Migratory and proliferative effect of platelet‐derived growth factor in rabbit retinal endothelial cells: Evidence of an autocrine pathway of platelet‐derived growth factor

Koyama, Noriyuki; Watanabe, Shiro; Tezuka, Mariko; Morisaki, Naho; Saitō, Yasushi; Yoshida, Sho

doi:10.1002/jcp.1041580102

Cited by 45 publications

(30 citation statements)

References 39 publications

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“…The endothelium is the production site for several factors with the ability to stimulate or inhibit endothelial cell function (McPherson et al 1981, Schweigerer et al 1987, Koyama et al 1994, Nomura et al 1995. Autocrine regulation provides an insight into the mechanism by which local differences of cell growth and differentiation are established within a capillary microenvironment that would determine, for example, the selection of a single endothelial cell to initiate a new capillary network.…”

Section: Discussionmentioning

confidence: 99%

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Human umbilical vein endothelial cells express multiple prolactin isoforms

Corbacho¹,

Macotela²,

Nava³

et al. 2000

Journal of Endocrinology

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Members of the prolactin (PRL) hormonal family have direct effects on endothelial cell proliferation, migration and tube formation. Moreover, isoforms of PRL may function as autocrine regulators of endothelial cells. Bovine brain capillary endothelial cells (BBCEC) express the PRL gene, while anti-PRL antibodies inhibit BBCEC proliferation. Here, we show the expression of the PRL gene into various PRL isoforms in endothelial cells from the human umbilical vein. Reverse transcription-polymerase chain reaction of total RNA from human umbilical vein endothelial cells (HUVEC) detected the full-length PRL mRNA as well as a 100 bp smaller PRL transcript similar to the one previously reported in BBCEC. HUVEC were positive to PRL immunocytochemistry. In addition, various PRL immunoreactive proteins were detected in HUVEC extracts and HUVEC conditioned media by metabolic labelling immunoprecipitation analysis. These PRL immunorelated proteins had apparent molecular masses of 60, 23, 21, 16 and 14 kDa. In contrast to previous findings in BBCEC, HUVEC conditioned media contained very little PRL bioactivity as determined by the selective bioassay of Nb2 cell proliferation. Moreover, some polyclonal or monoclonal antibodies directed against PRL stimulated HUVEC proliferation, in contrast to the inhibitory effect seen in BBCEC. The present findings extend the previous observations about the expression of PRL gene in endothelial cells from bovine brain capillaries to human cells of the umbilical vein, implicating that endothelium from different types of vessels and species share the expression of PRL gene but may differ in the putative autocrine role of the PRL isoforms expressed.

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Section: Discussionmentioning

confidence: 99%

“…Endothelial cells are known to produce and respond to their own angiogenic and anti-antiangiogenic factors, and thus exert an autocrine control of neovascularisation (McPherson et al 1981, Schweigerer et al 1987, Koyama et al 1994, Nomura et al 1995. Recent work has suggested that PRLs may contribute to this autocrine regulation.…”

Section: Introductionmentioning

confidence: 99%

Human umbilical vein endothelial cells express multiple prolactin isoforms

Corbacho¹,

Macotela²,

Nava³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…The endothelium is the production site for several factors with the ability to stimulate or inhibit the formation of new blood vessels (McPherson et al 1981, Schweigerer et al 1987, Klagsbrun & D'Amore 1991, Auerbach & Auerbach 1994, Koyama et al 1994, Nomura et al 1995. Autocrine angiogenic and antiangiogenic factors provide an insight into the mechanisms by which endothelial cell growth is selectively supported or prohibited locally within a tissue microenvironment.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover endothelial cells produce and respond to their own angiogenic or antiangiogenic factors (autocrine regulation). Endothelial peptides with autocrine effects include basic fibroblast growth factor (bFGF), plateletderived growth factor (PDGF), vascular endothelial growth factor (VEGF) and thrombospondin (McPherson et al 1981, Schweigerer et al 1987, Koyama et al 1994, Nomura et al 1995. Autocrine regulation could help explain the local differences of cell growth and differentiation that must be established in a capillary microenvironment and that are involved, for example, in the selection of a single endothelial cell to initiate a capillary network.…”

Section: Introductionmentioning

confidence: 99%

Expression of prolactin mRNA and of prolactin-like proteins in endothelial cells: evidence for autocrine effects

Clapp¹,

López-Gómez²,

Nava³

et al. 1998

Journal of Endocrinology

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Formation of new capillary blood vessels, termed angiogenesis, is essential for the growth and development of tissues and underlies a variety of diseases including tumor growth. Members of the prolactin hormonal family bind to endothelial cell receptors and have direct effects on cell proliferation, migration and tube formation. Because many angiogenic and antiangiogenic factors are produced by endothelial cells, we investigated whether endothelial cells expressed the prolactin gene. Here we show that bovine brain capillary endothelial cells (BBCEC) in culture express the full-length prolactin messenger RNA, in addition to a novel prolactin transcript, lacking the third exon of the gene. In addition cultures of BBCEC synthesize and secrete prolactin-like immunoreactive proteins with apparent molecular masses of 23, 21 and 14 kDa. The prolactin-like nature of these proteins is supported by the observation that Nb2-cells, a prolactin-responsive cell line, were stimulated to proliferate when co-cultured with endothelial cells and this stimulation was neutralized with prolactin-directed antibodies. Finally, consistent with a possible autocrine effect of endothelial-derived prolactins, polyclonal and monoclonal prolactin antibodies specifically inhibited basal and basic fibroblast growth-factorstimulated growth of endothelial cells. Taken together, the present findings support the hypothesis of the prolactin gene being expressed in endothelial cells as proteins that could act in an autocrine fashion to regulate cell proliferation.

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“…229,230 Additionally, significantly elevated concentrations of PDGF AB are found in the vitreous and preretinal membranes of patients with proliferative diabetic retinopathy (PDR). 231 PDGF may act directly on endothelial cells 232 that are engaged in angiogenesis or that express PDGF receptor beta-subunits. 233,234 However, it is reported that PDGF AB is also elevated in ischemic non-diabetic retinopathy, indicating that ischemia rather than diabetes per se might be a strong stimulator of PDGF production in the retina.…”

mentioning

confidence: 99%

The pathogenesis of diabetic retinopathy: old concepts and new questions

Cai

Boulton

2002

Eye

294

196

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Hyperglycaemia appears to be a critical factor in the aetiology of diabetic retinopathy and initiates downstream events including: basement membrane thickening, pericyte drop out and retinal capillary non-perfusion. More recently, focus has been directed to the molecular basis of the disease process in diabetic retinopathy. Of particular importance in the development and progression of diabetic retinopathy is the role of growth factors (eg vascular endothelial growth factor, placenta growth factor and pigment epithelium-derived factor) together with specific receptors and obligate components of the signal transduction pathway needed to support them. Despite these advances there are still a number of important questions that remain to be answered before we can confidently target pathological signals. How does hyperglycaemia regulate retinal vessels? Which growth factors are most important and at what stage of retinopathy do they operate? What is the preferred point in the growth factor signalling cascade for therapeutic intervention? Answers to these questions will provide the basis for new therapeutic interventions in a debilitating ocular condition.

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Migratory and proliferative effect of platelet‐derived growth factor in rabbit retinal endothelial cells: Evidence of an autocrine pathway of platelet‐derived growth factor

Cited by 45 publications

References 39 publications

Human umbilical vein endothelial cells express multiple prolactin isoforms

Human umbilical vein endothelial cells express multiple prolactin isoforms

Expression of prolactin mRNA and of prolactin-like proteins in endothelial cells: evidence for autocrine effects

The pathogenesis of diabetic retinopathy: old concepts and new questions

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