle independent of its canonical fibrinolytic function. After muscle injury, dystrophic calcifications either can be resorbed during the process of tissue healing, persist, or become organized into mature bone (HO). Without sufficient plasmin activity, dystrophic calcifications persist after muscle injury and are sufficient to induce HO. Downregulating the primary inhibitor of plasmin (α2-antiplasmin) or treating with pyrophosphate analogues prevents dystrophic calcification and subsequent HO in vivo. Because plasmin also supports bone homeostasis and fracture repair, increasing plasmin activity represents the first pharmacologic strategy to prevent soft tissue calcification without adversely affecting systemic bone physiology or concurrent muscle and bone regeneration. © 2016 American Society for Bone and Mineral Research.

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“…Radiographic imaging was performed as described . Briefly, following adequate anesthesia, digital radiographs (Faxitron, Tucson, AZ, USA) were collected at an exposure of 4 s at 35 kV.…”

Section: Methodssupporting

confidence: 89%

Plasmin Prevents Dystrophic Calcification After Muscle Injury

Mignemi

Yuasa

Baker

et al. 2016

Journal of Bone and Mineral Research

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“…Angiography. Perfusion with MICROFIL vascular contrast was conducted as previously described (61)(62)(63)(64). Briefly, mice were euthanized and positioned supine; a thoracotomy extending into a laparotomy was performed.…”

Section: Murine Femur Fracture Modelmentioning

confidence: 99%

Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification

Yuasa¹,

Mignemi²,

Nyman³

et al. 2015

J. Clin. Invest.

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“…All primary cells were harvested from femurs of male transgenic mice at 3 to 4 weeks of age. Chondrocytes were isolated from cartilage of the proximal epiphysis, which lacks a secondary ossification center . Briefly, the epiphysis was removed with a pair of tweezers and incubated in calcium‐ and magnesium‐free Hank's balanced salt solution with 0.2% bacterial collagenase (Sigma, St. Louis, MO, USA) for 3 to 4 hours at 37°C to release chondrocytes from their extracellular matrix.…”

Section: Methodsmentioning

confidence: 99%

Dynamics and Cellular Localization of Bmp2, Bmp4, and Noggin Transcription in the Postnatal Mouse Skeleton

Pregizer

Mortlock

2014

Journal of Bone and Mineral Research

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Transcription of Bone Morphogenetic Proteins (BMPs) and their antagonists in precise spatiotemporal patterns is essential for proper skeletal development, maturation, maintenance, and repair. Nevertheless, transcriptional activity of these molecules in skeletal tissues beyond embryogenesis has not been well-characterized. In this study, we used several transgenic reporter mouse lines to define the transcriptional activity of two potent BMP ligands, Bmp2 and Bmp4, and their antagonist Noggin in the postnatal skeleton. At 3–4 weeks of age, Bmp4 and Noggin reporter activity was readily apparent in most cells of the osteogenic or chondrogenic lineages, respectively, while Bmp2 reporter activity was strongest in terminally differentiated cells of both lineages. By 5–6 months, activity of the reporters had generally abated; however, the Noggin and Bmp2 reporters remained remarkably active in articular chondrocytes and persisted there indefinitely. We further found that endogenous Bmp2, Bmp4, and Noggin transcript levels in postnatal bone and cartilage mirrored the activity of their respective reporters in these tissues. Finally, we found that the activity of the Bmp2, Bmp4, and Noggin reporters in bone and cartilage at 3–4 weeks could be recapitulated in both osteogenic and chondrogenic culture models. These results reveal that Bmp2, Bmp4, and Noggin transcription persists to varying degrees in skeletal tissues postnatally, with each gene exhibiting its own cell-type specific pattern of activity. Illuminating these patterns and their dynamics will guide future studies aimed at elucidating both the causes and consequences of aberrant BMP signaling in the postnatal skeleton.

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Differential development of the distal and proximal femoral epiphysis and physis in mice

Cited by 41 publications

References 26 publications

Plasmin Prevents Dystrophic Calcification After Muscle Injury

Plasmin Prevents Dystrophic Calcification After Muscle Injury

Fibrinolysis is essential for fracture repair and prevention of heterotopic ossification

Dynamics and Cellular Localization of Bmp2, Bmp4, and Noggin Transcription in the Postnatal Mouse Skeleton

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