Expression pattern of osteogenic protein-1 (bone morphogenetic protein-7)                in human and mouse development.

Helder, Marco N.; Özkaynak, Engin; Sampath, Kuber T.; Luyten, F.P.; Latin, Višnja; Oppermann, Hermann; Vukičević, Slobodan

doi:10.1177/43.10.7560881

Cited by 175 publications

(127 citation statements)

References 8 publications

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“…Although BMP-7 was originally identified as a protein that induced bone and cartilage formation, with an important role in the morphogenesis of embryo and in postnatal life (37), it is also produced in kidney (37,38). Recent studies have shown that BMP-7 is able to prevent kidney damage in vivo in numerous animal models of disease.…”

Section: Discussionmentioning

confidence: 99%

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

Selbi¹,

Motte²,

Hascall³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Increased synthesis of hyaluronan (HA) in the renal corticointerstitium has been documented in renal injury, although the functional significance of this is unclear. The aim of the work presented in the current study was to examine the role of HA in monocyte binding by proximal tubular cells (PTC). Using the PTC line HK-2, the authors show that unstimulated cells formed pericellular HA cable-like structures that bound mononuclear leukocytes via their cell surface CD44. Stimulation with bone morphogenic protein-7 (BMP-7) led to increased formation of HA cable-like structures and also a dosedependent increase in CD44-dependent binding of radiolabeled

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Section: Discussionmentioning

confidence: 99%

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

Selbi¹,

Motte²,

Hascall³

et al. 2004

Journal of the American Society of Nephrology

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“…However, they are expressed in a wide range of non-skeletal tissues during mammalian development, including germ layer, whiskers, hair, teeth, urogenital system, gut, heart and brain (170,171). These observations suggest that BMPs have a much broader role in overall tissue morphogenesis, and in repair of other tissue systems.…”

Section: Other Areas Of Potential Clinical Use Of Bmpsmentioning

confidence: 99%

Bone morphogenetic proteins in human bone regeneration

Groeneveld

Burgér

2000

European Journal of Endocrinology

358

217

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Recently, the first clinical reports on bone regeneration by two recombinant human bone morphogenetic proteins (rhBMPs), BMP-2 and BMP-7 (also named osteogenic protein-1, OP-1) have been published (1-4) . Although both BMPs were able to support bone regeneration, a significant variation in individual response was observed with both proteins. Animal studies and laboratory experiments reveal a number of conditions that influence the osteoinductivity of BMP, such as BMP concentration, carrier properties and influence of local and systemic growth factors and hormones. In this paper, these studies and the clinical reports are reviewed, and the conditions that modulate the BMP-dependent osteoinduction are discussed. The information may provide clues as to how the performance of recombinant human BMP as bone-graft substitute in humans can be improved. European Journal of Endocrinology 142 9-21 BMP and demineralized bone matrixThe history of bone morphogenetic proteins (BMPs) began with the observation that demineralized bone matrix (DBM) is able to induce ectopic bone formation in subcutaneous and intramuscular pockets in rodents (5, 6). This bone induction process has been studied extensively (7-13). Histological and biochemical analyses showed that cartilage appears 5-10 days after implantation of active DBM (8). This cartilage mineralizes by day 7-14 and is subsequently replaced by bone (7-9). After 21 days, haematopoietic bone marrow formation can be observed (12). These cellular events observed after DBM implantation mimic embryonic bone development and normal fracture repair (11). As DBM-related bone formation was observed to occur at ectopic sites, it was assumed that pluripotent mesenchymal cells are attracted to the site of implantation. Isolation of the bone-inducing substance revealed that certain proteins were responsible, which were termed bone morphogenetic proteins (BMPs) or osteogenetic proteins (OPs).The use of DBM in treating bone defects has proven beneficial for bone regeneration both in animals and in humans (14-17). DBM has become widely accepted as a bone-graft substitute in clinical practice (18-22), but its bone inductive capacity has been questioned (23, 24). In several studies, including our own, histology revealed that new bone was generated by osteoconduction rather than osteoinduction (25-27) -that is, bone regeneration occurred by growth of existing host bone on the DBM granules, which acted as a scaffold, rather than by de novo differentiation of bone, independent of pre-existing bone. Lack of inductive properties of DBM may be related to the procedures of production of commercially available DBM, as preservation of osteoinductive activity can be affected by the processing (28-30) or sterilization procedures (31). It is also possible that DBM of human origin, which is preferred for use in clinical practice, is less osteoinductive than DBM derived from animals, which is commonly used in animal studies. Several studies show that DBM from long-lived species such as baboon and human...

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“…Bone morphogenetic protein 7 (BMP-7), a member or the transforming growth factor-␤ (TGF-␤) superfamily, is widely expressed during embryonic growth (15) and is an essential morphogen in renal, skeletal, and eye development (16 -18). The BMP-7 null mouse dies of perinatal renal failure due to hypoplastic dysplastic kidneys.…”

mentioning

confidence: 99%

BMP-7 Is an Efficacious Treatment of Vascular Calcification in a Murine Model of Atherosclerosis and Chronic Renal Failure

Davies

Lund²,

Hruska³

2003

Journal of the American Society of Nephrology

197

162

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Abstract. Chronic renal failure is complicated by high cardiovascular mortality. One key contributor to this mortality is vascular calcification, for which no therapy currently exists. Bone morphogenetic protein 7 is an essential renal morphogen that maintains renal tubular differentiation in the adult and is downregulated in renal failure. Several studies have demonstrated its efficacy in treating various renal diseases in rodents, and it was hypothesized that it would also be an effective treatment of vascular calcification in this setting. Uremia was imposed on LDL receptor null mice (a model of atherosclerosis), which were then treated with bone morphogenetic protein 7 for 15 wk. Uremic animals had increased vascular calcification by histology and chemical analysis. Calcification in treated animals was similar to or less than non-uremic control animals. Cells exhibiting an osteoblast-like phenotype in the vessel wall may be important in the etiology of vascular calcification. Expression of osteocalcin was assessed as a marker of osteoblastic function, and it is shown that it is increased in untreated uremic animals but downregulated to levels similar to non-uremic control animals with treatment.

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Expression pattern of osteogenic protein-1 (bone morphogenetic protein-7) in human and mouse development.

Cited by 175 publications

References 8 publications

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

Bone morphogenetic proteins in human bone regeneration

BMP-7 Is an Efficacious Treatment of Vascular Calcification in a Murine Model of Atherosclerosis and Chronic Renal Failure

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