cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.18094413.v1
title: Additional file 2 of Identification of the molecular subgroups in asthma by gene expression profiles: airway inflammation implications

description: Additional file 2: Table S2. The details of the genes in each of the WGCNA modules.
DOI: 10.6084/m9.figshare.12851546
title: Aberrant spliceosome expression and altered alternative splicing events correlate with maturation deficiency in human oocytes

description: Different strategies of ovarian stimulation are widely used in IVF to retrieve mature metaphase II (MII) oocytes for fertilization. On average, approximately 70% of recovered oocytes are mature, while personalized administration of hCG and/or GnRH agonist trigger and <i>in vitro</i> maturation (IVM) management can further improve the maturation rate. However, even under such conditions, a complete absence of oocyte maturation is still observed sporadically. The probable causes for such maturation-deficient (MD) oocytes – which arrest abnormally at metaphase I (MI) stage – are still under investigation. In the present study, using single-cell transcriptomic RNA sequencing (RNA-seq) and differential expression analysis, we showed that gene expression profiles were aberrant, and alternative splicing (AS) patterns were changed in MD oocytes when compared with normally mature (MN) oocytes. Gene ontology (GO) enrichment demonstrated that the differently expressed genes (DEGs) were mostly correlated with pre-mRNA splicing, RNA transportation, RNA processing, and mRNA regulation. Subsequently, analysis of AS events revealed that genes with altered AS patterns were primarily associated with metabolism and cell cycle. With these findings, we have demonstrated aberrant gene expression in complete maturation-deficient oocytes, and we propose that alterations in post-transcriptional regulation constitute a potential underlying mechanism governing oocyte maturation.
DOI: 10.6084/m9.figshare.12851546.v2
title: Aberrant spliceosome expression and altered alternative splicing events correlate with maturation deficiency in human oocytes

description: Different strategies of ovarian stimulation are widely used in IVF to retrieve mature metaphase II (MII) oocytes for fertilization. On average, approximately 70% of recovered oocytes are mature, while personalized administration of hCG and/or GnRH agonist trigger and <i>in vitro</i> maturation (IVM) management can further improve the maturation rate. However, even under such conditions, a complete absence of oocyte maturation is still observed sporadically. The probable causes for such maturation-deficient (MD) oocytes – which arrest abnormally at metaphase I (MI) stage – are still under investigation. In the present study, using single-cell transcriptomic RNA sequencing (RNA-seq) and differential expression analysis, we showed that gene expression profiles were aberrant, and alternative splicing (AS) patterns were changed in MD oocytes when compared with normally mature (MN) oocytes. Gene ontology (GO) enrichment demonstrated that the differently expressed genes (DEGs) were mostly correlated with pre-mRNA splicing, RNA transportation, RNA processing, and mRNA regulation. Subsequently, analysis of AS events revealed that genes with altered AS patterns were primarily associated with metabolism and cell cycle. With these findings, we have demonstrated aberrant gene expression in complete maturation-deficient oocytes, and we propose that alterations in post-transcriptional regulation constitute a potential underlying mechanism governing oocyte maturation.
DOI: 10.6084/m9.figshare.12851546.v1
title: Aberrant spliceosome expression and altered alternative splicing events correlate with maturation deficiency in human oocytes

description: Different strategies of ovarian stimulation are widely used in IVF to retrieve mature metaphase II (MII) oocytes for fertilization. On average, approximately 70% of recovered oocytes are mature, while personalized administration of hCG and/or GnRH agonist trigger and <i>in vitro</i> maturation (IVM) management can further improve the maturation rate. However, even under such conditions, a complete absence of oocyte maturation is still observed sporadically. The probable causes for such maturation-deficient (MD) oocytes – which arrest abnormally at metaphase I (MI) stage – are still under investigation. In the present study, using single-cell transcriptomic RNA sequencing (RNA-seq) and differential expression analysis, we showed that gene expression profiles were aberrant, and alternative splicing (AS) patterns were changed in MD oocytes when compared with normally mature (MN) oocytes. Gene ontology (GO) enrichment demonstrated that the differently expressed genes (DEGs) were mostly correlated with pre-mRNA splicing, RNA transportation, RNA processing, and mRNA regulation. Subsequently, analysis of AS events revealed that genes with altered AS patterns were primarily associated with metabolism and cell cycle. With these findings, we have demonstrated aberrant gene expression in complete maturation-deficient oocytes, and we propose that alterations in post-transcriptional regulation constitute a potential underlying mechanism governing oocyte maturation.
DOI: 10.6084/m9.figshare.12851552
title: MicroRNA-126 promotes proliferation, migration, invasion and endothelial differentiation while inhibits apoptosis and osteogenic differentiation of bone marrow-derived mesenchymal stem cells

description: Bone marrow-derived mesenchymal stem cells (BMSCs) are widely used for the treatment of inflammatory and immune diseases, and microRNA-126 (miR-126) is a critical regulator in inflammation as well as immunity. However, the mediating role of miR-126 in BMSCs is still not clear. Thus, this study aimed to preliminarily investigate the effect of miR-126 on proliferation, apoptosis, migration, invasion, differentiation, and its potential regulating pathways in BMSCs. Human BMSCs were obtained and infected with miR-126 overexpression lentivirus, control overexpression lentivirus, miR-126 knock-down lentivirus and control knock-down lentivirus, then cell functions, the PI3 K/AKT pathway and MEK1/ERK1 pathway were evaluated. Subsequently, PI3 K overexpression plasmid and MEK1 overexpression plasmid were transfected into BMSCs with miR-126 knockdown, then the cell functions were assessed as well. BMSCs with miR-126 overexpression displayed elevated proliferation, migration and invasion while decreased apoptosis; however, BMSCs with miR-126 knockdown presented with decreased proliferation, migration, invasion but increased apoptosis. As for differentiation, BMSCs with miR-126 overexpression showed higher levels of CD31, eNOS and VE-cadherin but lower expressions of ALP, OPN and RUNX2, while BMSCs with miR-126 knockdown disclosed the opposite results. Additionally, BMSCs with miR-126 overexpression showed elevated PI3 K, pAKT, MEK1 and pERK1 expressions, while BMSCs with miR-126 knockdown displayed opposite results. Furthermore, PI3 K overexpression and MEK1 overexpression both reversed the effects of miR-126 on cell functions in BMSCs. In conclusion, miR-126 is a genetic regulator in BMSCs via modulating multiple cell functions through the PI3 K/AKT and MEK1/ERK1 signaling pathways.
DOI: 10.6084/m9.figshare.12851552.v2
title: MicroRNA-126 promotes proliferation, migration, invasion and endothelial differentiation while inhibits apoptosis and osteogenic differentiation of bone marrow-derived mesenchymal stem cells

description: Bone marrow-derived mesenchymal stem cells (BMSCs) are widely used for the treatment of inflammatory and immune diseases, and microRNA-126 (miR-126) is a critical regulator in inflammation as well as immunity. However, the mediating role of miR-126 in BMSCs is still not clear. Thus, this study aimed to preliminarily investigate the effect of miR-126 on proliferation, apoptosis, migration, invasion, differentiation, and its potential regulating pathways in BMSCs. Human BMSCs were obtained and infected with miR-126 overexpression lentivirus, control overexpression lentivirus, miR-126 knock-down lentivirus and control knock-down lentivirus, then cell functions, the PI3 K/AKT pathway and MEK1/ERK1 pathway were evaluated. Subsequently, PI3 K overexpression plasmid and MEK1 overexpression plasmid were transfected into BMSCs with miR-126 knockdown, then the cell functions were assessed as well. BMSCs with miR-126 overexpression displayed elevated proliferation, migration and invasion while decreased apoptosis; however, BMSCs with miR-126 knockdown presented with decreased proliferation, migration, invasion but increased apoptosis. As for differentiation, BMSCs with miR-126 overexpression showed higher levels of CD31, eNOS and VE-cadherin but lower expressions of ALP, OPN and RUNX2, while BMSCs with miR-126 knockdown disclosed the opposite results. Additionally, BMSCs with miR-126 overexpression showed elevated PI3 K, pAKT, MEK1 and pERK1 expressions, while BMSCs with miR-126 knockdown displayed opposite results. Furthermore, PI3 K overexpression and MEK1 overexpression both reversed the effects of miR-126 on cell functions in BMSCs. In conclusion, miR-126 is a genetic regulator in BMSCs via modulating multiple cell functions through the PI3 K/AKT and MEK1/ERK1 signaling pathways.
DOI: 10.6084/m9.figshare.12851552.v1
title: MicroRNA-126 promotes proliferation, migration, invasion and endothelial differentiation while inhibits apoptosis and osteogenic differentiation of bone marrow-derived mesenchymal stem cells

description: Bone marrow-derived mesenchymal stem cells (BMSCs) are widely used for the treatment of inflammatory and immune diseases, and microRNA-126 (miR-126) is a critical regulator in inflammation as well as immunity. However, the mediating role of miR-126 in BMSCs is still not clear. Thus, this study aimed to preliminarily investigate the effect of miR-126 on proliferation, apoptosis, migration, invasion, differentiation, and its potential regulating pathways in BMSCs. Human BMSCs were obtained and infected with miR-126 overexpression lentivirus, control overexpression lentivirus, miR-126 knock-down lentivirus and control knock-down lentivirus, then cell functions, the PI3 K/AKT pathway and MEK1/ERK1 pathway were evaluated. Subsequently, PI3 K overexpression plasmid and MEK1 overexpression plasmid were transfected into BMSCs with miR-126 knockdown, then the cell functions were assessed as well. BMSCs with miR-126 overexpression displayed elevated proliferation, migration and invasion while decreased apoptosis; however, BMSCs with miR-126 knockdown presented with decreased proliferation, migration, invasion but increased apoptosis. As for differentiation, BMSCs with miR-126 overexpression showed higher levels of CD31, eNOS and VE-cadherin but lower expressions of ALP, OPN and RUNX2, while BMSCs with miR-126 knockdown disclosed the opposite results. Additionally, BMSCs with miR-126 overexpression showed elevated PI3 K, pAKT, MEK1 and pERK1 expressions, while BMSCs with miR-126 knockdown displayed opposite results. Furthermore, PI3 K overexpression and MEK1 overexpression both reversed the effects of miR-126 on cell functions in BMSCs. In conclusion, miR-126 is a genetic regulator in BMSCs via modulating multiple cell functions through the PI3 K/AKT and MEK1/ERK1 signaling pathways.
DOI: 10.6084/m9.figshare.7608674
title: Additional file 15: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S8. The significant functional genes in GIs of P. multocida. (XLSX 12 kb)
DOI: 10.6084/m9.figshare.7608674.v1
title: Additional file 15: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S8. The significant functional genes in GIs of P. multocida. (XLSX 12 kb)
DOI: 10.6084/m9.figshare.7608683
title: Additional file 16: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S9. The significant functional genes in the common part of the GIs and the unique genes of the pan-genome. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.7608683.v1
title: Additional file 16: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S9. The significant functional genes in the common part of the GIs and the unique genes of the pan-genome. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.7608689
title: Additional file 1: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S1. The origin and genomic characteristic of 114 P. multocida. (XLSX 26 kb)
DOI: 10.6084/m9.figshare.7608689.v1
title: Additional file 1: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S1. The origin and genomic characteristic of 114 P. multocida. (XLSX 26 kb)
DOI: 10.6084/m9.figshare.12851570
title: Effects of bone marrow mesenchymal stem cells on ovarian and testicular function in aging Sprague-Dawley rats induced by D-galactose

description: To investigate the effect of bone marrow mesenchymal stem cells (MSCs) on ovarian and testicular function of aging Sprague-Dawley (SD) rats induced by D-galactose (D-gal) and try to clarify the underlying functional mechanism. Adherent culture was used to isolate and purify rat MSCs. The status, proliferation and differentiation of MSCs were detected by hematoxylin-eosin staining, MTT, colony formation, flow cytometry and directional differentiation. The aging rat model was established by subcutaneous injection of D-gal, and the homing of MSCs was detected by fluorescence microscope after infusion of GFP-labeled MSCs through caudal vein. ELISA was used to detect the content of sex hormone in serum, and HE staining was used to observe the structure and morphology of testis and ovary. The isolated and purified MSCs were in good condition, and most of the cells were in G1 phase, which had strong abilities of cell proliferation, colony formation and differentiation. After GFP-labeled MSCs were infused, MSCs could be homed into the testis and ovary of rats. MSCs infusion could significantly improve the morphology of testis and ovary, increase the contents of P and E2 while decrease the contents of LH and FSH in female rats, and increase the content of testosterone in male rats (<i>P</i> &lt; 0.01). It also increased the activity of superoxide dismutase (SOD) in serum of ovary and testis and significantly decreased the content of malondialdehyde (MDA). MSCs affected the content of MDA and the activity of SOD by reducing the expression of cyclin-dependent kinase inhibitor 2A (p16) and increasing proliferating cell nuclear antigen (PCNA), consequently improving the aging and injury of reproductive organs.
DOI: 10.6084/m9.figshare.12851570.v1
title: Effects of bone marrow mesenchymal stem cells on ovarian and testicular function in aging Sprague-Dawley rats induced by D-galactose

description: To investigate the effect of bone marrow mesenchymal stem cells (MSCs) on ovarian and testicular function of aging Sprague-Dawley (SD) rats induced by D-galactose (D-gal) and try to clarify the underlying functional mechanism. Adherent culture was used to isolate and purify rat MSCs. The status, proliferation and differentiation of MSCs were detected by hematoxylin-eosin staining, MTT, colony formation, flow cytometry and directional differentiation. The aging rat model was established by subcutaneous injection of D-gal, and the homing of MSCs was detected by fluorescence microscope after infusion of GFP-labeled MSCs through caudal vein. ELISA was used to detect the content of sex hormone in serum, and HE staining was used to observe the structure and morphology of testis and ovary. The isolated and purified MSCs were in good condition, and most of the cells were in G1 phase, which had strong abilities of cell proliferation, colony formation and differentiation. After GFP-labeled MSCs were infused, MSCs could be homed into the testis and ovary of rats. MSCs infusion could significantly improve the morphology of testis and ovary, increase the contents of P and E2 while decrease the contents of LH and FSH in female rats, and increase the content of testosterone in male rats (<i>P</i> &lt; 0.01). It also increased the activity of superoxide dismutase (SOD) in serum of ovary and testis and significantly decreased the content of malondialdehyde (MDA). MSCs affected the content of MDA and the activity of SOD by reducing the expression of cyclin-dependent kinase inhibitor 2A (p16) and increasing proliferating cell nuclear antigen (PCNA), consequently improving the aging and injury of reproductive organs.
DOI: 10.6084/m9.figshare.12851570.v3
title: Effects of bone marrow mesenchymal stem cells on ovarian and testicular function in aging Sprague-Dawley rats induced by D-galactose

description: To investigate the effect of bone marrow mesenchymal stem cells (MSCs) on ovarian and testicular function of aging Sprague-Dawley (SD) rats induced by D-galactose (D-gal) and try to clarify the underlying functional mechanism. Adherent culture was used to isolate and purify rat MSCs. The status, proliferation and differentiation of MSCs were detected by hematoxylin-eosin staining, MTT, colony formation, flow cytometry and directional differentiation. The aging rat model was established by subcutaneous injection of D-gal, and the homing of MSCs was detected by fluorescence microscope after infusion of GFP-labeled MSCs through caudal vein. ELISA was used to detect the content of sex hormone in serum, and HE staining was used to observe the structure and morphology of testis and ovary. The isolated and purified MSCs were in good condition, and most of the cells were in G1 phase, which had strong abilities of cell proliferation, colony formation and differentiation. After GFP-labeled MSCs were infused, MSCs could be homed into the testis and ovary of rats. MSCs infusion could significantly improve the morphology of testis and ovary, increase the contents of P and E2 while decrease the contents of LH and FSH in female rats, and increase the content of testosterone in male rats (<i>P</i> &lt; 0.01). It also increased the activity of superoxide dismutase (SOD) in serum of ovary and testis and significantly decreased the content of malondialdehyde (MDA). MSCs affected the content of MDA and the activity of SOD by reducing the expression of cyclin-dependent kinase inhibitor 2A (p16) and increasing proliferating cell nuclear antigen (PCNA), consequently improving the aging and injury of reproductive organs.
DOI: 10.6084/m9.figshare.12851570.v2
title: Effects of bone marrow mesenchymal stem cells on ovarian and testicular function in aging Sprague-Dawley rats induced by D-galactose

description: To investigate the effect of bone marrow mesenchymal stem cells (MSCs) on ovarian and testicular function of aging Sprague-Dawley (SD) rats induced by D-galactose (D-gal) and try to clarify the underlying functional mechanism. Adherent culture was used to isolate and purify rat MSCs. The status, proliferation and differentiation of MSCs were detected by hematoxylin-eosin staining, MTT, colony formation, flow cytometry and directional differentiation. The aging rat model was established by subcutaneous injection of D-gal, and the homing of MSCs was detected by fluorescence microscope after infusion of GFP-labeled MSCs through caudal vein. ELISA was used to detect the content of sex hormone in serum, and HE staining was used to observe the structure and morphology of testis and ovary. The isolated and purified MSCs were in good condition, and most of the cells were in G1 phase, which had strong abilities of cell proliferation, colony formation and differentiation. After GFP-labeled MSCs were infused, MSCs could be homed into the testis and ovary of rats. MSCs infusion could significantly improve the morphology of testis and ovary, increase the contents of P and E2 while decrease the contents of LH and FSH in female rats, and increase the content of testosterone in male rats (<i>P</i> &lt; 0.01). It also increased the activity of superoxide dismutase (SOD) in serum of ovary and testis and significantly decreased the content of malondialdehyde (MDA). MSCs affected the content of MDA and the activity of SOD by reducing the expression of cyclin-dependent kinase inhibitor 2A (p16) and increasing proliferating cell nuclear antigen (PCNA), consequently improving the aging and injury of reproductive organs.
DOI: 10.6084/m9.figshare.12851573
title: The integrative analysis of DNA methylation and mRNA expression profiles confirmed the role of selenocompound metabolism pathway in Kashin-Beck disease

description: Kashin-Beck disease (KBD) is an endemic chronic osteochondropathy. The etiology of KBD remains unknown. In this study, we conducted an integrative analysis of genome-wide DNA methylation and mRNA expression profiles between KBD and normal controls to identify novel candidate genes and pathways for KBD. Articular cartilage samples from 17 grade III KBD patients and 17 healthy controls were used in this study. DNA methylation profiling of knee cartilage and mRNA expression profile data were obtained from our previous studies. InCroMAP was performed to integrative analysis of genome-wide DNA methylation profiles and mRNA expression profiles. Gene ontology (GO) enrichment analysis was conducted by online DAVID 6.7. The quantitative real-time polymerase chain reaction (qPCR), Western blot, immunohistochemistry (IHC), and lentiviral vector transfection were used to validate one of the identified pathways. We identified 298 common genes (such as COL4A1, HOXA13, TNFAIP6 and TGFBI), 36 GO terms (including collagen function, skeletal system development, growth factor), and 32 KEGG pathways associated with KBD (including Selenocompound metabolism pathway, PI3K-Akt signaling pathway, and TGF-beta signaling pathway). Our results suggest the dysfunction of many genes and pathways implicated in the pathogenesis of KBD, most importantly, both the integrative analysis and <i>in vitro</i> study in KBD cartilage highlighted the importance of selenocompound metabolism pathway in the pathogenesis of KBD for the first time.
DOI: 10.6084/m9.figshare.12851573.v1
title: The integrative analysis of DNA methylation and mRNA expression profiles confirmed the role of selenocompound metabolism pathway in Kashin-Beck disease

description: Kashin-Beck disease (KBD) is an endemic chronic osteochondropathy. The etiology of KBD remains unknown. In this study, we conducted an integrative analysis of genome-wide DNA methylation and mRNA expression profiles between KBD and normal controls to identify novel candidate genes and pathways for KBD. Articular cartilage samples from 17 grade III KBD patients and 17 healthy controls were used in this study. DNA methylation profiling of knee cartilage and mRNA expression profile data were obtained from our previous studies. InCroMAP was performed to integrative analysis of genome-wide DNA methylation profiles and mRNA expression profiles. Gene ontology (GO) enrichment analysis was conducted by online DAVID 6.7. The quantitative real-time polymerase chain reaction (qPCR), Western blot, immunohistochemistry (IHC), and lentiviral vector transfection were used to validate one of the identified pathways. We identified 298 common genes (such as COL4A1, HOXA13, TNFAIP6 and TGFBI), 36 GO terms (including collagen function, skeletal system development, growth factor), and 32 KEGG pathways associated with KBD (including Selenocompound metabolism pathway, PI3K-Akt signaling pathway, and TGF-beta signaling pathway). Our results suggest the dysfunction of many genes and pathways implicated in the pathogenesis of KBD, most importantly, both the integrative analysis and <i>in vitro</i> study in KBD cartilage highlighted the importance of selenocompound metabolism pathway in the pathogenesis of KBD for the first time.