Acidic fibroblast growth factor in the developing rat embryo.

Fu, Yiming; Spirito, Paolo; Yu, Zu‐Xi; Biro, Sadatoshi; Sasse, Joachim; Jun, Lei; Ferrans, Víctor J.; Epstein, Stephen E.; Casscells, Ward

doi:10.1083/jcb.114.6.1261

Cited by 107 publications

(62 citation statements)

References 59 publications

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“…Both FGFl and FGF2 have been found bound to HSPGs either on the cell surface or in the extracellular matrix (Klagsbrun, 1990) and HSPG-bound FGF1 has been shown to be 100x more mitogenic than heparinbound FGF1 (Gordon et al, 1989). FGF1 has been localized extracellularly in vivo in the developing heart (Engelmann et al, 1993), tooth (Cam et al, 1992), lungs, digestive system, CNS and eye (Fu et al, 1991) where it is thought to act both as a paracrine growth factor as well as stimulating capillary and neural invasion. Weiner and Swain (1989) have shown that neonatal cardiac myocytes deposit FGF1 into their extracellular matrix and FGFR1 transcipts have been localized on developing cardiomyocytes (Engelman et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

The location of acidic fibroblast growth factor in the breast is dependent on the activity of proteases present in breast cancer tissue

Coope

Browne²,

Yiangou³

et al. 1997

Br J Cancer

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Summary Acidic fibroblast growth factor (FGF1) and two of its receptors, FGFR1 and FGFR4, were localized in cryostat sections of normal, benign and malignant human breast tissue by immunohistochemistry. Without pretreatment, FGF1 staining was mainly seen in normal epithelial cells. However, polymerase chain reaction (PCR) analysis and immunoblotting of isolated normal epithelial and myoepithelial cells showed FGF1 mRNA and protein to be present in both cell types. Following incubation of frozen sections at 370C in phosphate-buffered saline, FGF1 staining was also revealed in myoepithelial cells and basement membrane adjacent to carcinoma cells. Treatment with protease inhibitors demonstrated that this effect was due to the activity of an endogenous protease. In contrast, FGF1 staining was found to be associated with the stroma adjacent to malignant cells only in the presence of protease inhibitors. FGFR1 and FGFR4 immunostaining was localized to both normal and malignant epithelial cells and to a lesser extent to myoepithelial cells. There was no difference in the staining intensity for the FGF receptors between normal and cancer samples. The change in location of FGF1 between normal and malignant tissues and the sensitivity of stored FGF1 to the action of endogenous proteases raises the possibility of both autocrine and paracrine roles for FGF1 in the normal and malignant human breast.Keywords: breast cancer; fibroblast growth factor 1; protease; immunohistochemistry Fibroblast growth factor 1 (FGF1) belongs to a family of multifunctional polypeptides that are involved in a wide array of biological processes, which include cellular proliferation and differentiation, angiogenesis, chemotaxis, embryonal development and tissue repair (Basilico and Moscatelli, 1992). To date, the FGFs consist of a family of nine homologous polypeptide growth factors that include FGF1 (acidic FGF), FGF2 (basic FGF), FGF3 (int-2), FGF4 (hst-l/Kaposi FGF), FGF5, FGF6 (hst-2), FGF7 (keratinocyte growth factor), FGF8 (androgen-induced growth factor) and FGF9 (glial-activating factor) (Basilico and Moscatelli, 1992;Tanaka et al, 1992;Miyamoto et al, 1993). These proteins share 35-50% overall homology of their amino acid sequences (Basilico and Moscatelli, 1992;Givol and Yayon, 1992).Unlike other members of the family, FGF1, FGF2 and FGF9 are synthesized without a signal peptide sequence and thus may remain sequestered in the cell (Basilico and Moscatelli, 1992;Cao and Pettersson, 1993). However, release of FGF may occur through leakage from damaged cells or from viable cells via a novel mechanism (Mignatti et al, 1992;Cao and Pettersson, 1993). Yeoman (1993) has postulated that proteoglycan-bound FGF may be released from the cell surface or extracellular matrix by the action of proteases, and Briozzo et al (1991) have shown that Received 10 June 1996 Revised 26 November 1996 Accepted 3 December 1996 Correspondence to: J Gomm MCF7 breast cancer cells secrete cathepsin D, which is able to digest the extracellular matrix and releas...

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Section: Discussionmentioning

confidence: 99%

The location of acidic fibroblast growth factor in the breast is dependent on the activity of proteases present in breast cancer tissue

Coope

Browne²,

Yiangou³

et al. 1997

Br J Cancer

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“…Synergistic Angiogenesis. Leptin has been found to be coexpressed with other angiogenic factors (including FGF-2 and VEGF) in adipose, placental, and fetal tissues, suggesting that leptin might modulate the angiogenic activity of these factors (3,7,11). To test this possibility, low doses of leptin and FGF-2 or VEGF were coimplanted into mouse corneas.…”

Section: Resultsmentioning

confidence: 99%

Leptin induces vascular permeability and synergistically stimulates angiogenesis with FGF-2 and VEGF

Cao

Bråkenhielm

Wahlestedt

et al. 2001

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

404

288

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Most endocrine hormones are produced in tissues and organs with permeable microvessels that may provide an excess of hormones to be transported by the blood circulation to the distal target organ. Here, we investigate whether leptin, an endocrine hormone, induces the formation of vascular fenestrations and permeability, and we characterize its angiogenic property in the presence of other angiogenic factors. We provide evidence that leptininduced new blood vessels are fenestrated. Under physiological conditions, capillary fenestrations are found in the leptin-producing adipose tissue in lean mice. In contrast, no vascular fenestrations were detected in the adipose tissue of leptin-deficient ob͞ob mice. Thus, leptin plays a critical role in the maintenance and regulation of vascular fenestrations in the adipose tissue. Leptin induces a rapid vascular permeability response when administrated intradermally. Further, leptin synergistically stimulates angiogenesis with fibroblast growth factor (FGF)-2 and vascular endothelial growth factor (VEGF), the two most potent and commonly expressed angiogenic factors. These findings demonstrate that leptin has another new function-the increase of vascular permeability.leptin ͉ obesity ͉ vascular fenestrations ͉ neovascularization

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“…The study by Fu et al (1991) also reported high and low molecular weight forms of FGF in SD rat embryos. In addition, they detected "faint staining in some nuclei" by immunohistochemistry, but did not state in which specific tissues this occurred or at what stages.…”

Section: Fgf Associated With Plasma Membranes and Nucleimentioning

confidence: 97%

“…11-16, NIH 3T3 cells. Fu et al (1991) suggested that extracellular pools of acidic FGF they immunostained in the central nervous system of embryonic rats could stimulate capillary invasion. In the present study, the demonstration of extracellular dense foci of FGF was a relatively infrequent finding.…”

Section: Immunolocalization Of Fgf Within Gonadotropes and Its Releasmentioning

confidence: 99%

Development of the vasculature of the anterior pituitary: Ontogeny of basic fibroblast growth factor

Schechter

Pattison

1993

Developmental Dynamics

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This study correlates the ontogeny of basic fibroblast growth factor (FGF) with the development of the vasculature of the anterior pituitary (AP) in two strains of rat, Sprague-Dawley (SD) and Fischer 344 (F344). Immunolocalization of FGF was followed from the first appearance of Rathke's pouch (RP) in 12-day (12d) fetuses, through each day of fetal development, and in 5,20, and 50d postnatal female rats. In addition, the ontogeny of folliculo-stellate cells (FSC) is described, since previous studies suggested that these unique cells might function as phagocytes in the regulation of FGF. In both rat strains, vascularization of the A P commenced in 16d fetuses. In 15-20d fetuses, dense foci of immunopositivity for extracellular FGF were apparent at sites of capillary penetration adjacent to partially disrupted, immature gonadotropes. Localization of FGF was first detected in immature gonadotropes in 18d fetuses and persisted in the cytosol of a subpopulation of gonadotropes thereafter. In 15d fetuses, FGF was localized within the cytosol intimately associated with the peripheral-facing plasma membranes of all cells of the adenohypophysis, and persisted to variable degrees in later fetal stages. Localization of FGF within nuclei of AP parenchymal cells was evident only in 16-17d fetuses. Although the ontogeny of FGF and vascularization of the AP was very similar in both rat strains, the ontogeny of FSC differed markedly. In both strains, follicular lumens contained FGF during late fetal and early postnatal development. However, both electron microscopy and immunostaining for S-100 marker protein revealed that the postero-lateral edges of the A P of F344 rats often lacked FSC when compared to SD rats, a situation which could compromise regulation of FGF by FSC at the A P periphery in that strain, and thereby contribute to the neovascularization from systemic blood vessels known to occur in that strain during prolactinoma formation.

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Acidic fibroblast growth factor in the developing rat embryo.

Cited by 107 publications

References 59 publications

The location of acidic fibroblast growth factor in the breast is dependent on the activity of proteases present in breast cancer tissue

The location of acidic fibroblast growth factor in the breast is dependent on the activity of proteases present in breast cancer tissue

Leptin induces vascular permeability and synergistically stimulates angiogenesis with FGF-2 and VEGF

Development of the vasculature of the anterior pituitary: Ontogeny of basic fibroblast growth factor

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