Clinical applications of heparin‐binding growth factors

Lobb, Roy R.

doi:10.1111/j.1365-2362.1988.tb01020.x

Eur J Clin Investigation

1988

DOI: 10.1111/j.1365-2362.1988.tb01020.x

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Clinical applications of heparin‐binding growth factors

Roy R. Lobb

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1989

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Cited by 78 publications

(39 citation statements)

References 129 publications

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“…Because the endothelial cell is considered to be the primary cell involved in all forms of angiogenesis, efforts have concentrated on the identity of polypeptide factors that control endothelial cell proliferation (1,2). Indeed, the heparinbinding growth factor (HBGF) family of polypeptides has gained general acceptance as initiators of angiogenesis especially during development (1)(2)(3)(4)(5)(6). This gene family includes the prototypes HBGF-1 (acidic fibroblast growth factor), HBGF-2 (basic fibroblast growth factor), and three additional HBGF-like structures, hst/KS, int-2, and fibroblast growth factor 5 (2,5).…”

mentioning

confidence: 99%

RETRACTED: Heparin-binding growth factor 1 induces the formation of organoid neovascular structures in vivo.

Thompson

Haudenschild

Anderson

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

125

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One of the promises of modem molecular biology has been the opportunity to use genetically modified human cells in a patient to permanently restore inborn errors of metabolism. Although it has been possible to introduce genes into mammalian cells and to control their expression, it has proven difficult to introduce mammalian cells as carriers of the modified genetic information into hosts. The successful implantation of selective cells cannot be achieved without adequate vascular support, an essential step toward integration and reconstitution of a new biological function. Although a partial solution to this problem has been found by inducing specific site-directed neovessel formation using heparinbinding growth factor 1 (HBGF-1) adsorbed to a collagen matrix, these implants function for only a short period (weeks). We now report the formation of organoid neovascular structures using polytetrafluoroethylene fibers coated with collagen and HBGF-1 implanted in the peritoneal cavity of the rat. The organoid structures contained readily visible vascular lumina and nonvascular structures that resemble nerve tissue. It was also possible to demonstrate that the vascular system on the implant is continuous with the vascular tree of the host. This feature was used to demonstrate that the organoid structures are capable of sustaining the biological function of implanted normal rat hepatocytes over long periods of time (months) in the homozygous Gunn rat, thereby facilitating future applications involving the delivery of new genetic information.Angiogenesis involves the orderly migration and proliferation of blood vessels and occurs during development (1,2). Although angiogenesis is an infrequent event in the adult, mainly associated with wound and fracture repair, exceptions are found in the female reproductive system, where this process occurs in the follicle during development, in the corpus luteum during ovulation, and in the placenta during pregnancy (1, 2). These physiologic, specific periods of angiogenesis are relatively brief and highly regulated in contrast to the pathologic angiogenic events associated with tumor growth, diabetic retinopathy, and other disorders. Because the endothelial cell is considered to be the primary cell involved in all forms of angiogenesis, efforts have concentrated on the identity of polypeptide factors that control endothelial cell proliferation (1,2). Indeed, the heparinbinding growth factor (HBGF) family of polypeptides has gained general acceptance as initiators of angiogenesis especially during development (1)(2)(3)(4)(5)(6). This gene family includes the prototypes HBGF-1 (acidic fibroblast growth factor), HBGF-2 (basic fibroblast growth factor), and three additional HBGF-like structures, hst/KS, int-2, and fibroblast growth factor 5 (2, 5). HBGF-1 and HBGF-2 are potent inducers of endothelial cell migration and/or proliferation in vitro (1, 2, 7) and are known to modulate the expression of endothelial cell-derived proteases (8-13). Further, the HBGF prototypes are tightl...

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mentioning

confidence: 99%

RETRACTED: Heparin-binding growth factor 1 induces the formation of organoid neovascular structures in vivo.

Thompson

Haudenschild

Anderson

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

125

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“…The angiogenic, neurotrophic, and growthpromoting effects of FGF2 suggest that FGF2 has potential therapeutic applications (Lobb, 1988). Conversely, inappropriate FGF2 expression may contribute to diverse pathologies, including diabetic retinopathy, tumor growth, renal injury, rheumatoid arthritis, and atherosclerosis (Folkman and Klagsbrun, 1987;Klagsbrun and Edelman, 1989;Hicks et al, 1991;Abboud, 1993).…”

mentioning

confidence: 99%

“…FGF2 probably is the most widely distributed mitogen yet characterized. It has been found without exception in all tissues so far examined and in most, although not all, cells (Lobb, 1988). The family of FGFRs is functionally present in wide variety of cells, if not all (for review, see Jaye et al, 1992).…”

mentioning

confidence: 99%

In Vivo Involvement of Heparan Sulfate Proteoglycan in the Bioavailability, Internalization, and Catabolism of Exogenous Basic Fibroblast Growth Factor

et al. 1999

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The in vivo bioavailability of exogenous fibroblast growth factor 2 (FGF2) was studied after i.v. injection of uniformly 14 C-labeled FGF2 into young rats.14 C-FGF2 was rapidly accumulated in almost all solid organs within 5 min. After 30 min, more than 65% of FGF2 was retained in liver, 4.5% in kidneys, 1.2% in spleen, 0.15% in adrenal glands, and trace amounts in bone marrow, eyes, lungs, and heart. Suborgan distribution of 14 C-FGF2 showed that for kidneys and adrenal glands, the labeling was mainly concentrated in the cortical zone. Incubation of organ sections with 2 M NaCl or heparin eluted all the radioactivity, indicating that labeling was due to FGF2-heparan sulfate proteoglycan (HSPG) interactions. Electrophoretic analysis show only native 14 C-FGF2 in the blood and extracellular matrix; however, FGF2 is continuously catabolized in solid organs, indicating that all participate in the clearance of FGF2 by cellular internalization and subsequent catabolism. All FGF2 catabolic fragments bound heparin, demonstrating the preservation of their HSPG-binding site during the in vivo intracellular catabolism of FGF2. Analysis of the high-affinity receptors of FGF2 (FGFR-1 and FGFR-3) and the mitogen-activated protein kinase did not show any increase in either FGFR tyrosine phosphorylation or in mitogen-activated protein kinase activation. This study shows for the first time that exogenous FGF2 is cleared by HSPG cellular internalization and catabolism without inducing the activation of FGFRs within at least five organs in vivo, which strongly suggests that the HSPG-dependent internalization and catabolism pathway may control the in vivo bioavailability of FGF2.

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“…To date, however, no studies have been re ported on the efficacy of aFGF for healing chronic experimental gastric ulcers. There fore, the purposes of the present study were: (1) to assess the capability of human recombi nant aFGF [10], when administered orally, to heal acetic-acid-induced gastric ulcers in rats: (2) to compare the healing effect of aFGF to that of standard antiulcer agents (famotidine, Maalox): (3) to determine whether combined aFGF and Maalox treatment would enhance the healing of experimental gastric ulcers, and (4) to assess whether orally administered aFGF stimulated angiogenesis in the aceticacid-induced gastric ulcer bed.…”

mentioning

confidence: 99%

“…Growth factors like epidermal growth fac tor, platelet-derived growth factor, transform ing growth factor and fibroblast growth fac tors (FGFs) are potential therapeutic agents for wound healing [1], FGF is present in a wide variety of tissues [1][2][3] and is found in macrophages [4] as well as endothelial cells [2], At very low concentrations, FGF can stimulate the angiogenic process [1][2][3][4], which is thought to play an important role in wound healing.…”

mentioning

confidence: 99%

Acidic Fibroblast Growth Factor Accelerates the Healing of Acetic-Acid-lnduced Gastric Ulcers in Rats

Fitzpatrick¹,

Jakubowska²,

Martin³

et al. 1992

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Acidic fibroblast growth factor (aFGF) was evaluated for the healing of acetic-acid-induced gastric ulcers in rats. The effect of aFGF on angiogenesis in the gastric ulcer bed was determined by the carmine dye infusion method, while its effect on gastric acid secretion was assessed in chronic gastric fistula rats. Oral treatment with aFGF, in the presence of heparin, reduced (ED₅₀ value = 30.2 μg/kg/day) the acetic-acid-induced gastric ulcer area, when assessed 1 week later. aFGF was about 1,333-fold more potent than famotidine for healing such ulcers. At a dose of 200 μg/kg/day, aFGF increased the carmine density 3-fold and correspondingly reduced (80%) the gastric ulcer area. Thus, the ulcer healing effect of this agent involves angiogenesis in the gastric ulcer bed. This effect of aFGF appears to be unrelated to an inhibition of gastric acid secretion, as it was ineffective in chronic gastric fistula rats. In summary, oral aFGF significantly accelerates the healing of experimental gastric ulcers in rats. It may be a potent and effective agent for the treatment of peptic ulcers in humans.

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Clinical applications of heparin‐binding growth factors

Cited by 78 publications

References 129 publications

RETRACTED: Heparin-binding growth factor 1 induces the formation of organoid neovascular structures in vivo.

RETRACTED: Heparin-binding growth factor 1 induces the formation of organoid neovascular structures in vivo.

In Vivo Involvement of Heparan Sulfate Proteoglycan in the Bioavailability, Internalization, and Catabolism of Exogenous Basic Fibroblast Growth Factor

Acidic Fibroblast Growth Factor Accelerates the Healing of Acetic-Acid-lnduced Gastric Ulcers in Rats

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