Expression of bone morphogenetic proteins in normal human intramembranous and endochondral bones

Suttapreyasri, Srisurang; Koontongkaew, Sittichai; Phongdara, Amornrat; Leggat, U.

doi:10.1016/j.ijom.2006.01.021

Cited by 39 publications

(37 citation statements)

References 44 publications

(35 reference statements)

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“…These include bone morphogenesis, functions of hepatic reticuloendothelial system, hematopoiesis, neuronal differentiation, glucose homeostasis, iron homeostasis, and angiogenesis (18,(20)(21)(22)(23)(24)(25). It is interesting to note that although the expression of BMP-9 was initially thought to be restricted to the liver (18,26), recent studies have found BMP-9 mRNA expression to occur in a number of cells and tissues, including the central nervous system and bone in recent studies (22,27). The nonparenchymal cells of the liver (endothelial, Kupffer, and stellate cells), rather than hepatocytes, are thought to be the major source of BMP-9 in the body (28).…”

Section: Introductionmentioning

confidence: 99%

Bone Morphogenetic Protein-9 Induces Apoptosis in Prostate Cancer Cells, the Role of Prostate Apoptosis Response-4

Ye¹,

Kynaston

Jiang³

2008

Molecular Cancer Research

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Bone morphogenetic proteins (BMP) have been implicated in the development of bone metastases in prostate cancer. In this study, we investigated the role which BMP-9 played in prostate cancer and found that the expression of BMP-9 was decreased or absent in prostate cancer, particularly in the foci of higher grade disease. We further investigated the influence of BMP-9 on the biological behaviors of prostate cancer cells. The forced overexpression of BMP-9 prevented the in vitro growth, cell-matrix adhesion, invasion, and migration of prostate cancer cells. We also elucidated that BMP-9 induced apoptosis in PC-3 cells through the up-regulation of prostate apoptosis response-4. Among the receptors which have been implicated in the signaling of BMP-9, BMPR-IB and BMPR-II have also been implicated in the development and progression of prostate cancer. Knockdown of BMPR-IB or BMPR-II using respective hammerhead ribozyme transgenes could promote cell growth in vitro. We also found that BMPR-II is indispensable for the Smad-dependent signal transduction by BMP-9 in PC-3 cells, in which Smad-1 was phosphorylated and translocated from the cytoplasm into the nuclei. Taken together, BMP-9 inhibits the growth of prostate cancer cells due to the induced apoptosis, which is related to an up-regulation of prostate apoptosis response-4 through a Smad-dependent pathway. BMP-9 could also prevent the migration and invasiveness of prostate cancer. This suggests that BMP-9 may function as a tumor suppressor and apoptosis regulator in prostate cancer. (Mol Cancer Res

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Section: Introductionmentioning

confidence: 99%

Bone Morphogenetic Protein-9 Induces Apoptosis in Prostate Cancer Cells, the Role of Prostate Apoptosis Response-4

Ye¹,

Kynaston

Jiang³

2008

Molecular Cancer Research

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“…Only BMPs-2, -4, -6, -7, and -9 induce complete bone morphogenesis [25] and are found in both normal human membranous and endochondral bones [28]. BMPs are present in demineralized bone tissue at a concentration of about 2 μg/kg, and the concentration of BMP-9 in the blood plasma is 2-12 ng/mL [29][30][31].…”

Section: Tgf-β and Vegfmentioning

confidence: 99%

Bone repair: New developments in growth factor delivery systems and their mathematical modeling

Lauzon

Bergeron

Marcos

et al. 2012

Journal of Controlled Release

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“…When the bony microenvironment is altered; however, other BMPs may manifest (Suttapreyasri et al 2006). BMP-2 is expressed during murine embryonal skeletogenesis; it stimulates osteoblast differentiation from uncommitted progenitors both in vitro and in vivo (Chikazu et al 2002).…”

Section: Tgf-β Superfamilymentioning

confidence: 99%

A Comprehensive Clinicopathologic Analysis Suggests that Vascular Endothelial Growth Factor (VEGF) is the Most Likely Mediator of Periosteal New Bone Formation (PNBF) Associated with Diverse Etiologies

Lakey

Klein

Faye-Petersen

2008

Clinical medicine. Arthritis and musculoskeletal disorders

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Abstract:Periosteal new bone formation (PNBF) is the means by which appositional bone growth normally takes place on the surfaces of compact bone. Alterations in the periosteal microenvironment trigger complex interactions between osteoblasts and endothelial cells to promote PNBF. Physiologic processes like mechanical stress result in normal PNBF; but, a variety of pathologic processes result in excessive PNBF. The production of suffi cient bone to be detectable by conventional radiography is a common feature of diverse etiologies, including infection; infl ammation; prostaglandin E 2 administration for ductal-dependent congenital heart disease; metabolic and hormonal abnormalities; neoplasms; fracture repair; systemic hypoxia; and hypertrophic osteoarthropathy. While the clinical settings and distribution of affected bone sites in these conditions are different, the histopathology of the PNBF is essentially identical; so, it seems logical that a common pathway might mediate them all. By combining the observations and insights gained from osseous research and studying the clinical pathology of these diverse conditions, we constructed a comprehensive pathway to explain PNBF. In doing so, it seems likely that Vascular Endothelial Growth Factor (VEGF) is the most likely common mediator of the pathways that lead to PNBF.

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Expression of bone morphogenetic proteins in normal human intramembranous and endochondral bones

Cited by 39 publications

References 44 publications

Bone Morphogenetic Protein-9 Induces Apoptosis in Prostate Cancer Cells, the Role of Prostate Apoptosis Response-4

Bone Morphogenetic Protein-9 Induces Apoptosis in Prostate Cancer Cells, the Role of Prostate Apoptosis Response-4

Bone repair: New developments in growth factor delivery systems and their mathematical modeling

A Comprehensive Clinicopathologic Analysis Suggests that Vascular Endothelial Growth Factor (VEGF) is the Most Likely Mediator of Periosteal New Bone Formation (PNBF) Associated with Diverse Etiologies

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