bFGF Promotes the Proliferation of Rat Peripheral Blood Mesenchymal Stem Cells Through β-Catenin Signaling

bFGF (basic fibroblast growth factor, bFGF) could promote the proliferation of bone marrow and cord blood mesenchymal stem cells. However, the effect of bFGF on the proliferation of peripheral blood mesenchymal stem cells (PBMSCs) needs further research. This study aimed to investigate the role of bFGF on the culture and expansion of PBMSCs in vitro. Firstly, arterial blood was collected from rats abdominal aorta. After mononuclear cells (MNCs) were separated with Ficoll separation fluid, MNCs were cultured in the DMEM medium without bFGF (served as control group) or with bFGF (10, 20 ng/mL, served as 10 or 20 ng/mL bFGF group). PBMSCs were obtained by adherent culture method. The third passage of PBMSCs was detected for the MSC surface markers and the effect of bFGF on the cell cycle of PBMSCs using flow cytometry. The effects of bFGF on colony formation, cell growth, and the expressions of cyclin D1, cyclin E, p21 and β-catenin were evaluated. PBMSCs showed no difference in morphology among the three groups. PBMSC clonies appeared 14 days after cultivation. Compared with the control group, the cell growth confluence of PBMSCs was obviously increased by 40% and 80% in groups treated with 10 ng/mL bFGF or 20 ng/mL bFGF respectively after culture of 21 days (all P<0.05). Compared with the group treated with 10 ng/mL bFGF, the confluence of PBMSCs in 20 ng/mL group was further increased by 28% (P<0.05). Cells of the third passage were positively stained for CD29 and CD90, while were negative for CD45. These results were consistent with the phenotypic characteristics of MSCs. Compared with the control group, the colony number of PBMSCs in the 10 ng/mL and 20 ng/mL bFGF groups was increased by 51% (P<0.05) and 92% (P<0.05), respectively. Compared with the 10 ng/mL group, the colony number of PBMSCs was further increased in 20 ng/mL group by 14% (P<0.05). The growth curve of PBMSCs showed that after 7 days of culture, the number of PBMSCs in 10 ng/mL bFGF group and 20 ng/mL bFGF group was increased by 41% (P<0.05) and 61% (P<0.05), respectively. Moreover, the cell number had a statistically significant difference between these two groups (P<0.05). Results from flow cytometry cell cycle showed that the numbers of PBMSCs in the G1 phase of experimental groups were significantly decreased as the concentration of bFGF increased when compared with the control group (P<0.05), whereas the number of PBMSCs in the S phase was significantly increased (P<0.05). Immunofluorescence experiments showed that, compared with the control group, bFGF significantly promoted the nuclear translocation and expression of β-catenin in PBMSCs. Compared with the 10 ng/mL group, the PBMSCs in 20 ng/mL bFGF group showed stronger nuclear translocation and expression of β-catenin. Western blot experiments showed that the levels of β-catenin and its target proteins cyclinD1 and cyclinE were significantly increased (all P<0.05), whereas expression of p21 was significantly decreased in PBMSCs in the bFGF groups in a concentration dependent pattern when compared with control group (P<0.05). The study firstly confirms that bFGF promotes the proliferation of PBMSCs by regulating the β-catenin signaling pathway, which may facilitate the aquisition of larger number of PBMSCs for stem cell engineering in vitro.     

基于“无废理念”的纺织服装工业区绿色化改造模式研究

通过对中国工业区,特别是纺织服装工业区"产废"情况的梳理,明确针对污染严重,经济效益不高的工业区进行改造的必要性。为实现对纺织服装工业区绿色化改造,从"无废理念"出发,重点研究纺织服装工业区绿色化改造的可实施路径。在研究方法上将纺织服装工业区作为研究整体,基于可持续发展思想,构建纺织服装工业区经济、社会、环境复合生态系统,运用层次分析法,选取对于该类工业园区具有代表性的经济、社会、环境指标进行评价,通过评价后总的分值,结合生命周期规律,将需要改造的纺织服装工业区进行初步筛选。同时,利用经济、社会、环境各子系统的分值,对具体改造模式加以判别。文章通过对纺织服装工业区不可持续性的内涵挖掘,将工业区绿色化改造模式与改造内容建立关联,可以通过产业绿色化改造和建成空间绿色化改造,来实现工业园区的升级与转型,进而实现可持续发展。最后,根据模式判别结果,针对不同模式在产业与建成空间的不同特征,提出相应的绿色化改造方法和政策建议。在结论中总结基于"无废理念"纺织服装工业区绿色化改造与可持续发展的辩证关系。此方法适用于其他类型的工业区改造模式判别,以促进工业区的可持续发展。     

IgA肾病患者与健康人肠道菌群的比较

目的通过16S rRNA高通量基因测序方法对IgA肾病患者与健康人的肠道菌群进行比较。方法纳入生活于同一地区的40例IgA肾病患者与10例健康人,收集研究对象的新鲜粪便样本,提取粪便细菌总DNA,通过PCR扩增后上机测序,然后进行可操作分类单元聚类、物种分类分析及Alpha多样性分析、Beta多样性分析,最后比较两组之间的肠道菌群差异。结果与健康人相比,IgA肾病患者肠道菌群丰富度指数(Ace、Chao1)下降(u=2.308,P=0.033;u=2.259,P=0.039),多样性指数(Shannon、Simpson)升高(u=5.370,P0.001;u=4.601,P=0.007);相对丰度方面,IgA肾病患者的厚壁菌门、拟杆菌门、放线菌门细菌数量增加(t=2.301,P=0.037;t=6.729,P=0.005;t=5.285,P=0.006),而变形菌门细菌数量减少(t=4.138,P=0.009);拟杆菌属、链球菌属细菌数量增加(t=9.037,P=0.003;t=6.001,P=0.008),而unidentified_Enterobacteriaceae数量减少(t=2.198,P=0.033)。PCoA图提示两组肠道菌群有显著差异。LDA差异贡献分析发现两组之间共有15个物种存在显著差异,其中造成显著差异影响力最大的5个物种依次是γ-变形菌纲、unidentified_Enterobacteriaceae、肠杆菌科、肠杆菌目、变形菌门(t=9.930,P=0.002;t=2.198,P=0.033;t=2.604,P=0.015;t=2.393,P=0.021;t=4.138,P=0.009),它们刚好落在同一个进化树上,在IgA肾病组的相对丰度显著降低。结论 IgA肾病患者存在肠道菌群失调,显著减少的肠杆菌科的未知属可能是IgA肾病的特征菌,其对机体免疫的影响及在IgA肾病发生发展中的作用尚不清楚,进一步研究可能为IgA肾病的防治提供新的靶点。     

The AKR1B1 inhibitor epalrestat suppresses the progression of cervical cancer

Molecular Biology Reports - Cervical cancer is the leading cause of cancer-related death among women worldwide. Identifying an effective treatment with fewer side effects is imperative, because all...     

Activation of the bitter taste sensor TRPM5 prevents high salt-induced cardiovascular dysfunction

Science China Life Sciences - High salt intake is a known risk factor of cardiovascular diseases. Our recent study demonstrated that long-term high salt intake impairs transient receptor potential...     

Identification of SRY‐box 30 as an age‐related essential gatekeeper for male germ‐cell meiosis and differentiation

Although important factors governing the meiosis have been reported in the embryonic ovary, meiosis in postnatal testis remains poorly understood. Herein, we first report that SRY‐box 30 (Sox30) is an age‐related and essential regulator of meiosis in the postnatal testis. Sox30‐null mice exhibited uniquely impaired testis, presenting the abnormal arrest of germ‐cell differentiation and irregular Leydig cell proliferation. In aged Sox30‐null mice, the observed testicular impairments were more severe. Furthermore, the germ‐cell arrest occurred at the stage of meiotic zygotene spermatocytes, which is strongly associated with critical regulators of meiosis (such as Cyp26b1, Stra8 and Rec8) and sex differentiation (such as Rspo1, Foxl2, Sox9, Wnt4 and Ctnnb1). Mechanistically, Sox30 can activate Stra8 and Rec8, and inhibit Cyp26b1 and Ctnnb1 by direct binding to their promoters. A different Sox30 domain required for regulating the activity of these gene promoters, providing a “fail‐safe” mechanism for Sox30 to facilitate germ‐cell differentiation. Indeed, retinoic acid levels were reduced owing to increased degradation following the elevation of Cyp26b1 in Sox30‐null testes. Re‐expression of Sox30 in Sox30‐null mice successfully restored germ‐cell meiosis, differentiation and Leydig cell proliferation. Moreover, the restoration of actual fertility appeared to improve over time. Consistently, Rec8 and Stra8 were reactivated, and Cyp26b1 and Ctnnb1 were reinhibited in the restored testes. In summary, Sox30 is necessary, sufficient and age‐associated for germ‐cell meiosis and differentiation in testes by direct regulating critical regulators. This study advances our understanding of the regulation of germ‐cell meiosis and differentiation in the postnatal testis.     

Home‐site fidelity and homing behavior of the big‐headed turtle Platysternon megacephalum

Site fidelity refers to the restriction of dispersal distance of an animal and its tendency to return to a stationary site. To our knowledge, the homing ability of freshwater turtles and their fidelity is reportedly very low in Asia. We examined mark–recapture data spanning a 4‐year period in Diaoluoshan National Nature Reserve, Hainan Province, China, to investigate the site fidelity and homing behavior of big‐headed turtles Platysternon megacephalum. A total of 11 big‐headed turtles were captured, and all individuals were used in this mark–recapture study. The site fidelity results showed that the adult big‐headed turtles (n = 4) had a 71.43% recapture rate in the original site after their release at the same site, whereas the juveniles (n = 1) showed lower recapture rates (0%). Moreover, the homing behavior results showed that the adults (n = 5) had an 83.33% homing rate after displacement. Adult big‐headed turtles were able to return to their initial capture sites (home) from 150 to 2,400 m away and precisely to their home sites from either upstream or downstream of their capture sites or even from other streams. However, none of the juveniles (n = 4) returned home, despite only being displaced 25–150 m away. These results indicated that the adult big‐headed turtles showed high fidelity to their home site and strong homing ability. In contrast, the juvenile turtles may show an opposite trend but further research is needed.     

Arid1a regulates neural stem/progenitor cell proliferation and differentiation during cortical development

ObjectiveNeurodevelopmental diseases are common disorders caused by the disruption of essential neurodevelopmental processes. Recent human exome sequencing and genome‐wide association studies have shown that mutations in the subunits of the SWI/SNF (BAF) complex are risk factors for neurodevelopmental diseases. Clinical studies have found that ARID1A (BAF250a) is the most frequently mutated SWI/SNF gene and its mutations lead to mental retardation and microcephaly. However, the function of ARID1A in brain development and its underlying mechanisms still remain elusive.MethodsThe present study used Cre/loxP system to generate an Arid1a conditional knockout mouse line. Cell proliferation, cell apoptosis and cell differentiation of NSPCs were studied by immunofluorescence staining. In addition, RNA‐seq and RT‐PCR were performed to dissect the molecular mechanisms of Arid1a underlying cortical neurogenesis. Finally, rescue experiments were conducted to evaluate the effects of Neurod1 or Fezf2 overexpression on the differentiation of NSPCs in vitro.ResultsConditional knockout of Arid1a reduces cortical thickness in the developing cortex. Arid1a loss of function inhibits the proliferation of radial glial cells, and increases cell death during late cortical development, and leads to dysregulated expression of genes associated with proliferation and differentiation. Overexpression of Neurod1 or Fezf2 in Arid1a cKO NSPCs rescues their neural differentiation defect in vitro.ConclusionsThis study demonstrates for the first time that Arid1a plays an important role in regulating the proliferation and differentiation of NSPCs during cortical development, and proposes several gene candidates that are worth to understand the pathological mechanisms and to develop novel interventions of neurodevelopment disorders caused by Arid1a mutations.