1T-rich MoS2 nanosheets anchored on conductive porous carbon as effective polysulfide promoters for lithium-sulfur batteries.

The practical applications of lithium-sulfur (Li-S) batteries have severely been hindered by notorious shuttle effect and sluggish redox kinetics of lithium polysulfide intermediates (LiPSs), which bring about rapid capacity degradation, low coulombic efficiency and poor cycling stability. In this work, 1T-rich MoS2 nanosheets are in-situ developed onto the conductive porous carbon matrix (1T-rich MoS2@PC) as efficient polysulfide promotors for high-performance Li-S batteries. The porous carbon skeleton tightly anchors MoS2 nanosheets to prevent their reaggregation and ensures accessible electrical channels, and at the same time provides a favorable confined space that promotes the generation of 1T-rich MoS2 structure. More importantly, the uniformly distributed metallic 1T-rich MoS2 nanosheets not only affords rich sulfphilic sites and high binding energy for immobilizing LiPSs, but also favors rapid electron transfer and LiPSs conversation kinetics, substantially regulating sulfur chemistry in working cells. Consequently, the Li-S cell assembled with 1T-rich MoS2@PC modified separator delivers a remarkable cycling stability with ultralow capacity decay rate of 0.067% over 500 cycles at 1C. Encouragingly, under harsh conditions (high sulfur loading of 4.78 mg cm-2 and low E/S ratio of 8 µL mg-1), a favorable electrochemical performance can still be demonstrated. This study highlights the profitable design of 1T-rich MoS2/carbon based electrocatalyst for suppressing shuttle effect and promoting catalytic conversation of LiPSs, and has the potential to be applied to in other energy storage systems.

[Retracted] Antagonist targeting miR­106b­5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the EdU staining assay data shown in Figs. 4C and 5C and the western blotting data shown in Fig. 4E were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been submitted for publication elsewhere prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 48: 169, 2021; DOI: 10.3892/ijmm.2021.5002].

What role does PDL1 play in EMT changes in tumors and fibrosis?

Epithelial-mesenchymal transformation (EMT) plays a pivotal role in embryonic development, tissue fibrosis, repair, and tumor invasiveness. Emerging studies have highlighted the close association between EMT and immune checkpoint molecules, particularly programmed cell death ligand 1 (PDL1). PDL1 exerts its influence on EMT through bidirectional regulation. EMT-associated factors, such as YB1, enhance PDL1 expression by directly binding to its promoter. Conversely, PDL1 signaling triggers downstream pathways like PI3K/AKT and MAPK, promoting EMT and facilitating cancer cell migration and invasion. Targeting PDL1 holds promise as a therapeutic strategy for EMT-related diseases, including cancer and fibrosis. Indeed, PDL1 inhibitors, such as pembrolizumab and nivolumab, have shown promising results in clinical trials for various cancers. Recent research has also indicated their potential benefit in fibrosis treatment in reducing fibroblast activation and extracellular matrix deposition, thereby addressing fibrosis. In this review, we examine the multifaceted role of PDL1 in immunomodulation, growth, and fibrosis promotion. We discuss the challenges, mechanisms, and clinical observations related to PDL1, including the limitations of the PD1/PDL1 axis in treatment and PD1-independent intrinsic PDL1 signaling. Our study highlights the dynamic changes in PDL1 expression during the EMT process across various tumor types. Through interplay between PDL1 and EMT, we uncover co-directional alterations, regulatory pathways, and diverse changes resulting from PDL1 intervention in oncology. Additionally, our findings emphasize the dual role of PDL1 in promoting fibrosis and modulating immune responses across multiple diseases, with potential implications for therapeutic approaches. We particularly investigate the therapeutic potential of targeting PDL1 in type II EMT fibrosis: strike balance between fibrosis modulation and immune response regulation. This analysis provides valuable insights into the multifaceted functions of PDL1 and contributes to our understanding of its complex mechanisms and therapeutic implications.

GMrepo v2: a curated human gut microbiome database with special focus on disease markers and cross-dataset comparison.

GMrepo (data repository for Gut Microbiota) is a database of curated and consistently annotated human gut metagenomes. Its main purposes are to increase the reusability and accessibility of human gut metagenomic data, and enable cross-project and phenotype comparisons. To achieve these goals, we performed manual curation on the meta-data and organized the datasets in a phenotype-centric manner. GMrepo v2 contains 353 projects and 71,642 runs/samples, which are significantly increased from the previous version. Among these runs/samples, 45,111 and 26,531 were obtained by 16S rRNA amplicon and whole-genome metagenomics sequencing, respectively. We also increased the number of phenotypes from 92 to 133. In addition, we introduced disease-marker identification and cross-project/phenotype comparison. We first identified disease markers between two phenotypes (e.g. health versus diseases) on a per-project basis for selected projects. We then compared the identified markers for each phenotype pair across datasets to facilitate the identification of consistent microbial markers across datasets. Finally, we provided a marker-centric view to allow users to check if a marker has different trends in different diseases. So far, GMrepo includes 592 marker taxa (350 species and 242 genera) for 47 phenotype pairs, identified from 83 selected projects. GMrepo v2 is freely available at: https://gmrepo.humangut.info.

Neutrophil-to-Lymphocyte Ratio and Treatment Failure in Peritoneal Dialysis-Associated Peritonitis.

Objective: We sought to explore if there is an association between neutrophil-to-lymphocyte ratio (NLR) and treatment failure in patients with peritoneal dialysis-associated peritonitis (PDAP). Methods: Our cohort involved 337 episodes of PDAP experienced by 202 patients who were undergoing continuous ambulatory peritoneal dialysis at a single center from 1 July 2013 to 30 June 2018. The exposures were log-transformed NLR and a categorical variable grouped by the tertiles of NLR levels (T1, <3.75; T2, 3.75-6.53; and T3, >6.53) at baseline. Generalized estimating equation (GEE) and restricted cubic spline (RCS) analyses were done to determine the association between NLR and treatment failure, defined as catheter removal or all-cause mortality during therapy. Results: After adjusting for other potential predictors, the log-transformed NLR exhibited an incremental relationship with the risk of treatment failure (odds ratio, 1.82; 95% confidence interval, 1.05-3.15). RCS analyses showed that the relationship was positively and linearly correlated (P for nonlinearity = 0.104). As a three-level categorical variable, in reference to T1, the T3 of NLR showed a 3.41-fold increased venture of treatment failure in fully adjusted model. Subgroup analyses suggested that the prognostic relevance of NLR in PDAP was particularly significant in gram-negative peritonitis. Conclusions: A greater level of NLR at baseline was remarkably associated with a higher incidence of treatment failure among PDAP episodes regardless of other potential risk factors.

Antagonist targeting miR­106b­5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.

Acute renal injury (ARI) is a life­threatening condition and a main contributor to end­stage renal disease, which is mainly caused by ischemia­reperfusion (I/R). miR­106b­5p is a kidney function­related miRNA; however, whether miR­106b­5p regulates the progression of ARI remains unclear. The present study thus aimed to examine the effects of miR­106b­5p antagonist on the regulation of ARI progression. It was found that miR­106b­5p expression was upregulated in the renal tissue of rats with I/R­induced ARI and in NRK­52E rat renal proximal tubular epithelial cells subjected to hypoxia­reoxygenation (H/R). In vitro, H/R induction suppressed the proliferation, and promoted the apoptosis and autophagy of NRK­52E cells, whereas miR­106b­5p antagonist (inhibition of miR­106b­5p) promoted the proliferation, and attenuated the apoptosis and autophagy of NRK­52E cells under the H/R condition. Dual luciferase reporter gene assay validated that transcription factor 4 (TCF4) was a target of miR­106b­5p. It was further found that TCF4 overexpression promoted the proliferation, and inhibited the apoptosis and autophagy of NRK­52E cells subjected to H/R. Moreover, the effects of miR­106b­5p antagonist on NRK­52E cell proliferation, apoptosis and autophagy were mediated through the regulation of TCF4. In vivo, miR­106b­5p antagonist reduced the severity of renal injury, decreased cell proliferation in renal tissues and lowered the serum creatinine (Scr) and blood urea nitrogen (BUN) levels in the blood samples from rats with I/R­induced ARI. On the whole, the findings presented herein demonstrate that miR­106b­5p antagonist attenuates ARI by promoting the proliferation, and suppressing the apoptosis and autophagy of renal cells via upregulating TCF4.

Prevalence and risk factors of relapse in patients with ANCA-associated vasculitis receiving cyclophosphamide induction: a systematic review and meta-analysis of large observational studies.

BACKGROUND: Clinical relapses are common in patients with ANCA-associated vasculitis (AAV). The aim of this systematic review was to estimate time-point prevalence and risk factors of relapse. METHODS: We searched PubMed, Embase, and Cochrane Library databases from their inception to March 30, 2020. Cohorts and post-hoc studies were included for the estimation of summary cumulative relapse rates (CRRs) and adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs). Sensitivity and meta-regression analyses were also performed. RESULTS: Of the 42 eligible studies, 24 studies with 6236 participants were used for the pooled analyses of CRRs. The summary 1-year, 3-year, and 5-year CRRs were 0.12 (95% CI, 0.10-0.14), 0.33 (0.29-0.38), and 0.47 (0.42-0.52), respectively. In meta-regressions, the baseline age was positively associated with 1-year CRR. The proportion of granulomatosis with polyangiitis was positively associated with 5-year CRR. Twenty-eight studies with 5390 participants were used for the meta-analysis of risk factors for relapse, including a lower level of baseline serum creatine, proteinase 3 (PR3)-ANCA positivity at diagnosis, an ANCA rise, extrarenal organ involvement (including lung, cardiovascular, upper respiratory, and gastrointestinal involvement), intravenous (vs oral) cyclophosphamide induction, a shorter course of immunosuppressant maintenance, and maintenance with mycophenolate mofetil (vs azathioprine). CONCLUSIONS: Our systematic review demonstrated that the 1-year, 3-year, and 5-year cumulative probabilities of relapse were ∼12%, 33%, and 47% in AAV patients receiving cyclophosphamide induction, respectively. Early identification of risk factors for relapse is helpful to the risk stratification of patients so as to achieve personalized treatment.

OGEE v3: Online GEne Essentiality database with increased coverage of organisms and human cell lines.

OGEE is an Online GEne Essentiality database. Gene essentiality is not a static and binary property, rather a context-dependent and evolvable property in all forms of life. In OGEE we collect not only experimentally tested essential and non-essential genes, but also associated gene properties that contributes to gene essentiality. We tagged conditionally essential genes that show variable essentiality statuses across datasets to highlight complex interplays between gene functions and environmental/experimental perturbations. OGEE v3 contains gene essentiality datasets for 91 species; almost doubled from 48 species in previous version. To accommodate recent advances on human cancer essential genes (as known as tumor dependency genes) that could serve as targets for cancer treatment and/or drug development, we expanded the collection of human essential genes from 16 cell lines in previous to 581. These human cancer cell lines were tested with high-throughput experiments such as CRISPR-Cas9 and RNAi; in total, 150 of which were tested by both techniques. We also included factors known to contribute to gene essentiality for these cell lines, such as genomic mutation, methylation and gene expression, along with extensive graphical visualizations for ease of understanding of these factors. OGEE v3 can be accessible freely at https://v3.ogee.info.

Red blood cell distribution width and peritoneal dialysis-associated peritonitis prognosis.

Objective: Red blood cell distribution width (RDW) is a parameter of the heterogeneity of circulating erythrocyte size. Recent researches have pointed out a link among RDW, chronic kidney disease, and inflammation. We sought to investigate the prognostic value of baseline RDW in patients with peritoneal dialysis-associated peritonitis (PDAP).Methods: Our study included 337 peritonitis episodes experienced by 202 patients who were undergoing continuous ambulatory peritoneal dialysis (CAPD) at a single center from 2013 to 2018. Episodes were categorized according to the tertiles of baseline RDW levels (T1, <13.2%; T2, 13.2-14.3%; T3, >14.3%). Routine logistic regression and generalized estimating equation (GEE) were used to estimate the association between RDW and treatment failure, which was defined as relapse/recurrent episodes, catheter removal, or death during therapy.Results: After adjusting for other potential predictors, RDW exhibited an incremental relationship with the risk of treatment failure. The baseline RDW of T3 indicated a 43% and 52% increased venture of treatment failure in logistic and GEE analyses, respectively, compared with T1. As a continuous variable, the fitting curve based on restricted cubic spiline showed that the relationship was nonlinearly but positively correlated. The multivariate model A (combined RDW with baseline age, albumin, serum ferritin, and duration on CAPD) showed an area under the curve of 0.671 (95% confidence interval, 0.5920.749) for the prediction of treatment failure.Conclusions: A Higher baseline level of RDW was significantly associated with a greater rate of treatment failure among PDAP episodes independent of other potential predictors.

Biomimetic Matrix Stiffness Modulates Hepatocellular Carcinoma Malignant Phenotypes and Macrophage Polarization through Multiple Modes of Mechanical Feedbacks.

The extracellular matrix (ECM) stiffening is an important sign of local microenvironment change, which is considered as a hallmark of many diseases including hepatocellular carcinoma (HCC). The fates of both cancer cells and immune cells can be regulated by mechanical feedbacks acquired from ECM, but there is a lack of a precise study of mechanical feedback modes in different cell phenotypes following with the progressively increasing ECM stiffness. Herein, we used a biopolymeric film without further modification of adhesive molecules, as a natural local niche to mimic a gradually stiffening manner from HCC onset in liver cirrhosis to its metastasis in the spinal cord. Three distinct manners of mechanical feedbacks were found: the gradual manner in HCC cell spreading, migration and early apoptosis to oxaliplatin, the stepwise manner in HCC cell adhesion, proliferation, focal adhesion (FA) formation, drug resistance, and macrophage M1 polarization; the specific manner in the stages of the progression of epithelial-mesenchymal transition at different stiffness ranges. Further investigation of molecular mechanisms confirmed those mechanical feedback manners by signaling activation of FA kinase, phosphatidylinositol 3-kinase, and expression of pro-/antiapoptotic and pro-/anti-inflammatory genes. Our results pave a novel avenue to know about mechanical feedbacks from ECM, which could be used for future cancer studies and in vitro drug screening applications.

GMrepo: a database of curated and consistently annotated human gut metagenomes.

GMrepo (data repository for Gut Microbiota) is a database of curated and consistently annotated human gut metagenomes. Its main purpose is to facilitate the reusability and accessibility of the rapidly growing human metagenomic data. This is achieved by consistently annotating the microbial contents of collected samples using state-of-art toolsets and by manual curation of the meta-data of the corresponding human hosts. GMrepo organizes the collected samples according to their associated phenotypes and includes all possible related meta-data such as age, sex, country, body-mass-index (BMI) and recent antibiotics usage. To make relevant information easier to access, GMrepo is equipped with a graphical query builder, enabling users to make customized, complex and biologically relevant queries. For example, to find (1) samples from healthy individuals of 18 to 25 years old with BMIs between 18.5 and 24.9, or (2) projects that are related to colorectal neoplasms, with each containing >100 samples and both patients and healthy controls. Precomputed species/genus relative abundances, prevalence within and across phenotypes, and pairwise co-occurrence information are all available at the website and accessible through programmable interfaces. So far, GMrepo contains 58 903 human gut samples/runs (including 17 618 metagenomes and 41 285 amplicons) from 253 projects concerning 92 phenotypes. GMrepo is freely available at: https://gmrepo.humangut.info.

[Spatial-temporal Distribution of Aerosol Optical Depth and Its Main Influence Types in China During 1990-2017].

In order to accurately understand the optical characteristics of aerosols in China, based on Mann-Kendall(MK) and Sen's slope trend analysis methods, the spatiotemporal variations of aerosol optical depth(AOD) derived from MERRA-2 reanalysis datasets were estimated in China for the period of 1990-2017. The results showed that ① for the interannual scale, there was a significant increasing trend in the annual mean AOD in China during 1990-2017. Besides, high aerosol loadings were observed in spring and summer, and the seasonal difference between the eastern and western regions was large. This was mainly due to the topographic and meteorological factors. ② At the spatial scale, the annual mean AOD values increased from the northwest to the southeast, with characteristically high AOD values occurring in Sichuan Pendi and the Tarim and Turpan basins and low values in the Qinghai-Xizang plateau region. Similarly, the AOD MK value and Sen's slope value showed significant decreasing trends from the southeast to the northwest, which was closely related to climate change and the human activity intensity. ③ In regard to black carbon aerosol, dust aerosol, organic carbon aerosol, sea salt aerosol, and SO4 aerosol, dust and SO4 aerosols were affected by the air humidity and human activity intensity, which have obvious regional differences in China.

Role of Endothelial Cells in Renal Fibrosis.

Renal fibrosis has been regarded as the common pathway of end-stage renal failure. Understanding the fundamental mechanism that leads to renal fibrosis is essential for developing better therapeutic options for chronic kidney diseases. So far, the main abstractions are on the injury of tubular epithelial cells, activation of interstitial cells, expression of chemotactic factor and adhesion molecule, infiltration of inflammatory cells and homeostasis of ECM. However, emerging studies revealed that endothelial cells (ECs) might happen to endothelial-to-mesenchymal transition (EndMT) dependent and/or independent endothelial dysfunction, which were supposed to accelerate renal fibrosis and are identified as new mechanisms for the proliferation of myofibroblasts as well. In this chapter, we are about to interpret the role of ECs in renal fibrosis and analyze the related molecules and pathways of both EndMT and EndMT independent endothelial dysfunction.

Immobilized Transforming Growth Factor-Beta 1 in a Stiffness-Tunable Artificial Extracellular Matrix Enhances Mechanotransduction in the Epithelial Mesenchymal Transition of Hepatocellular Carcinoma.

Cancer progression is regulated by multiple factors of extracellular matrix (ECM). Understanding how cancer cells integrate multiple signaling pathways to achieve specific behaviors remains a challenge because of the lack of appropriate models to copresent and modulate ECM properties. Here we proposed a strategy to build a thin biomaterial matrix by poly(l-lysine) and hyaluronan as an artificial stiffness-tunable ECM. Transforming growth factor-beta 1 (TGF-ß1) was used as a biochemical cue to present in an immobilized and spatially controlled manner, with a high loading efficiency of 90%. Either soft matrix with immobilized TGF-ß1 (i-TGF) or bare stiff matrix could only promote HCC cells to form the epithelial phenotype, whereas stiff matrix with i-TGF was the only condition to induce the mesenchymal phenotype. Further investigation revealed that i-TGF increased the specific TGF-ß1 receptor (TßRI) expression to activate PI3K pathway. i-TGF-TßRI interactions also promoted HCC cell adhesion to enlarge contact area for stiffness sensing, resulting in the raising expression of the mechano-sensor (ß1 integrin). Mechanotransduction would then be enhanced by the ß1 integrin/vinculin/p-FAK pathway, leading to a noble PI3K activation. Using our model, a novel mechanism was discovered to elucidate regulation of cell fates by coupling mechanotransduction and biochemical signaling.

High expression of RAB38 promotes malignant progression of pancreatic cancer.

Ras­Related Protein Rab­38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome­related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the present study, an immunohistochemical assay was performed to analyze the expression of RAB38 in pancreatic adenocarcinoma tumor specimens from 82 patients, and the clinicopathological characteristics and survival rate of these patients were further examined. To validate the role of RAB38 in tumors, the effect of RAB38 on tumor cell proliferation, migration and invasion was assessed by establishing RAB38 knockdown cell lines. Reverse transcription­quantitative polymerase chain reaction and western blotting were used to examine the expression levels of proteins associated with the cancer cell behavior. In addition, the inhibitory effect of RAB38 silencing on pancreatic cancer was examined in mice. The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients. Further investigation indicated that RAB38 downregulation significantly suppressed the proliferation, migration and invasive capacity of pancreatic cancer cells, as well as decreased the expression levels of Ki67, proliferating cell nuclear antigen, and matrix metalloproteinases 2 and 9. RAB38 silencing also inhibited the development of pancreatic cancer in vivo. Taken together, a high level of RAB38 was significantly associated with the malignant phenotypes of pancreatic cancer, suggesting that RAB38 may serve as a novel biomarker and a potential therapeutic target for pancreatic cancer.

Effect of Serum Vitamin D Levels on Cellular Immunity and Antiviral Effects in Chronic Hepatitis B Patients.

BACKGROUND: To study the effect of 25-hydroxyl vitamin D3 on peripheral blood T lymphocyte immune function and antiviral effects in chronic hepatitis B patients. METHODS: The clinical data for 70 patients with chronic hepatitis B were analyzed. Serum 25-hydroxyl vitamin D was determined by electrochemical luminescence, and hepatitis B virus serological markers were determined by fluorescence quantitative polymerase chain reaction. Subsets of T lymphocytes were determined by immune fluorescence labeling method. These patients were divided into three groups based on serum 25-hydroxyl vitamin D level. After six months of pegylated interferon treatment, three groups have their number of T lymphocyte, liver functions, and virological indexes examined at the corresponding time. RESULTS: The years and ratio of gender have no statistical differences in these three groups. The proportion of CD3+, CD4+ T lymphocytes and the ratio of CD4+/CD8+ significantly increased (p < 0.05) as the level of 25-hydroxyl vitamin D increased, but the proportion of CD8+ decreased. Interferon treatment can improve the T cells subgroup, and the high level group of serum 25-hydroxyl vitamin D improved more obviously. The positive ratio of HBeAg, HBsAg and the titer of HBV DNA decreased with the increase of serum vitamin D, and the difference between the high and low level 25-hydroxyl vitamin D groups was significant (p < 0.05). The treatment of interferon can obviously improve the hepatitis B virus serological markers; the high level group of serum 25-hydroxyl vitamin D can obtain better virological response. However, there was no significant difference between the three groups of serological markers of liver function. CONCLUSIONS: Vitamin D may play a part in the immunologic function adjustment and immune tolerance in the natural course of chronic HBV infection, and high levels of vitamin D may be able to achieve sustained virological response. These findings may shed light on the research and treatment of chronic hepatitis B pathogenesis.

MicroRNA-7/NF-κB signaling regulatory feedback circuit regulates gastric carcinogenesis.

MicroRNAs play essential roles in gene expression regulation during carcinogenesis. Here, we investigated the role of miR-7 and the mechanism by which it is dysregulated in gastric cancer (GC). We used genome-wide screenings and identified RELA and FOS as novel targets of miR-7. Overexpression of miR-7 repressed RELA and FOS expression and prevented GC cell proliferation and tumorigenesis. These effects were clinically relevant, as low miR-7 expression was correlated with high RELA and FOS expression and poor survival in GC patients. Intriguingly, we found that miR-7 indirectly regulated RELA activation by targeting the IκB kinase IKKε. Furthermore, IKKε and RELA can repress miR-7 transcription, which forms a feedback circuit between miR-7 and nuclear factor κB (NF-κB) signaling. Additionally, we demonstrate that down-regulation of miR-7 may occur as a result of the aberrant activation of NF-κB signaling by Helicobacter pylori infection. These findings suggest that miR-7 may serve as an important regulator in GC development and progression.

Inhibiting gastric cancer-associated angiogenesis by CIAPIN1 siRNA.

Angiogenesis plays an essential role in tumor growth and metastasis and is a promising target for cancer therapy. We characterized the effects of selective CIAPIN1 inhibition on the angiogenesis gastric cancer cell line SGC7901 by stable transfection of CIAPIN1 siRNA. Our study has been shown that CIAPIN1 play the determined role in tumor growth and multidrug resistance. The conditioned media obtained from SGC7901 treated with CIAPIN1 siRNA suppressed in vitro the proliferation, migration and tube formation of human umbilical vein endothelial cells compared with untransfected cells or cells transfected with control vector alone. Furthermore, the stable transfection of CIAPIN1 siRNA inhibited in vivo tumorigenicity and angiogenesis. Our findings support that selective inhibition of CIAPIN1 alone plays an instrumental role on gastric cancer associated angiogenesis.

[Effects of mouse NIH3T3 cells transfected with VEGF gene on neovascularization of ischemic flaps].

OBJECTIVE: To investigate the feasibility of applying NIH3T3 cells transfected by VEGF gene to the treatment of ischemic random skin flaps. METHODS: Plasmid PcDNA3.1(-)/VEGF(165) containing VEGF gene was transduced into the mouse NIH3T3 cells by liposome. Immunohistochemistry was used to detect the expression of VEGF protein of mouse NIH/3T3 cells in vitro. The NIH3T3 cells were stained with CM-DiI before the transplantation. Thirty mice were randomized into 3 groups: Groups A, B and C, and were respectively injected with NIH/3T3 cells transfected with PcDNA3.1(-)/VEGF(165) plasmid, NIH/3T3 cells and medium only. On the 4th day after the injection, random dorsal skin flaps with an area of 4.0 cm x 1.5 cm were established. The survival, neovascularization and blood flow recovery of the flaps were detected. RESULTS: VEGF-transduced NIH3T3 cells expressed VEGF highly in vitro and in vivo. The results showed that flap survival rate in group A (95.1% +/- 3.1%) was significantly higher than those in group B (37.4% +/- 6.3%) and group C (26.2% +/- 5.6%). The capillary density and the blood perfusion of the flaps in group A were significantly higher than those in other two groups. CONCLUSIONS: VEGF-transfected NIH3T3 cells can improve ischemic flap neovascularization and extend survival areas.