Effects of endothelial cell growth factor on bone remodelling in vitro.

Canalis, Ernesto; Lorenzo, Joseph; Burgess, W H; Maciag, Thomas

doi:10.1172/jci112807

Cited by 72 publications

(23 citation statements)

References 35 publications

(25 reference statements)

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“…As a result of its mitogenic effect, bFGF also stimulated NCP synthesis, indicating that its actions were not specific for collagen. Although bone matrix (10). However, bFGF had a somewhat more pronounced effect on DNA synthesis than ECGF, and while heparin clearly enhanced the ECGF effect, it only caused a marginal enhancement of the bFGF effect on DNA synthesis.…”

Section: Discussionmentioning

confidence: 85%

“…Conversely, heparin increases the affinity of aFGF to its receptor (21), and this does not seem to occur with bFGF. Although ECGF was shown to stimulate prostaglandin E2 synthesis, neither its effects nor those of bFGF could be attributed to prostaglandin production, since the response to these agents was not modified by indomethacin (10).…”

Section: Discussionmentioning

confidence: 94%

“…Calvariae were homogenized in 0.5 M acetic acid and an aliquot of this homogenate and of the respective culture medium was hydrolyzed in 6 N HCI at 107°C for 24 h. The samples were dried, derivatized with phenylisothiocyanate, and the [3HIproline (used for the labeling) and [3H]-hydroxyproline (representing newly labeled collagen) separated by reverse-phase high pressure liquid chromatography using an amino acid analysis PICO-TAG column (Waters Assoc., Div. of Millipore Corp., Milford, MA) and an acetonitrile gradient (10 …”

Section: Collagen Degradationmentioning

confidence: 99%

“…This suggests that aFGF and bFGF are either preferentially trapped by the bone matrix or are synthesized by skeletal cells; in either case, they may play a role in the local regulation of bone remodeling. Endothelial cell growth factor (ECGF), a form of aFGF, was shown to stimulate bone cell replication and, as a result, bone collagen synthesis, but the effects of bFGF on bone formation have not been reported (10). Studies using partially purified preparations of FGF indicated that it was mitogenic for bone cultures, but pure preparations of recombinant bFGF have not been tested, and its function in the process of bone remodeling has not been defined (1 1).…”

Section: Introductionmentioning

confidence: 99%

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Effects of basic fibroblast growth factor on bone formation in vitro.

Canalis¹,

Centrella²,

McCarthy³

1988

J. Clin. Invest.

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365

192

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Basic fibroblast growth factor (bFGF) was studied for its effects on bone formation in cultured rat calvariae. bFGF at 0.1-100 ng/ml stimulated [3Hlthymidine incorporation into DNA by up to 4.4-fold. bFGF also increased the number of colcemid-induced metaphase arrested cells and the DNA content. Transient (24 h) treatment with bFGF enhanced 1H1-proline incorporation into collagen 24-48 h after the factor was removed; this effect was DNA synthesis dependent and blocked by hydroxyurea. The collagen stimulated by bFGF was type I, and this effect was observed primarily in the periosteum-free bone. In contrast, continuous treatment with bFGF for 24-96 h inhibited VHlproline incorporation into type I collagen. bFGF did not alter collagen degradation. In conclusion, bFGF stimulates calvarial DNA synthesis, which causes an increased number of collagen-synthesizing cells, but bFGF has a direct inhibitory effect on collagen synthesis.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 94%

Section: Collagen Degradationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of basic fibroblast growth factor on bone formation in vitro.

Canalis¹,

Centrella²,

McCarthy³

1988

J. Clin. Invest.

Self Cite

365

192

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show abstract

“…The mitogenic effect of heparin on HUVEC also appears to be dependent on its interaction with ECGF and is not seen with increased concentrations of heparin alone (up to 900 ,g/ml) (14). A similar interaction has been observed in fetal rat calvariae where ECGF stimulates DNA synthesis (38). Heparin has been shown to increase the affinity of ECGF for its receptor, probably through a conformational change in the ECGF peptide (15).…”

mentioning

confidence: 70%

The addition of endothelial cell growth factor and heparin to human umbilical vein endothelial cell cultures decreases plasminogen activator inhibitor-1 expression.

Konkle¹,

Ginsburg²

1988

J. Clin. Invest.

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Plasminogen activator inhibitor-i (PAI-1) is a specific and rapid inhibitor of tissue plasminogen activator (tPA) and urokinase. Clinical studies suggest that PAM-i may play a crucial role in the regulation of fibrinolysis. A number of factors modulate PAM-i activity in endothelial cell culture, and the isolation of PAM-i cDNA now allows study of PAM-i regulation at the mRNA level. We examined the effect of endothelial cell growth factor (ECGF) and heparin on PAM-i expression in human umbilical vein endothelial cell (HUVEC) culture. The addition of ECGF and heparin to HUVEC cultures results in a 3-10-fold decrease in the PAM-i activity secreted into the conditioned media. This effect is mediated at the mRNA level. A decrease in PAM-i is also seen with higher concentrations of ECGF alone, but is greatly enhanced by the addition of heparin. No significant change in tPA antigen or mRNA levels was observed.

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Mechanisms of bone metastasis

Mundy¹

1997

Cancer

483

198

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Mechanisms of Bone MetastasisSolid cancers metastasize to bone by a multistep process that involves interactions Gregory R. Mundy, M.D.between tumor cells and normal host cells. Some tumors, most notably breast and prostate carcinomas, grow avidly in bone because the bone microenvironment University of Texas Health Science Center, San Antonio, Texas.provides a favorable soil. In the case of breast carcinoma, the final step in bone metastasis (namely bone destruction) is mediated by osteoclasts that are stimulated by local production of the tumor peptide parathyroid hormone-related peptide (PTH-rP), whereas prostate carcinomas stimulate osteoblasts to make new bone. Production of PTH-rP by breast carcinoma cells in bone is enhanced by growth factors produced as a consequence of normal bone remodeling, particularly activated transforming growth factor-b (TGF-b). Thus, a vicious cycle exists in bone between production by the tumor cells of mediators such as PTH-rP and subsequent production by bone of growth factors such as TGF-b, which enhance PTH-rP production. The metastatic process can be interrupted either by neutralization of PTH-rP or by rendering the tumor cells unresponsive to TGF-b, both of which can be accomplished experimentally. The osteoclast is another available site for therapeutic intervention in the bone metastatic process. Osteoclasts can be inhibited by drugs such as the new-generation bisphosphonates; as a consequence of this inhibition, there is a marked reduction in the skeletal events associated with metastatic cancer to bone, such as pain, fracture, and hypercalcemia. However and possibly even more importantly, there is also a reduction of tumor burden in bone. In experimental situations, this has clearly been shown to affect not only morbidity but also survival. The precise mechanism by which bisphosphonates inhibit osteoclasts is still unclear and may represent a combination of inhibition of osteoclast formation as well as increased apoptosis in mature osteoclasts. However, studies with potent bisphosphonates such as ibandronate, pamidronate, and risedronate have clearly documented that reduction of bone turnover and osteoclast activity leads to beneficial effects not only on skeletal complications associated with metastatic cancer, but also on tumor burden in bone.

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Effects of endothelial cell growth factor on bone remodelling in vitro.

Cited by 72 publications

References 35 publications

Effects of basic fibroblast growth factor on bone formation in vitro.

Effects of basic fibroblast growth factor on bone formation in vitro.

The addition of endothelial cell growth factor and heparin to human umbilical vein endothelial cell cultures decreases plasminogen activator inhibitor-1 expression.

Mechanisms of bone metastasis

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