Growth factors最新文献

{"title":"Characterisation of mesenchymal stem cells conditioned media obtained at different conditioning times: their effect on glial cells in <i>in vitro</i> scratch model.","authors":"Eva Székiová, Zuzana Michalová, Juraj Blaško, Rastislav Mucha, Lucia Slovinská, Martin Kello, Ivo Vanický","doi":"10.1080/08977194.2023.2182145","DOIUrl":"10.1080/08977194.2023.2182145","url":null,"abstract":"<p><p>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. <i>In vitro</i>, 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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 2","pages":"57-70"},"PeriodicalIF":1.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10092369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knock-down of IGFBP2 ameliorates lung fibrosis and inflammation in rats with severe pneumonia through STAT3 pathway.","authors":"Yuyu Wang, Jianjiang Huang, Fang Zhang, Keli Shen, Bin Qiu","doi":"10.1080/08977194.2023.2259497","DOIUrl":"10.1080/08977194.2023.2259497","url":null,"abstract":"<p><strong>Objective: </strong>To observe the mechanism of IGFBP2 knock-down in improving lung fibrosis and inflammation through STAT3 pathway in rats with severe pneumonia.</p><p><strong>Materials and methods: </strong>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.</p><p><strong>Results: </strong>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 <i>(p</i> < 0.05), while PaCO₂, CO₂, and SaO₂, IL-4 and IL-10 levels, and the proportion of M2 type AMs decreased (<i>p</i> < 0.05). However, the knockdown of IGFBP2 reversed the above index trends.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"210-220"},"PeriodicalIF":1.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41095376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of transforming growth factor-β in airway remodelling in bronchiolitis obliterans.","authors":"Ziwei Wang","doi":"10.1080/08977194.2023.2239356","DOIUrl":"10.1080/08977194.2023.2239356","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":" ","pages":"192-209"},"PeriodicalIF":1.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10242088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative evaluation of autologous platelet-rich plasma and platelet lysate in patients with knee osteoarthritis.","authors":"Sareh Hosseini,&nbsp;Mohammad Sadegh Soltani-Zangbar,&nbsp;Majid Zamani,&nbsp;Yoda Yaghoubi,&nbsp;Reza Rikhtegar Ghiasi,&nbsp;Roza Motavalli,&nbsp;Ali Ghassabi,&nbsp;Rahim Iranzad,&nbsp;Amir Mehdizadeh,&nbsp;Seyed Kazem Shakouri,&nbsp;Alireza Pishgahi,&nbsp;Mehdi Yousefi","doi":"10.1080/08977194.2023.2227273","DOIUrl":"https://doi.org/10.1080/08977194.2023.2227273","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 3","pages":"165-177"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9904259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription factor ETV1-induced lncRNA MAFG-AS1 promotes migration, invasion, and epithelial-mesenchymal transition of pancreatic cancer cells by recruiting IGF2BP2 to stabilize ETV1 expression.","authors":"Hanqin Weng, Weijian Feng, Fengling Li, Dong Huang, Liangyi Lin, Zaiguo Wang","doi":"10.1080/08977194.2023.2227272","DOIUrl":"10.1080/08977194.2023.2227272","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 3","pages":"152-164"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9892950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of hepatocyte growth factor-transfected mesenchymal stem cell transplantation in canine injured vocal folds.","authors":"Xingqiao Xie,&nbsp;Xumao Li,&nbsp;Xinsheng Lin,&nbsp;Xiangyu Chen,&nbsp;Chenshan Zhang,&nbsp;Guangbin Sun","doi":"10.1080/08977194.2023.2227270","DOIUrl":"https://doi.org/10.1080/08977194.2023.2227270","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 3","pages":"130-139"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10277765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Production of a biosimilar version of aflibercept to improve VEGF blocker cytotoxicity on endothelial cells.","authors":"Amin Ramezani,&nbsp;Mohammadrasul Zareinejad,&nbsp;Elham Mahmoudi Maymand,&nbsp;Elina Kaviani,&nbsp;Abbas Ghaderi","doi":"10.1080/08977194.2023.2227271","DOIUrl":"https://doi.org/10.1080/08977194.2023.2227271","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 3","pages":"140-151"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9901941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microfracture technique combined with mesenchymal stem cells inducer represses miR-708-5p to target special at-rich sequence-binding protein 2 to drive cartilage repair and regeneration in rabbit knee osteoarthritis.","authors":"YongChao Wang,&nbsp;Qin Su,&nbsp;HaiRong Tang,&nbsp;Qiang Tian,&nbsp;Xin Lin,&nbsp;MeiChun Fu,&nbsp;RenMing Zhang,&nbsp;ZhangFeng Luo,&nbsp;KeYun Zhang","doi":"10.1080/08977194.2023.2227269","DOIUrl":"https://doi.org/10.1080/08977194.2023.2227269","url":null,"abstract":"<p><p>Knee osteoarthritis (KOA) is a degenerative joint illness which leads to knee pain and functional limitation. In this study, we combined microfracture surgery with kartogenin (KGN), a small bioactive molecule used to promote the differentiation of mesenchymal stem cells (MSCs), and explored its impact on cartilage repair and possible latent mechanisms of action. The research offers a brand-new idea for the clinical cure of KOA. The microfracture technique in combination with KNG treatment was performed on a rabbit model of KOA. Animal behaviour was evaluated after the intra-articular injection of miR-708-5p and Special AT-rich sequence binding protein 2 (SATB2) lentiviruses. Later, the expression of the tumour necrosis factor α (TNF-α) and interleukin- 1 (IL-1), the pathology of synovial tissue and cartilage tissue, and the positive cartilage type II collagen, MMP-1, MMP-3 and TIMP-1 were detected. Finally, a luciferase assay was conducted to verify the interaction of miR-708-5p and SATB2. Our results showed that miR-708-5p was elevated in the rabbit KOA model; however, the expression of SATB2 was reduced. Meanwhile, the microfracture technology combined with MSCs inducer KGN drove cartilage repair and regeneration in rabbit KOA by repressing the miR-708-5p expression. We also found that miR-708-5p directly targeted the SATB2 mRNA to regulate its expression. Furthermore, our data urged that elevating miR-708-5p or restraining SATB2 may reverse the therapeutic effect of the microfracture technique combined with MSCs inducer on rabbit KOA. Microfracture technique combined with MSCs inducer represses miR-708-5p to target SATB2 to drive cartilage repair and regeneration in rabbit KOA. This indicates that the microfracture technique combined with MSCs inducers is supposed to be an effective latent method for osteoarthritis cure.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 3","pages":"115-129"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10259865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The polymethoxylated flavone hexamethylquercetagetin suppresses NF-κB signaling and inhibits cell survival in cervical carcinoma.","authors":"Yanan Sun,&nbsp;Nan Li,&nbsp;Yuru Cai,&nbsp;Xingnan Zhao,&nbsp;Hongyu Yang","doi":"10.1080/08977194.2022.2144282","DOIUrl":"https://doi.org/10.1080/08977194.2022.2144282","url":null,"abstract":"<p><p>Nuclear factor-κB (NF-κB) contributes to the development and progression of cervical carcinoma. To construct a xenograft model, Ca Ski cells were subcutaneously inoculated into BALB/c nude mice. The relative protein expression of NF-κB p65, p-p65, IκBα, and p-IκBα were detected in hexamethylquercetagetin (HTQC) treated cervical carcinoma cells with or without tumor necrosis factor (TNF)α stimulation, or representative tumors tissues in xenograft mice. HTQC could prohibit NF-κB-derived luciferase activity in Ca Ski and C-33 A cells and inhibit the relative NF-κB p-p65 and p-IκBα expression with or without TNFα stimulation. At the same time, HTQC inhibited <i>in vitro</i> cell survival in a concentration-dependent manner and suppressed the tumor volume and weight in xenograft models. In summary, HTQC functions as an NF-κB inhibitor to prohibit the survival and proliferation of cervical carcinoma, which can be considered as an NF-κB target remedy in future clinical practice.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 1","pages":"1-7"},"PeriodicalIF":1.8,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9129275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinoic acid signaling is critical for generation of pancreatic progenitors from human embryonic stem cells.","authors":"Niloufer P Dumasia,&nbsp;Aparna P Khanna,&nbsp;Prasad S Pethe","doi":"10.1080/08977194.2022.2144284","DOIUrl":"https://doi.org/10.1080/08977194.2022.2144284","url":null,"abstract":"<p><p>Retinoic acid (RA) is essential for gut endoderm development and has been extensively used for <i>in vitro</i> pancreatic differentiation from human pluripotent stem cells. However, the gene regulatory network triggered by RA signaling remains poorly addressed. Also, whether RA signals control histone modifiers such as the Polycomb group proteins during pancreatic specification remains to be explored. Here, we assess the role of RA on pancreas-specific genes during the differentiation of human embryonic stem cells (hESCs). We demonstrate that RA helps cells exit the definitive endoderm stage and proceed toward a pancreatic fate. Inhibition of the RA pathway using the pharmacological inhibitor LE135 impairs the induction of pancreatic endoderm (PE) markers <i>FOXA2</i>, <i>HNF4α</i>, <i>HNF1β</i>, <i>HHEX</i>, and <i>PDX1</i>. We further determine that RA signals alter the expression of epigenetic-associated genes <i>BMI1</i> and <i>RING1B</i> in the hESC-derived pancreatic progenitors. These findings broaden our understanding of the mechanisms that drive early PE specification.</p>","PeriodicalId":12782,"journal":{"name":"Growth factors","volume":"41 1","pages":"8-19"},"PeriodicalIF":1.8,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9129276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}