cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6926987
title: Supplementary Material for: BAIBA Attenuates the Expression of Inflammatory Cytokines and Attachment Molecules and ER Stress in HUVECs and THP-1 Cells

description: <b><i>Objective:</i></b> β-Aminoisobutyric acid (BAIBA), a myokine, is a thymine catabolite that is induced during exercise, leading to browning of white fat, hepatic fatty acid oxidation, and suppression of hepatic lipogenesis. However, the effects of BAIBA on the progression of atherosclerosis remain unclear. <b><i>Methods:</i></b> We performed a Western blot analyses to determine various protein expression. ELISAs (enzyme-linked immunosorbent assays), cell adhesion assays, and cell viability assays were also performed on human umbilical vascular endothelial cells (HUVECs) and human monocytes (THP-1 cells). <b><i>Results:</i></b> In the current study, we demonstrate that BAIBA suppresses atherosclerotic reactions caused by lipopolysaccharide (LPS) treatment via an AMPK-dependent pathway. Treatment of HUVECs and THP-1 cells with BAIBA inhibited the LPS-induced phosphorylation of nuclear factor-κB (NFκB) and the secretion of proinflammatory cytokines. In HUVECs, expression of adhesion molecules and LPS-stimulated adhesion of THP-1 cells to the endothelium were significantly decreased after BAIBA treatment. Furthermore, LPS-induced endoplasmic reticulum (ER) stress and cell toxicity were significantly decreased after BAIBA treatment of HUVECs. Notably, all of these proatherosclerotic effects were fully abrogated by treatment with small interfering RNA targeting AMPK. <b><i>Conclusion:</i></b> BAIBA ameliorates LPS-induced atherosclerotic reactions via AMPK-mediated suppression of inflammation and ER stress.
DOI: 10.7910/dvn/jdfd2b/zwqfop
title: 0-40.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.7910/dvn/jdfd2b/49fkgm
title: 0-3.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.7910/dvn/jdfd2b/4nyegg
title: 0-16.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.7910/dvn/jdfd2b/t46kze
title: 0-39.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.7910/dvn/jdfd2b/kpxjkk
title: 0-41.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923516
title: Supplementary Material for: A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients

description: <b><i>Background/Aims:</i></b> CDH18 (cadherin 18) is specifically expressed in the central nervous system and associated with various neuropsychiatric disorders. In this study, the role of CDH18 in glioma carcinogenesis and progression was investigated. <b><i>Methods:</i></b> The expression of CDH18 and its prognostic value in patients with gliomas were analyzed in public database and validated by real-time PCR/immunohistochemical staining (IHC) in our cohort. CCK-8 assay, transwell migration assay, wound healing assay, clonogenic assay and tumorigenicity assay were used to compare the proliferation, invasion and migration ability of glioma cells with different expressions of CDH18. iTRAQ-based quantitative proteomic analysis were used to reveal the downstream target of CDH18. Rescue experiments were conducted to further validate the relationship between UQCRC2 and CDH18. <b><i>Results:</i></b> The expression of CDH18 was depressed in a ladder-like pattern from normal tissues to WHO IV gliomas, and was an independent prognostic factor in TCGA (The Cancer Genome Atlas), CGGA (the Chinese glioma genome-atlas) and our glioma cohorts (n=453). Functional experiments <i>in vitro</i> and <i>in vivo</i> demonstrated that CDH18 inhibited invasion/migration, enhanced chemoresistance and suppressed tumorigenicity of glioma cells. UQCRC2 was identified as the downstream target of CDH18 by proteomic analysis. The expression of UQCRC2 was gradually absent as the WHO grades of gliomas escalated and was positively correlated with the expression of CDH18. Furthermore, <i>in vitro</i> assays demonstrated that down-regulation of UQCRC2 partly reversed the inhibition of invasion/migration ability and chemoresistance in CDH18 overexpressed glioma cell lines. Survival analysis demonstrated that combined CDH18/UQCRC2 biomarkers significantly influenced the prognosis of glioma patients. <b><i>Conclusions:</i></b> The present research demonstrated that CDH18 exerted its tumor-suppressor role via UQCRC2 in glioma cells and CDH18 might serve as a therapeutic target for treating gliomas.
DOI: 10.7910/dvn/jdfd2b/0jrirr
title: 0-8.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923447
title: Analytical Data of Xanthocidins isolated from Streptomyces sp. AcE210

description: NMR raw data of xanthocidin and xanthocidin derivetives isolated from Streptomyces sp. AcE210<br>
DOI: 10.6084/m9.figshare.6923447.v1
title: Analytical Data of Xanthocidins isolated from Streptomyces sp. AcE210

description: NMR raw data of xanthocidin and xanthocidin derivetives isolated from Streptomyces sp. AcE210<br>
DOI: 10.7910/dvn/jdfd2b/p4nxxb
title: 0-10.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923516.v1
title: Supplementary Material for: A Novel Tumor-Suppressor, CDH18, Inhibits Glioma Cell Invasiveness Via UQCRC2 and Correlates with the Prognosis of Glioma Patients

description: <b><i>Background/Aims:</i></b> CDH18 (cadherin 18) is specifically expressed in the central nervous system and associated with various neuropsychiatric disorders. In this study, the role of CDH18 in glioma carcinogenesis and progression was investigated. <b><i>Methods:</i></b> The expression of CDH18 and its prognostic value in patients with gliomas were analyzed in public database and validated by real-time PCR/immunohistochemical staining (IHC) in our cohort. CCK-8 assay, transwell migration assay, wound healing assay, clonogenic assay and tumorigenicity assay were used to compare the proliferation, invasion and migration ability of glioma cells with different expressions of CDH18. iTRAQ-based quantitative proteomic analysis were used to reveal the downstream target of CDH18. Rescue experiments were conducted to further validate the relationship between UQCRC2 and CDH18. <b><i>Results:</i></b> The expression of CDH18 was depressed in a ladder-like pattern from normal tissues to WHO IV gliomas, and was an independent prognostic factor in TCGA (The Cancer Genome Atlas), CGGA (the Chinese glioma genome-atlas) and our glioma cohorts (n=453). Functional experiments <i>in vitro</i> and <i>in vivo</i> demonstrated that CDH18 inhibited invasion/migration, enhanced chemoresistance and suppressed tumorigenicity of glioma cells. UQCRC2 was identified as the downstream target of CDH18 by proteomic analysis. The expression of UQCRC2 was gradually absent as the WHO grades of gliomas escalated and was positively correlated with the expression of CDH18. Furthermore, <i>in vitro</i> assays demonstrated that down-regulation of UQCRC2 partly reversed the inhibition of invasion/migration ability and chemoresistance in CDH18 overexpressed glioma cell lines. Survival analysis demonstrated that combined CDH18/UQCRC2 biomarkers significantly influenced the prognosis of glioma patients. <b><i>Conclusions:</i></b> The present research demonstrated that CDH18 exerted its tumor-suppressor role via UQCRC2 in glioma cells and CDH18 might serve as a therapeutic target for treating gliomas.
DOI: 10.7910/dvn/jdfd2b/uuszbx
title: 0-44.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923354
title: Supplementary Material for: The RNA-Binding Protein PCBP1 Functions as a Tumor Suppressor in Prostate Cancer by Inhibiting Mitogen Activated Protein Kinase 1

description: <b><i>Background/Aims:</i></b> Poly r(C) binding protein (PCBP) 1 or heterogeneous ribonucleoprotein (hnRNP) E1 is a RNA binding protein functional in multiple biological processes. In prostate cancer (PCa), PCBP1 loss was shown to be involved with increased stemness in PCacells; however, the underlying mechanism remains unclear. <b><i>Method:</i></b> The role of PCBP1 in prostate tumor formationwas determined by xenograft assays. Immunoprecipitationand mass spectrometry were performed to find the pathways altered after PCBP1 knockdown. Cell proliferation, migration, invasion, and soft agar colony formationassays and xenograft assays were used to determine the role of target protein pathogenesis regulation and formation of PCa. QRT-PCR was performedto quantify relative mRNA expression. <b><i>Results:</i></b> The expression of mitogen activated protein kinase 1 (MAPK1) or extracellular signal regulated kinase 2 (ERK2) was increased following PCBP1 loss. Attenuation of MAPK1 inhibited <i>in vitro</i> and <i>in vivo</i> tumorigenicity and metastasis in PCa cell line, PC3. Overexpression of MAPK1 in the PC3 cells increased the tumorigenicity and metastasis. Analysis of PCBP1 and MAPK1 mRNA levels in 25 PCa patients compared to tumor-adjacent normal tissue confirmed an inverse correlation between PCBP1 and MAPK1 expression. <b><i>Conclusions:</i></b> PCBP1 can act as a suppressor of tumor in prostate epithelial cells by inhibiting MAPK1 expression.
DOI: 10.7910/dvn/jdfd2b/5hlvbx
title: 0-48.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923261
title: Supplementary Material for: MicroRNA-224 Promotes Pancreatic Cancer Cell Proliferation and Migration by Targeting the TXNIP-Mediated HIF1α Pathway

description: <b><i>Background/Aims:</i></b> MicroRNAs (miRNAs) have been shown to participate in the development of pancreatic ductal adenocarcinoma (PDAC) by modulating multiple cellular processes. Increased miR-224 expression enhances proliferation and metastasis in human cancers. This study aimed to investigate the role of miR-224 and its underlying mechanism of action in PDAC. <b><i>Methods:</i></b> BrdU, MTT, and cell migration assays were performed to determine cell proliferation, viability, and migration, respectively. The binding sites of miR-224 were identified using a luciferase reporter system, whereas protein expression of target genes was determined by immunoblotting and immunofluorescence analyses. A BALB/c nude mouse xenograft model was used to evaluate the role of miR-224 <i>in vivo</i>. <b><i>Results:</i></b> We demonstrated that miR-224 expression was enhanced in PDAC cells and tissues, and was related to migration and proliferation. Noticeably, miR-224 overexpression promoted the proliferation, migration, and metastasis of Panc1 cells, while miR-224 inhibition had the reverse effect on PDAC cells. Moreover, we found that thioredoxin-interacting protein (TXNIP) is a target of miR-224. The results also indicated that miR-224 inversely regulated TXNIP by binding directly to its 3′-untranslated region, which resulted in the activation of hypoxia-inducible factor 1α (HIF1α). Further, either TXNIP re-expression or HIF1α depletion abolished the effects of miR-224 on the proliferation and migration of PDAC cells <i>in vitro</i> and <i>in vivo</i>. Regarding the relationship of TXNIP and HIF1α, we found that TXNIP mediated the nuclear export of HIF1α and its degradation by forming a complex with HIF1α. <b><i>Conclusion:</i></b> The miR-224-TXNIP-HIF1α axis may be useful in developing novel therapies for PDAC.
DOI: 10.7910/dvn/jdfd2b/5qyfrn
title: 0-38.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6923261.v1
title: Supplementary Material for: MicroRNA-224 Promotes Pancreatic Cancer Cell Proliferation and Migration by Targeting the TXNIP-Mediated HIF1α Pathway

description: <b><i>Background/Aims:</i></b> MicroRNAs (miRNAs) have been shown to participate in the development of pancreatic ductal adenocarcinoma (PDAC) by modulating multiple cellular processes. Increased miR-224 expression enhances proliferation and metastasis in human cancers. This study aimed to investigate the role of miR-224 and its underlying mechanism of action in PDAC. <b><i>Methods:</i></b> BrdU, MTT, and cell migration assays were performed to determine cell proliferation, viability, and migration, respectively. The binding sites of miR-224 were identified using a luciferase reporter system, whereas protein expression of target genes was determined by immunoblotting and immunofluorescence analyses. A BALB/c nude mouse xenograft model was used to evaluate the role of miR-224 <i>in vivo</i>. <b><i>Results:</i></b> We demonstrated that miR-224 expression was enhanced in PDAC cells and tissues, and was related to migration and proliferation. Noticeably, miR-224 overexpression promoted the proliferation, migration, and metastasis of Panc1 cells, while miR-224 inhibition had the reverse effect on PDAC cells. Moreover, we found that thioredoxin-interacting protein (TXNIP) is a target of miR-224. The results also indicated that miR-224 inversely regulated TXNIP by binding directly to its 3′-untranslated region, which resulted in the activation of hypoxia-inducible factor 1α (HIF1α). Further, either TXNIP re-expression or HIF1α depletion abolished the effects of miR-224 on the proliferation and migration of PDAC cells <i>in vitro</i> and <i>in vivo</i>. Regarding the relationship of TXNIP and HIF1α, we found that TXNIP mediated the nuclear export of HIF1α and its degradation by forming a complex with HIF1α. <b><i>Conclusion:</i></b> The miR-224-TXNIP-HIF1α axis may be useful in developing novel therapies for PDAC.
DOI: 10.7910/dvn/jdfd2b/zsdtxr
title: 0-36.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6921917
title: Supplementary Material for: To Be Or Not to Be: the “Smoker’s Paradox” – An in-Vitro Study

description: <b><i>Background/Aims:</i></b> Clinical studies have reported a better outcome of smokers after myocardial infarction compared to non-smokers. The data are controversial, as some clinical studies did not observe this effect. The cell biological processes involved, which might account for a ‘Smoker’s Paradox’, have not been investigated yet. Therefore, the aim was to elucidate the effect of cigarette smoke on the viability of cardiomyocytes in the context of hypoxia and reperfusion. <b><i>Methods:</i></b> HL-1 cells were incubated with different concentrations of cigarette smoke extract (CSE) and subjected to hypoxia/reperfusion to further evaluate influence of CSE on viability of HL-1 cells using flow cytometry analyses, Western Blot and immunofluorescence staining. <b><i>Results:</i></b> Incubation with CSE led to a concentration-dependent reduction in HL-1 viability. Adding hypoxia as a stressor enhanced cell death. Caspase-independent apoptosis was the observed type of cell death partly induced by P53 and apoptosis-inducing-factor. Yet a significant increase in LDH release in cardiomyocytes incubated with 4%, 8% and 16% CSE suggests necrosis with rapid DNA depletion. Interestingly, after hypoxia a decreased LDH release under lower CSE concentrations was observed. Moreover, a concentration-dependent increase in proliferation and a trend for increased ATP availability under hypoxic conditions was shown. <b><i>Conclusions:</i></b> The trend for less LDH release in hypoxia after low-level CSE incubation might represent a switch from necrosis to apoptosis, which in combination with the increase in metabolic activity and ATP availability might account for the ‘Smoker’s Paradox’. These findings could partly explain inconsistent results of previous clinical studies as the data showed strong evidence for the crucial relevance of the amount of cigarettes smoked. We are in need of future studies distinguishing between different types of smokers to finally verify or falsify the ‘Smoker’s Paradox’.
DOI: 10.6084/m9.figshare.6922631
title: Supplementary Material for: Therapeutic Potential of Human Adipose-Derived Stem Cell Exosomes in Stress Urinary Incontinence – An in Vitro and in Vivo Study

description: <b><i>Background/Aims:</i></b> To evaluate whether local injection of exosomes derived from human adipose-derived stem cells (hADSCs) facilitates recovery of stress urinary incontinence (SUI) in a rat model. <b><i>Methods:</i></b> For the <i>in vitro</i> study, a Cell Counting Kit-8 (CCK-8) array and proteomic analysis were performed. For the <i>in vivo</i> study, female rats were divided into four groups: sham, SUI, adipose-derived stem cell (ADSC), and exosomes (<i>n</i> = 12 each). The SUI model was generated by pudendal nerve transection and vaginal dilation. Vehicle, hADSCs, or exosomes were injected into the peripheral urethra. After 2, 4, and 8 weeks, the rats underwent cystometrography and leak point pressure (LPP) testing, and tissues were harvested for histochemical analyses. <b><i>Results:</i></b> The CCK-8 experiment demonstrated that ADSC-derived exosomes could enhance the growth of skeletal muscle and Schwann cell lines in a dose-dependent manner. Proteomic analysis revealed that ADSC-derived exosomes contained various proteins of different signaling pathways. Some of these proteins are associated with the PI3K-Akt, Jak-STAT, and Wnt pathways, which are related to skeletal muscle and nerve regeneration and proliferation. <i>In vivo</i> experiments illustrated that rats of the exosome group had higher bladder capacity and LPP, and had more striated muscle fibers and peripheral nerve fibers in the urethra than rats of the SUI group. Both urethral function and histology of rats in the exosome group were slightly better than those in the ADSC group. <b><i>Conclusions:</i></b> Local injection of hADSC-derived exosomes improved functional and histological recovery after SUI.
DOI: 10.7910/dvn/jdfd2b/6j40oe
title: 0-33.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6919700
title: testtest

description: This item is a draft(metadata required for publication missing)
DOI: 10.6084/m9.figshare.6921917.v1
title: Supplementary Material for: To Be Or Not to Be: the “Smoker’s Paradox” – An in-Vitro Study

description: <b><i>Background/Aims:</i></b> Clinical studies have reported a better outcome of smokers after myocardial infarction compared to non-smokers. The data are controversial, as some clinical studies did not observe this effect. The cell biological processes involved, which might account for a ‘Smoker’s Paradox’, have not been investigated yet. Therefore, the aim was to elucidate the effect of cigarette smoke on the viability of cardiomyocytes in the context of hypoxia and reperfusion. <b><i>Methods:</i></b> HL-1 cells were incubated with different concentrations of cigarette smoke extract (CSE) and subjected to hypoxia/reperfusion to further evaluate influence of CSE on viability of HL-1 cells using flow cytometry analyses, Western Blot and immunofluorescence staining. <b><i>Results:</i></b> Incubation with CSE led to a concentration-dependent reduction in HL-1 viability. Adding hypoxia as a stressor enhanced cell death. Caspase-independent apoptosis was the observed type of cell death partly induced by P53 and apoptosis-inducing-factor. Yet a significant increase in LDH release in cardiomyocytes incubated with 4%, 8% and 16% CSE suggests necrosis with rapid DNA depletion. Interestingly, after hypoxia a decreased LDH release under lower CSE concentrations was observed. Moreover, a concentration-dependent increase in proliferation and a trend for increased ATP availability under hypoxic conditions was shown. <b><i>Conclusions:</i></b> The trend for less LDH release in hypoxia after low-level CSE incubation might represent a switch from necrosis to apoptosis, which in combination with the increase in metabolic activity and ATP availability might account for the ‘Smoker’s Paradox’. These findings could partly explain inconsistent results of previous clinical studies as the data showed strong evidence for the crucial relevance of the amount of cigarettes smoked. We are in need of future studies distinguishing between different types of smokers to finally verify or falsify the ‘Smoker’s Paradox’.
DOI: 10.6084/m9.figshare.6922631.v1
title: Supplementary Material for: Therapeutic Potential of Human Adipose-Derived Stem Cell Exosomes in Stress Urinary Incontinence – An in Vitro and in Vivo Study

description: <b><i>Background/Aims:</i></b> To evaluate whether local injection of exosomes derived from human adipose-derived stem cells (hADSCs) facilitates recovery of stress urinary incontinence (SUI) in a rat model. <b><i>Methods:</i></b> For the <i>in vitro</i> study, a Cell Counting Kit-8 (CCK-8) array and proteomic analysis were performed. For the <i>in vivo</i> study, female rats were divided into four groups: sham, SUI, adipose-derived stem cell (ADSC), and exosomes (<i>n</i> = 12 each). The SUI model was generated by pudendal nerve transection and vaginal dilation. Vehicle, hADSCs, or exosomes were injected into the peripheral urethra. After 2, 4, and 8 weeks, the rats underwent cystometrography and leak point pressure (LPP) testing, and tissues were harvested for histochemical analyses. <b><i>Results:</i></b> The CCK-8 experiment demonstrated that ADSC-derived exosomes could enhance the growth of skeletal muscle and Schwann cell lines in a dose-dependent manner. Proteomic analysis revealed that ADSC-derived exosomes contained various proteins of different signaling pathways. Some of these proteins are associated with the PI3K-Akt, Jak-STAT, and Wnt pathways, which are related to skeletal muscle and nerve regeneration and proliferation. <i>In vivo</i> experiments illustrated that rats of the exosome group had higher bladder capacity and LPP, and had more striated muscle fibers and peripheral nerve fibers in the urethra than rats of the SUI group. Both urethral function and histology of rats in the exosome group were slightly better than those in the ADSC group. <b><i>Conclusions:</i></b> Local injection of hADSC-derived exosomes improved functional and histological recovery after SUI.
DOI: 10.7910/dvn/jdfd2b/bp2jrr
title: 0-5.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.6084/m9.figshare.6919700.v1
title: testtest

description: This item is a draft(metadata required for publication missing)
DOI: 10.7910/dvn/jdfd2b/ozr1pm
title: 0-24.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;
DOI: 10.7910/dvn/jdfd2b/av2oda
title: 0-7.25V

description: sigma=0.25V; This is a FITS file with 1 (primary) HDU. The following recognized metadata keys have been found in the FITS file: NAXIS2; NAXIS; NAXIS1; NAXIS0;