Role of fibroblast growth factor-binding protein in the pathogenesis of HIV-associated hemolytic uremic syndrome

Ray, Patricio E.; Tassi, E.; Li, Xuehui; Wellstein, Anton

doi:10.1152/ajpregu.00492.2005

Cited by 39 publications

(56 citation statements)

References 51 publications

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“…FGF-BP binds to FGF-1 and FGF-2 in a noncovalent, reversible manner facilitating the release of the growth factor from the ECM and presenting it to FGF receptors (87-90). Moreover, FGF-BP is likely to supplement the role of heparan sulfate in mediating FGF-dependent signaling and mitogenesis (91). Indeed, we and others have shown that heparin, heparan sulfate, and other heparinoids are able to compete with FGF-BP binding to FGF-2 as well as a direct binding of FGF-BP to perlecan, thereby indicating a potential role for FGF-BP in releasing FGF proteins tightly bound to ECM molecules (90,92).…”

Section: Fibroblast Growth Factors and Fibroblast Growth Factor-bindimentioning

confidence: 81%

“…Numerous studies conducted in our laboratory have confirmed a role for FGF-BP as an extracellular chaperone for FGFs that enhances FGF-dependent biochemical and biologic functions. In murine NIH-3T3 fibroblasts as well as in bovine GM7373 endothelial cells, FGF-BP was shown to enhance FGF-2-induced MAPK signaling pathway and cell proliferation and we showed recently that the interaction domain with FGF-2 is a short domain in the C-terminus of the FGF-BP protein (90,91,93). Furthermore, FGF-BP was responsible for enhancing FGF-2-mediated angiogenesis in a chick chorioallantoic membrane (CAM) assay (90).…”

Section: Fibroblast Growth Factors and Fibroblast Growth Factor-bindimentioning

confidence: 99%

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The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

Tassi

Wellstein

2006

Seminars in Oncology

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Tumor angiogenesis has been related to the initiation as well as progression toward more aggressive behavior of human tumors. We will discuss genetic events underlying the initiation and progression of colorectal and pancreatic adenocarcinoma with a particular focus on the modulation of angiogenesis. A secreted fibroblast growth factor (FGF) binding protein (FGF-BP), which is an extracellular chaperone molecule for FGFs, has been shown to enhance FGF-mediated biochemical and biologic events and to be a crucial rate-limiting factor for tumor-dependent angiogenesis. Histochemical and in situ hybridization studies with archival samples show that FGF-BP is induced early during the initiation of colorectal and pancreatic adenocarcinoma. We will discuss the potential of this secreted protein as a serum marker to identify at-risk subjects.

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Section: Fibroblast Growth Factors and Fibroblast Growth Factor-bindimentioning

confidence: 81%

Section: Fibroblast Growth Factors and Fibroblast Growth Factor-bindimentioning

confidence: 99%

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

Tassi

Wellstein

2006

Seminars in Oncology

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“…Following that, we demonstrate that KLF5 promotes breast tumorigenesis in vivo by using the MCF7 breast cancer cell line (Figures 5d and e). As a KLF5 direct target gene, FGF-BP has been well documented to promote cell proliferation, migration, anchorage-independent growth, angiogenesis and tumorigenesis (Czubayko et al, 1994a(Czubayko et al, , b, 1997Aigner et al, 2001;Ray et al, 2006;Tassi et al, 2006). These results suggest that KLF5 may actually promote breast cancer progression.…”

Section: Discussionmentioning

confidence: 95%

Krüppel-like factor 5 promotes breast cell proliferation partially through upregulating the transcription of fibroblast growth factor binding protein 1

et al. 2009

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The Kru¨ppel-like factor 5 (KLF5) is a zinc-finger transcription factor promoting cell proliferation, cellcycle progression and survival. A high expression level of KLF5 mRNA has been shown to be associated with shorter breast cancer patient survival. However, the mechanism of KLF5 action in breast cancer is still not clear. In this study, we found that both KLF5 and its downstream gene fibroblast growth factor binding protein 1 (FGF-BP) are co-expressed in breast cell lines and primary tumors. Manipulation of the KLF5 expression can positively regulate the FGF-BP mRNA and protein levels in multiple breast cell lines. In addition, the secreted FGF-BP protein in the conditional medium is also regulated by KLF5. Furthermore, we demonstrated that KLF5 binds and activates the FGF-BP promoter through a GC box by luciferase reporter, oligo pull down and chromatin immunoprecipitation (ChIP) assays. When FGF-BP is depleted by siRNA, KLF5 fails to promote cell proliferation in MCF10A, SW527 and TSU-Pr1. We further demonstrated that overexpression or addition of FGF-BP rescues the KLF5-knockdown-induced growth arrest in MCF10A cells. Finally, KLF5 significantly promotes MCF7 breast cancer cell xenograft growth in athymic nude mice. These findings suggest that KLF5 may promote breast cancer cell proliferation at least partially through directly activating the FGF-BP mRNA transcription. Understanding the mechanism of KLF5 action in breast cancer may result in useful diagnostic and therapeutic targets.

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“…21 On the other hand, BP1 expression was found upregulated in blood vessels of mice that succumb to premature atherogenesis, 63 a disease that is linked to inflammation and pathological repair of vascular endothelia. Furthermore, BP1 was found to be upregulated after spinal cord injury and in HIV-induced kidney damage, 64,65 in different malignancies such as colon, breast, prostate, 19,44,66 and skin cancers, 17 and has been proposed as an angiogenic switch that is turned on during malignant progression. 16 These findings suggest that BP1 can play a role in the maintenance and repair, as well as the pathology, of a variety of tissues.…”

Section: Fgfbp1 Conditional Expression In Mice 2229mentioning

confidence: 99%

Impact of Fibroblast Growth Factor-Binding Protein–1 Expression on Angiogenesis and Wound Healing

Tassi

McDonnell

Gibby

et al. 2011

The American Journal of Pathology

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Fibroblast growth factors (FGFs) participate in embryonic development, in maintenance of tissue homeostasis in the adult, and in various diseases. FGF-binding proteins (FGFBP) are secreted proteins that chaperone FGFs stored in the extracellular matrix to their receptor, and can thus modulate FGF signaling. FGFBP1 (alias BP1, FGF-BP1, or HBp17) expression is required for embryonic survival, can modulate FGF-dependent vascular permeability in embryos, and is an angiogenic switch in human cancers. To determine the function of BP1 in vivo, we generated tetracycline-regulated conditional BP1 transgenic mice. BP1-expressing adult mice are viable, fertile, and phenotypically indistinguishable from their littermates. Induction of BP1 expression increased mouse primary fibroblast motility in vitro, increased angiogenic sprouting into subcutaneous matrigel plugs in animals and accelerated the healing of excisional skin wounds. FGF-receptor kinase inhibitors blocked these effects. Healing skin wounds showed increased macrophage invasion as well as cell proliferation after BP1 expression. Also, BP1 expression increased angiogenesis during the healing of skin wounds as well as after ischemic injury to hindlimb skeletal muscles. We conclude that BP1 can enhance FGF effects that are required for the healing and repair of injured tissues in adult animals. The family of fibroblast growth factors (FGFs) encompasses 18 distinct FGF receptor ligands, with a wide expression range and a significant role in angiogenesis, tumor progression, wound healing, and embryonic development.1-4 Many members of the FGF family, such as FGF1 and FGF2, are immobilized in the extracellular matrix (ECM) bound to heparan sulfate proteoglycans (HSPGs) and released from this storage site by proteases and heparanases. 4 -6 The involvement of carrier proteins that shuttle FGFs from their storage site to their receptors represents an alternative mode of regulation of FGF release from the ECM. 1,7 FGF-binding protein 1 (BP1, FGFBP1, FGF-BP1, or HBp17), 8 the best characterized of the three known secreted FGFBPs, 9 is an extracellular chaperone that binds FGF1, 2, 7, 10, and 22 in a reversible, noncovalent manner. 8,10 -12 Binding of the C-terminus of the BP1 protein is sufficient for its interaction with FGF2.13 After binding to BP1, the biochemical and biological activities of FGF are positively modulated.14 Several findings from different laboratories indicate that BP1 can contribute to embryonic development, 15 angiogenesis, tumor growth, and malignant progression, 11,12,14 -20 as well as the maintenance and reinnervation of the neuromuscular junction. 21 We reported earlier that expression of BP1 in SW13 cells induces FGF2 release from the cells, FGF-dependent colony formation in soft agar, and the growth of highly vascularized tumors in nude mice.11 In contrast, depletion of endogenous BP1 from ME180 cells was observed to reduce the release of ECM bound FGF2 into the cell supernatants and to increase FGF2 immobilized on the cell surface.16 Consisten...

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Role of fibroblast growth factor-binding protein in the pathogenesis of HIV-associated hemolytic uremic syndrome

Abstract: Wellstein. Role of fibroblast growth factor-binding protein in the pathogenesis of HIV-associated hemolytic uremic syndrome.

Cited by 39 publications

References 51 publications

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

Krüppel-like factor 5 promotes breast cell proliferation partially through upregulating the transcription of fibroblast growth factor binding protein 1

Impact of Fibroblast Growth Factor-Binding Protein–1 Expression on Angiogenesis and Wound Healing

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