BACKGROUND: In vivo and in vitro studies demonstrate the important roles of fibroblast growth factor (FGF) and FGF receptors (FGFRs) in neural survival, neurogenesis, oxidative stress, and emotional behavior. However, evidence on the role of FGF and FGFR in the pathophysiology of major depressive disorder (MDD) remains limited and inconclusive.
OBJECTIVE: This preliminary meta-analysis aimed to examine changes in peripheral or central FGF and FGFR levels in patients with MDD.
METHODS: Electronic research through platform of PubMed and ClinicalTrials.gov.
METHODS: We used the inclusion criteria: articles discussing the comparisons of FGF levels, either in peripheral or central environment, in patients with MDD and in healthy controls (HC); articles on clinical trials in humans; and case-control trials. Case reports or series and nonclinical trials were excluded.
METHODS: Using a thorough literature search, the FGF/FGFR levels in patients with MDD and HC were compared. Four studies on peripheral FGF-2 and 3 on central FGF-2 and FGFR1 levels were included.
RESULTS: The findings reveal significantly higher peripheral FGF-2 protein and central FGFR1 RNA levels in patients with MDD than in HC (P = 0.005 and 0.006, separately), but no significant association with clinical variables. There was also no significant difference in the central FGF-2 levels in patients with MDD and in HC (P = 0.180).
CONCLUSIONS: The study has limitations of a small number of included studies, lack of meta-analysis of the FGF changes along with treatment, and lack of direct evidence on correlation of peripheral FGF-2 with central FGF-2 levels.
CONCLUSIONS: This preliminary meta-analysis points out a new direction for future studies investigating the relationship among MDD, oxidative stress, and the FGF family.

The rapid development of angiogenic growth factor therapy for patients with advanced ischemic heart disease over the last 5 years offers hope of a new treatment strategy based on generation of new blood supply in the diseased heart. However, as the field of therapeutic coronary angiogenesis is maturing from basic and preclinical investigations to clinical trials, many new and presently unresolved issues are coming into focus. These include in-depth understanding of the biology of angiogenesis, selection of appropriate patient populations for clinical trials, choice of therapeutic end points and means of their assessment, choice of therapeutic strategy (gene versus protein delivery), route of administration, and the side effect profile. The present article presents a summary statement of a panel of experts actively working in the field, convened by the Angiogenesis Foundation and the Angiogenesis Research Center during the 72nd meeting of the American Heart Association to define and achieve a consensus on the challenges facing development of therapeutic angiogenesis for coronary disease.

Platelet-derived growth factor-B (PDGF-B) is a potent paracrine-acting mitogen in Kaposi\'s sarcoma (KS) lesions. Interferon-alpha is widely used for clinical treatment of KS. Here we show that platelet-derived growth factor-B activates proliferation and migration of cultivated AIDS-KS spindle cells whereas interferon-alpha acts as an inhibitor. At the molecular level, these opposite activities of platelet-derived growth factor-B and interferon-alpha converged onto the adverse regulation of the c-myc gene expression. Platelet-derived growth factor-B induced c-myc mRNA and protein synthesis in cultivated AIDS-KS spindle cells whereas interferon-alpha inhibited these processes. Using c-myc-specific phoshothioate antisense oligodeoxynucleotides, we demonstrated that down-regulation of c-myc expression is sufficient to inhibit proliferation and migration of KS spindle cells in vitro. This indicated that c-Myc protein may be an important regulatory molecule of KS spindle cell proliferation and migration. High amounts of the c-Myc protein were detected in the nuclei of KS spindle cells in histological sections of AIDS-KS biopsies. This suggested that the c-myc gene may also regulate proliferation and migration of AIDS-KS spindle cells in vivo. In this case, c-myc may play an important role in the focus of major pathogenic and therapeutic pathways of KS.

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Synthetic genes encoding the 146 and 155 amino acid forms of human basic fibroblast growth factor (bFGF) were constructed with codon usage biased towards the polyhedrin-encoding gene of Autographa californica nuclear polyhedrosis virus (AcNPV). Expression of both bFGF genes in Spodoptera frugiperda (SF-21) suspension cell culture using a recombinant baculovirus yielded approximately 2.5 mg of mitogenically fully active protein per 10(9) cells following heparin-affinity chromatography. To improve translational efficiency, the Kozak consensus sequence was introduced and it was found that neither the replacement of a pyrimidine by a purine at position -3, nor the nature of the base at position +4 had any noticeable effect on the final levels of bFGF expression in SF-21 cells. The bases at these critical points in the consensus do not therefore play a major role in expression levels of the bFGF synthetic genes. The two synthetic genes were also expressed in Escherichia coli as native proteins using the T7 expression system. 5 mg of mitogenically fully active bFGF were obtained from 1 l of bacterial culture. Both insect cell- and E. coli-derived bFGF were equally mitogenic for Swiss 3T3 fibroblasts.