Growth factors最新文献

Adoption of organoid/tumoroid propagation of normal and malignant intestinal epithelia has provided unparalleled opportunities to compare cell growth factor and signaling dependencies. These 3D structures recapitulate tumours in terms of gene expression regarding the tumor cells but also allow deeper insights into the contribution of the tumour microenvironment (TME). Elements of the TME can be manipulated or added back in the form of infiltrating cytotoxic lymphocytes and/or cancer associated fibroblasts. The effectiveness of chemo-, radio- and immunotherapies can be explored within weeks of deriving these patient-derived tumour avatars informing treatment of these exact patients in a timely manner. Entrenched paths to colorectal cancer (CRC) from the earliest steps of conventional adenoma or serrated lesion formation, and the recognition of further sub-categorisations embodied by consensus-molecular-subtypes (CMS), provide genetic maps allowing a molecular form of pathologic taxonomy. Recent advances in organoid propagation and scRNAseq are reshaping our understanding of CMS and CRC.

Notably the integration of additives such as growth factors, vitamins, and drugs with scaffolds promoted nerve tissue engineering. This study tried to provide a concise review of all these additives that facilitates nerve regeneration. An attempt was first made to provide information on the main principle of nerve tissue engineering, and then to shed light on the effectiveness of these additives on nerve tissue engineering. Our research has shown that growth factors accelerate cell proliferation and survival, while vitamins play an effective role in cell signalling, differentiation, and tissue growth. They can also act as hormones, antioxidants, and mediators. Drugs also have an excellent and necessary effect on this process by reducing inflammation and immune responses. This review shows that growth factors were more effective than vitamins and drugs in nerve tissue engineering. Nevertheless, vitamins were the most commonly used additive in the production of nerve tissue.

Thyroid cancer (TC) is a relatively prevalent endocrine tumor among women, the incidence of which is rapidly rising. In this present study, we aimed to provide new therapeutic targets from the aspect of transcription factor-target gene interaction. TP63 and KRT17 were both highly expressed in TC tissues and cells. The results of ChIP and dual-luciferase assays confirmed TP63 to bind the KRT17 promoter. Cell function assays revealed that knockdown of TP63 could repress TC cell progression. Furthermore, the rescue assay verified that TP63 could facilitate KRT17 expression to activate the AKT signaling pathway, which in turn stimulated TC cell invasion and migration, and induced EMT. All these results verified that TP63 facilitates TC malignant progression by promoting KRT17 expression and inducing EMT.

In this study, the bone marrow mesenchymal stem cells conditioned media (BMMSC-CM) obtained by conditioning for 24(CM24), 48(CM48) and 72(CM72) hours was characterised. In vitro, the impact of BMMSC-CM on the astrocyte migratory response and oligodendrocyte density was evaluated using the scratch model. The proteomic profiles of individual secretomes were analysed by mass spectrometry and the concentrations of four selected neurotrophins (BDNF, NGF, GDNF and VEGF) were determined by ELISA. Our results revealed an increased number of proteins at CM72, many of which are involved in neuroregenerative processes. ELISA documented a gradual increase in the concentration of two neurotrophins (NGF, VEGF), peaking at CM72. In vitro, the different effect of individual BMMSC-CM on astrocyte migration response and oligodendrocyte density was observed, most pronounced with CM72. The outcomes demonstrate that the prolonged conditioning results in increased release of detectable proteins, neurotrophic factors concentration and stronger effect on reparative processes in neural cell cultures.

Objective: To observe the mechanism of IGFBP2 knock-down in improving lung fibrosis and inflammation through STAT3 pathway in rats with severe pneumonia.

Materials and methods: First, SP rat model was established. Then rats were divided into the Control group, the SP group, the SP + Lv-vector shRNA group, the SP + Lv-IGFBP2 shRNA group, the SP + Lv-vector group, and the SP + Lv-IGFBP2 group. The mRNA and protein levels of IGFBP2, NOS, CD206 and Arg 1 were detected by RT-qPCR and Western blot. IHC was used to check the positive expression of IGFBP2 and MCP1. A fully automated blood gas analyzer was used to detected PaCO₂, CO₂ content, PaO2 and SaO2. HE and Masson staining were performed to observe the lung tissue injury and collagen deposition of rats in each group. ELISA assays were used to calculate the levels of inflammatory factors IL-1β, IL-6, TNF-α, IL-4, and IL-10. Flow cytometry was conducted to acquire the ratio of M1-type AMs and M2-type AMs.

Results: Compared with the Control group, IGFBP2, iNOS, CD206, and Arg1 mRNA and protein expression levels, IGFBP2 and MCP1 positive expressions, PaCO₂, p-STAT3/STAT3, p-JAK2/JAK2, IL-1β, IL-6, and TNF-α levels, the number of AMs and neutrophils, the proportion of M1 type AMs and the expressions of α-SMA, Collagen-I, Collagen III, and Fibronectin were significantly increased in SP rats (p < 0.05), while PaCO₂, CO₂, and SaO₂, IL-4 and IL-10 levels, and the proportion of M2 type AMs decreased (p < 0.05). However, the knockdown of IGFBP2 reversed the above index trends.

Conclusion: Knock-down of IGFBP2 ameliorated lung injury in SP rats, inhibited inflammation and pulmonary fibrosis, and promoted M2-type transformation of AMs by activating the STAT3 pathway.

Airway remodelling is the main pathological mechanism of bronchiolitis obliterans (BO). Several studies have found that transforming growth factor-β (TGF-β) expression is increased in BO during airway remodelling, where it plays an important role in various biological processes by binding to its receptor complex to activate multiple signalling proteins and pathways. This review examines the role of TGF-β in airway remodelling in BO and its potential as a therapeutic target, highlighting the mechanisms of TGF-β activation and signalling, cellular targets of TGF-β actions, and research progress in TGF-β signalling and TGF-β-mediated processes.

Autologous platelet-rich plasma (PRP) and platelet lysate (PL) are nowadays promising candidates in the treatment of articular cartilage lesions. We aimed to compare PRP and PL injection effectiveness in patients with knee osteoarthritis (KOA). A total of fifty women with KOA were included in the study. Patients were treated with intra-articular injections of PRP and PL. Clinical outcomes were evaluated using the comparison of VAS, WOMAC, and ROM scores. The concentration levels of growth factors and cytokines were measured by ELISA. All patients showed significant improvements in pain and function following treatment of KOA with PL and PRP compared to baseline. Moreover, PL's concentration of growth factors was significantly higher than PRP. A significant increase was also observed in all of the aforementioned mediators in both PRP and PL products compared to control. These results can introduce PL as a promising and alternative option for KOA therapy in the future.

We investigated the mechanism of ETS-translocation variant 1 (ETV1)/lncRNA-MAFG-AS1 in pancreatic cancer (PC). MAFG-AS1 and ETV1 levels in PC cell lines and HPNE cells were determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting (WB). After transfection with sh-MAFG-AS1, PC cell invasion, migration, proliferation, and epithelial-mesenchymal transition (EMT)-related proteins were measured by 5-ethynyl-2'-deoxyuridine (EdU), Transwell assay, and WB. The binding between ETV1 and MAFG-AS1 was studied using dual-luciferase assay and chromatin immunoprecipitation. The interactions between MAFG-AS1, IGF2BP2, and ETV1 were tested. Combined experiments were further performed using sh-MAFG-AS1 and pcDNA-ETV1 simultaneously. ETV1/MAFG-AS1 was highly expressed in PC cells. Blocking MAFG-AS1 inhibited the malignant behaviors of PC cells. ETV1 induced MAFG-AS1 transcription in PC cells. MAFG-AS1 stabilized ETV1 mRNA by recruiting IGF2BP2. ETV1 overexpression partially antagonized the suppression of silencing MAFG-AS1 on PC cells. ETV1-induced MAFG-AS1 stabilized the ETV1 expression by recruiting IGF2BP2 and promoted PC cell migration, invasion, proliferation, and EMT.

This study aimed to assess the efficacy of hepatocyte growth factor (HGF)-transfected adipose-derived mesenchymal stem cell (ADSC) transplantation in the injured vocal folds (VFs) of canines. A lentiviral vector encoding HGF was successfully produced via Gateway cloning, which was used to infect ADSCs. Four weeks after transoral laser microsurgery (type II) with CO₂ laser, the beagles of each group were injected with HGF-transfected ADSCs or uninfected ADSCs into VFs. The results showed that the retention of HGF-transfected ADSCs in the VFs persisted about three months post-injection. The VFs in the HGF-transfected ADSCs group exhibited a closer-to-normal structure with less collagen deposition and higher amounts of hyaluronic acid (HA) in the third month. The short microvilli in the HGF-transfected ADSCs group showed a dense and uniform distribution. These results revealed that HGF-transfected ADSC is a potential treatment option for injured VFs.

This project aimed to produce a biosimilar version of aflibercept (AFL) and evaluate the effect of the co-treatment of AFL with other vascular endothelial growth factor (VEGF) blocker drugs. For this purpose, the optimized gene was inserted into the pCHO1.0 plasmid and transfected into the CHO-S cell line. The final concentration of biosimilar-AFL for the selected clone was 782 mg/L. Results revealed that the inhibition potential of the biosimilar-AFL on HUVEC cells was significant at 10 and 100 nM concentrations and in a dose-dependent manner. Furthermore, co-treatment of biosimilar-AFL with Everolimus (EVR), Lenvatinib (LEN), and Sorafenib (SOR) could reduce HUVEC cell viability/proliferation, more than when used alone. When LEN and SOR were co-treated with biosimilar-AFL, their cytotoxicity increased 10-fold. The most and least efficient combination was seen when biosimilar-AFL combined with LEN and EVR, respectively. Finally, biosimilar-AFL may improve the efficiency of LEN, EVR, and SOR in reducing the VEGF effect on endothelial cells.