Growth factors最新文献

Since its introduction in 2001, multiple platelet-rich fibrin (PRF) centrifugation protocols have emerged, but the variations in growth factor release that result from these protocols remain unclear. This review aimed to evaluate growth factor release across three PRF protocols: leukocyte-PRF (L-PRF), advanced-PRF (A-PRF/+), and injectable-PRF (i-PRF). A comprehensive search was conducted using the MEDLINE and Embase databases, identifying 14 studies that met the inclusion criteria. Due to significant heterogeneity in study designs and methodologies, a meta-analysis was not feasible. However, our findings suggest that lower-speed centrifugation protocols, such as A-PRF/+ and i-PRF, tend to provide a more uniform cell distribution and sustain higher growth factor release over time compared to the conventional L-PRF protocol. Despite these observations, the current evidence is insufficient to draw definitive conclusions about the growth factor release levels among L-PRF, A-PRF/+, and i-PRF. Further well-designed, comparative studies are required to clarify these differences and establish optimal protocols for clinical use.

Psoriasis pathogenisis remain unknown despite the fact that it is considered as the most common autoimmune skin disease. We raised the hypothesis whether the selected biomarkers in this study provide actual evidence of psoriasis presence and severity. We aim in a first level to study serum level of pro-angiogenic marker VEGF variation and its correlation with MMP-9 and its specific inhibitor TIMP-2 in psoriatic patients serum. The study included 115 psoriatic patients and 51 controls. The biological parameters were measured by ELISA methods. Logistic regression analysis showed that VEGF, MMP-9, and inflammation Z-score are associated with psoriasis. ROC analysis showed that VEGF has low discriminant power for PsVG, However TIMP-2 and inflammation Z-scorewell discriminate this variant of psoriasis. The combined analysis of VEGF-TIMP-2 resulted in a significant increase in discriminant power for PsVG. Increase inflammatory phase may be reflecting the tissue destruction byMMP-9, emphasizing the deleterious expanse and the architectural changes of the skin which are more severe in PsP.

Platelet-derived growth factor (PDGF)-induced signalling via PDGF receptor β (PDGFRβ) leads to activation of downstream signalling pathways which regulate multiple cellular responses. It is unclear how PDGFRβ is degraded; both lysosomal and proteasomal degradation have been suggested. In this study, we have characterised the proteolytic cleavage of ligand-activated PDGFRβ, which results in two fragments: a larger fragment containing the extracellular domain, the transmembrane segment, and a part of the intracellular juxtamembrane region with a molecular mass of ∼130 kDa, and an intracellular ∼70 kDa fragment released into the cytoplasm. The proteolytic processing did not take place without internalisation of PDGFRβ. In addition, chelation of intracellular Ca²⁺ inhibited proteolytic processing. Inhibition of the proteasome affected signal transduction by increasing the phosphorylation of PDGFRβ, PLCγ, and STAT3 while reducing it on Erk1/2 and not affecting Akt. The proteolytic cleavage was observed in fibroblasts or cells that had undergone epithelial-mesenchymal transition.

Diabetic foot ulcers (DFUs) are a severe microvascular complication. Platelet-rich plasma (PRP) pitches in DFU treatment. This study explored the mechanism of PRP facilitating wound repair in DFU mice via vascular endothelial growth factor A (VEGFA)/VEGF receptor 2 (VEGFR2)/extracellular signal-regulated kinase (ERK) pathway. The DFU mouse model was established, with wound skin injected with PRP, followed by the detections of wound area, histopathological changes, and CD31-positive cells. IL-6/TNF-α/VEGFA/VEGFR2/p-VEGFR2/(ERK1/2)/(p-ERK1/2) levels in wound tissue homogenates were assessed. VEGFA-VEGFR2 interaction was evaluated. PRP-treated DFU mice were simultaneously treated with fruquintinib/PD98059. PRP reduced wound area, IL-6 and TNF-α levels, elevated epidermal dermal thickness, CD31-positive cell number, and aligned tissue structure, which were mitigated by fruquintinib/PD98059. PRP promoted VEGFR2 phosphorylation. PRP and fruquintinib/PD98059 abated p-VEGFR2/VEGFR2 or p-ERK1/2/ERK1/2 levels in DFU mice. PRP activated the ERK pathway through VEGFA/VEGFR2. Collectively, PRP promoted VEGFR2 phosphorylation and activated the ERK pathway, thereby facilitating wound repair in DFU mice.

In this study, we aim to explore the involvement of growth differentiation factor 15 (GDF15) in both corneal neovascularization (CNV) and retinoblastoma (RB) progression. Cell migration and proliferation were assessed through Scratch assays and CCK-8 assays. Apoptosis was quantified using flow cytometry. In vitro angiogenesis was evaluated through a tube formation assay. RT-PCR and western blot analyses were employed to assess the angiogenesis-related factors. Results demonstrated that RhGDF15 has a promotional effect on the migration of RB cells. Conversely, si-GDF15 demonstrated an opposite effect. RhGDF15 exhibited an enhancement the tube formation, the levels of HIF-1α and SDF, as well as cell migration. Conversely, si-GDF15 demonstrated an opposite effect. The levels of factors were elevated by rhGDF15 in both HREC and RB cell lines. In conclusion, the downregulation of GDF15 has the potential to inhibit corneal angiogenesis and impede the migration of RB cells. These effects may be dependent on the AKT/ERK pathway.

Background: Congenital cyanotic heart disease (CHD) in children is associated with several complications, amongst these complications is growth retardation which is believed to be multifactorial.

Objectives: The objective of this study is to find out the role of leptin and Insulin-Like Growth Factor-1 (IGF-1) in the growth of paediatric patients with cyanotic CHD of different anatomical defects.

Design/methods: This is a cross-sectional study involving thirty-nine children known to suffer from congenital cyanotic heart disease followed by the cardiology outpatient department, and forty-seven matched controls. Serum leptin and IGF-1 were evaluated in all the enrolled subjects besides anthropometric measurement and assessment of average oxygen saturation.

Results: The patients' group showed statistically significant lower height, weight, Body mass index (BMI), leptin levels, and IGF-1. In addition, the patient group had a significant positive correlation between serum leptin and BMI, as well as a positive correlation of IGF-1 with average oxygen saturation.

Conclusion: Children suffering from congenital cyanotic heart disease have a higher probability of developing poor growth. Serum leptin and IGF-1 are lower in affected children with congenital cyanotic cardiac defects suggesting that they may play a role in their poor growth.

The coding sequence of human basic fibroblast growth factor (hbFGF) was optimised for expression in rice. An expression cassette was constructed by fusing the PCR-amplified RAmy3D promoter, along with its 5'UTR, 3'UTR, and terminator sequences, to the codon-optimised hbFGF sequence. This cassette was inserted into the pCAMBIA1304 shuttle vector, which also contained the RAmy3D signal peptide. Agrobacterium tumefaciens strain LBA 4404 was used to transform rice callus. Among the transformed lines, the callus expressing the highest level of bFGF (38.1 mg/kg fresh weight) was identified via ELISA and selected for establishing a cell suspension culture. Expression and secretion of the recombinant bFGF into the culture medium were observed three days after incubating the transgenic rice cells in sucrose-free medium. The presence of recombinant bFGF was confirmed through Western blot and SDS-PAGE analyses. Furthermore, the rice-derived bFGF effectively stimulated the proliferation of NIH/3T3 cells, demonstrating a comparable biological activity to that of commercial bFGF.

Bile acid-induced hepatotoxicity is inevitable in Cholestasis pathogenesis and L-Glutamine (L-Gln) has been reported to prevent total parenteral nutrition (TPN)-induced cholestasis in premature neonates. While mechanisms remain unknown, we hypothesize that bile acids impair growth factor (GF) function in hepatocytes which L-glutamine prevents through NAPDH oxidase (NOX) modulation. Glycochenodeoxycholic acid (GCDC, 0-100 µM) when added to primary hepatocyte cultures significantly (p < 0.01) decreased the FBS-induced BrdU incorporation, however inhibition of Fibroblast Growth factor (FGF)- or Hepatocyte growth factor (HGF)-induced DNA synthesis was more pronounced (p < 0.001). L-Gln markedly attenuated GCDC-mediated inhibition of DNA synthesis in both FBS and GF-treated cells. GCDC significantly increased the NADPH oxidase activity and NOX-1 protein expression that were markedly reduced by L-Gln and protein kinase c (PKC) inhibitor, LY-333531. Apocynin (APCN) and diphenyliodonium (DPI) significantly blocked the GCDC-mediated inhibition of GF-induced DNA synthesis. This study demonstrates that bile acid-induced hepatotoxicity involves dysfunction of certain growth factors via protein kinase c (PKC)- mediated NOX modulation which can be corrected, at least partly, by L-glutamine.

This study proposes to investigate the therapeutic efficacy and mechanism of combining tibial transverse transport (TTT) with platelet-rich plasma (PRP) for diabetic foot ulcer (DFU). The diabetic rabbit model was constructed with Streptozotocin, which was intervened with TTT and PRP. PRP injection combined with TTT significantly promoted vascularisation and enhanced CD31, VEGFA, and VEGFR2 expressions compared to traditional TTT. However, the VEGFR2 inhibitor suppressed these phenomena. In the in vitro injury model, PRP reversed the diminished human umbilical vein endothelial cells (HUVECs) function and vascularisation caused by high-glucose damage. Additionally, PRP reduced inflammation and oxidative stress (approximately 47% ROS level) and enhanced VEGFA and VEGFR2 expression in HUVECs. However, the knockdown of VEGFR2 reversed the effect of PRP. In conclusion, TTT combined with intraosseous flap injection of PRP sustained-release microspheres activated the VEGFA/VEGFR2 pathway to promote microcirculatory reconstruction in DFU. These findings may provide new potential therapeutic strategies for DFU.

Aims: This study aims to explore the potential role of vascular endothelial growth factor-B (VEGF-B) in the pathogenesis of diabetic peripheral neuropathy (DPN). The expression of VEGFRs were reanalysed by using gene arrays of peripheral nerve samples from mouse models of DPN retrieved from the GEO database. 213 T2D patients as well as 31 healthy individuals were recruited. The serum VEGF-B was detected and its relationship with DPN was analysed. The elevated VEGFR1 was the only change of VEGFR gene expression in the peripheral nerve from mouse models of DPN. The level of serum VEGF-B in T2D patients with DPN was higher than that in T2D patients without DPN and healthy people. Analysis of correlation and binary logistic regression confirmed that the increased serum VEGF-B level was an independent risk factor of DPN in T2D patients. VEGF-B-VEGFR1 signaling pathway may be involved in the development of DPN.