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CapitalBio Corporation exosomal mirna microarray analysis
NK-derived exosomes from lean mice attenuate obesity-induced insulin resistance. a Fasting blood glucose of NCD and HFD mice after group feeding. b – d OGTT ( b ), ITT ( c ), and HOMA-IR index ( d ) of HFD mice and NCD mice ( n = 48) were recorded at 42 days after group feeding. HOMA-IR = Fasting blood glucose value × fasting serum insulin value/22.5. e Transmission electron micrographs of NK-derived exosomes. Scale bar, 100 nm. f NanoSight particle tracking analysis showing the particle size of NK-derived exosomes isolated from NCD and HFD mice. g Western blot assays of <t>exosomal</t> markers TSG101, HSP70, CD63, and CD9. h – k After blank liposomes, NCD-Exos, and HFD-Exos were separately injected into NCD or HFD mice via tail vein, fasting blood glucose ( h ), OGTT ( i ), ITT ( j ), and HOMA-IR ( k ) were assessed in each group. G1: HFD mice treated with blank liposomes ( n = 3); G2: HFD mice treated with HFD-Exos ( n = 3); G3: HFD mice treated with NCD-Exos ( n = 3); G4: NCD mice treated with blank liposomes ( n = 3); G5: NCD mice treated with HFD-Exos ( n = 3); and G6: NCD mice treated with NCD-Exos ( n = 3). l After NCD-Exos labeled with PKH26 were transferred into recipient mice, fluorescence images of the liver, islets, SATs, VATs, and skeletal muscles were observed by in vitro imaging system. Scale bar, 5 mm. m The weight of VATs from HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. n Liver triglyceride content of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. o , p ELISA assays of IL-6, IL-1β, and TNF-α expression in VATs and livers of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t-test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)
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1) Product Images from "Natural killer cell-derived exosomal miR-1249-3p attenuates insulin resistance and inflammation in mouse models of type 2 diabetes"

Article Title: Natural killer cell-derived exosomal miR-1249-3p attenuates insulin resistance and inflammation in mouse models of type 2 diabetes

Journal: Signal Transduction and Targeted Therapy

doi: 10.1038/s41392-021-00805-y

NK-derived exosomes from lean mice attenuate obesity-induced insulin resistance. a Fasting blood glucose of NCD and HFD mice after group feeding. b – d OGTT ( b ), ITT ( c ), and HOMA-IR index ( d ) of HFD mice and NCD mice ( n = 48) were recorded at 42 days after group feeding. HOMA-IR = Fasting blood glucose value × fasting serum insulin value/22.5. e Transmission electron micrographs of NK-derived exosomes. Scale bar, 100 nm. f NanoSight particle tracking analysis showing the particle size of NK-derived exosomes isolated from NCD and HFD mice. g Western blot assays of exosomal markers TSG101, HSP70, CD63, and CD9. h – k After blank liposomes, NCD-Exos, and HFD-Exos were separately injected into NCD or HFD mice via tail vein, fasting blood glucose ( h ), OGTT ( i ), ITT ( j ), and HOMA-IR ( k ) were assessed in each group. G1: HFD mice treated with blank liposomes ( n = 3); G2: HFD mice treated with HFD-Exos ( n = 3); G3: HFD mice treated with NCD-Exos ( n = 3); G4: NCD mice treated with blank liposomes ( n = 3); G5: NCD mice treated with HFD-Exos ( n = 3); and G6: NCD mice treated with NCD-Exos ( n = 3). l After NCD-Exos labeled with PKH26 were transferred into recipient mice, fluorescence images of the liver, islets, SATs, VATs, and skeletal muscles were observed by in vitro imaging system. Scale bar, 5 mm. m The weight of VATs from HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. n Liver triglyceride content of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. o , p ELISA assays of IL-6, IL-1β, and TNF-α expression in VATs and livers of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t-test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)
Figure Legend Snippet: NK-derived exosomes from lean mice attenuate obesity-induced insulin resistance. a Fasting blood glucose of NCD and HFD mice after group feeding. b – d OGTT ( b ), ITT ( c ), and HOMA-IR index ( d ) of HFD mice and NCD mice ( n = 48) were recorded at 42 days after group feeding. HOMA-IR = Fasting blood glucose value × fasting serum insulin value/22.5. e Transmission electron micrographs of NK-derived exosomes. Scale bar, 100 nm. f NanoSight particle tracking analysis showing the particle size of NK-derived exosomes isolated from NCD and HFD mice. g Western blot assays of exosomal markers TSG101, HSP70, CD63, and CD9. h – k After blank liposomes, NCD-Exos, and HFD-Exos were separately injected into NCD or HFD mice via tail vein, fasting blood glucose ( h ), OGTT ( i ), ITT ( j ), and HOMA-IR ( k ) were assessed in each group. G1: HFD mice treated with blank liposomes ( n = 3); G2: HFD mice treated with HFD-Exos ( n = 3); G3: HFD mice treated with NCD-Exos ( n = 3); G4: NCD mice treated with blank liposomes ( n = 3); G5: NCD mice treated with HFD-Exos ( n = 3); and G6: NCD mice treated with NCD-Exos ( n = 3). l After NCD-Exos labeled with PKH26 were transferred into recipient mice, fluorescence images of the liver, islets, SATs, VATs, and skeletal muscles were observed by in vitro imaging system. Scale bar, 5 mm. m The weight of VATs from HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. n Liver triglyceride content of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. o , p ELISA assays of IL-6, IL-1β, and TNF-α expression in VATs and livers of HFD mice treated with NCD-Exos, HFD-Exos, or blank liposomes. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t-test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)

Techniques Used: Derivative Assay, Transmission Assay, Isolation, Western Blot, Liposomes, Injection, Labeling, Fluorescence, Muscles, In Vitro, Imaging, Enzyme-linked Immunosorbent Assay, Expressing

NK-derived exosomal miR-1249-3p mediates cellular insulin sensitivity and inflammation. a Microarray analysis of significantly expressed exosomal miRNAs between NCD-Exos and HFD-Exos was presented in a heatmap. b qRT-PCR assay of miR-1249-3p expression in splenic NK cells, NK-derived exosomes, and circulating exosomes from NCD or HFD mice. c NK cells transfected with a Cy3-labeled miR-1249-3p mimic were co-cultured with 3T3-L1 adipocytes or AML12 cells in a Transwell TM plate (membrane pore = 0.4 mm) plate. Scale bar, 100 μm. d – g After transfecting with miR-1249-3p mimic, miR-NC, inhibitor, and inh-NC, the glucose uptake content of 3T3-L1 adipocytes ( d ) and glucose production content of AML12 cells ( f ) were measured, and the concentrations of IL-6, TNF-α, and IL-1β secreted by 3T3-L1 adipocytes ( e ) and AML12 cells ( g ) were detected by ELISA. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)
Figure Legend Snippet: NK-derived exosomal miR-1249-3p mediates cellular insulin sensitivity and inflammation. a Microarray analysis of significantly expressed exosomal miRNAs between NCD-Exos and HFD-Exos was presented in a heatmap. b qRT-PCR assay of miR-1249-3p expression in splenic NK cells, NK-derived exosomes, and circulating exosomes from NCD or HFD mice. c NK cells transfected with a Cy3-labeled miR-1249-3p mimic were co-cultured with 3T3-L1 adipocytes or AML12 cells in a Transwell TM plate (membrane pore = 0.4 mm) plate. Scale bar, 100 μm. d – g After transfecting with miR-1249-3p mimic, miR-NC, inhibitor, and inh-NC, the glucose uptake content of 3T3-L1 adipocytes ( d ) and glucose production content of AML12 cells ( f ) were measured, and the concentrations of IL-6, TNF-α, and IL-1β secreted by 3T3-L1 adipocytes ( e ) and AML12 cells ( g ) were detected by ELISA. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)

Techniques Used: Derivative Assay, Microarray, Quantitative RT-PCR, Expressing, Transfection, Labeling, Cell Culture, Membrane, Enzyme-linked Immunosorbent Assay

Exosomal miR-1249-3p directly targets SKOR1 to mediate insulin sensitivity. a The potential targets of miR-1249-3p were predicted by integrating the results of two databases (TargetScan and miRDB). b Western blot analysis of SKOR1 in 3T3-L1 adipocytes and AML12 cells with the indicated treatments. c The wild-type and a mutated type of binding site between miR-1249-3p and SKOR1. d Relative luciferase activity of AML12 cells in the presence of indicated treatments. e Western blot analysis of SKOR1 expression in the VATs and livers of HFD mice after NCD-Exos or HFD-Exos treatment. f – i The effect of sh-SKOR1 on glucose uptake capacity in 3T3-L1 adipocytes ( f ), glucose production capacity in AML12 cells ( g ), and expression levels of IL-6, TNF-α, and IL-1β ( h , i ). j – q Glucose uptake content of 3T3-L1 adipocytes ( j ) and glucose production content of AML12 cells ( n ) with the indicated treatments were measured, as well as the expression levels of IL-6, TNF-α, and IL-1β ( k – m and o – q ). Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)
Figure Legend Snippet: Exosomal miR-1249-3p directly targets SKOR1 to mediate insulin sensitivity. a The potential targets of miR-1249-3p were predicted by integrating the results of two databases (TargetScan and miRDB). b Western blot analysis of SKOR1 in 3T3-L1 adipocytes and AML12 cells with the indicated treatments. c The wild-type and a mutated type of binding site between miR-1249-3p and SKOR1. d Relative luciferase activity of AML12 cells in the presence of indicated treatments. e Western blot analysis of SKOR1 expression in the VATs and livers of HFD mice after NCD-Exos or HFD-Exos treatment. f – i The effect of sh-SKOR1 on glucose uptake capacity in 3T3-L1 adipocytes ( f ), glucose production capacity in AML12 cells ( g ), and expression levels of IL-6, TNF-α, and IL-1β ( h , i ). j – q Glucose uptake content of 3T3-L1 adipocytes ( j ) and glucose production content of AML12 cells ( n ) with the indicated treatments were measured, as well as the expression levels of IL-6, TNF-α, and IL-1β ( k – m and o – q ). Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)

Techniques Used: Western Blot, Binding Assay, Luciferase, Activity Assay, Expressing

MiR-1249-3p relieves insulin resistance and inflammation via the SKOR1-SMAD6-TLR4-NF-κB axis. a – c After transfection with a miR-1249-3p mimic, miR-NC, or specific siRNA to SKOR1 or SMAD6, qRT-PCR analysis of miR-1249-3p ( a ), SKOR1 ( b ) and SMAD6 ( c ) expression in 3T3-L1 adipocytes cells with the indicated treatments was performed. d , g The expression of p-p65 and p65 in 3T3-L1 adipocytes cells with the indicated treatments was performed by western blot. e , f , h IL-1β, IL-6, and TNF-α expression in 3T3-L1 adipocytes cells subjected to the indicated treatments was assessed by ELISA. i The signaling pathway through which NK-derived exosomal miR-1249-3p regulates insulin resistance in type 2 diabetes mice. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)
Figure Legend Snippet: MiR-1249-3p relieves insulin resistance and inflammation via the SKOR1-SMAD6-TLR4-NF-κB axis. a – c After transfection with a miR-1249-3p mimic, miR-NC, or specific siRNA to SKOR1 or SMAD6, qRT-PCR analysis of miR-1249-3p ( a ), SKOR1 ( b ) and SMAD6 ( c ) expression in 3T3-L1 adipocytes cells with the indicated treatments was performed. d , g The expression of p-p65 and p65 in 3T3-L1 adipocytes cells with the indicated treatments was performed by western blot. e , f , h IL-1β, IL-6, and TNF-α expression in 3T3-L1 adipocytes cells subjected to the indicated treatments was assessed by ELISA. i The signaling pathway through which NK-derived exosomal miR-1249-3p regulates insulin resistance in type 2 diabetes mice. Experiments were performed at least in triplicate, and the results are shown as the mean ± s.d. Student’s t -test was used to analyze the data. (* P < 0.05; ** P < 0.01; *** P < 0.001)

Techniques Used: Transfection, Quantitative RT-PCR, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Derivative Assay



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Differentially expressed miRNA in exosomes from tuberculous pleural effusion and transudative pleural effusion (as control) by miRNAs sequencing. A Heatmap of differential exosomes miRNAs expression in pleural effusion between control individuals and tuberculous pleurisy patients; n = 9. RPKM values are represented by gradient colors and shown for each sample. Red represents a higher RPKM; blue represents a lower RPKM. Results are based on nine RNA sequencing samples. B Venn diagram showing the overlap between differentially expressed miRNAs in TPE exosomes and transudate exosomes. C Volcanic map of differential exosomes miRNAs expression in pleural effusion between control individuals and tuberculous pleurisy patients. Adjusted P value < 0.05 and fold change > 1 was set as restrictive conditions to identify the differentially expressed genes. D Pathway enrichment analysis showed the significant target genes of differentially expressed miRNAs associated with various KEGG pathways. E The expression of three differentially expressed miRNAs in TPE exosomes and transudate exosomes was verified by RT-qPCR and normalized by the U6. Data are expressed as mean ± SEM. n = 6, **** P < 0.0001 (Paired student’s t-test)

Journal: Respiratory Research

Article Title: Exosomal microRNAs of tuberculous pleural effusion orchestrating TGF-β signaling mediate pleural fibrosis

doi: 10.1186/s12931-026-03541-5

Figure Lengend Snippet: Differentially expressed miRNA in exosomes from tuberculous pleural effusion and transudative pleural effusion (as control) by miRNAs sequencing. A Heatmap of differential exosomes miRNAs expression in pleural effusion between control individuals and tuberculous pleurisy patients; n = 9. RPKM values are represented by gradient colors and shown for each sample. Red represents a higher RPKM; blue represents a lower RPKM. Results are based on nine RNA sequencing samples. B Venn diagram showing the overlap between differentially expressed miRNAs in TPE exosomes and transudate exosomes. C Volcanic map of differential exosomes miRNAs expression in pleural effusion between control individuals and tuberculous pleurisy patients. Adjusted P value < 0.05 and fold change > 1 was set as restrictive conditions to identify the differentially expressed genes. D Pathway enrichment analysis showed the significant target genes of differentially expressed miRNAs associated with various KEGG pathways. E The expression of three differentially expressed miRNAs in TPE exosomes and transudate exosomes was verified by RT-qPCR and normalized by the U6. Data are expressed as mean ± SEM. n = 6, **** P < 0.0001 (Paired student’s t-test)

Article Snippet: Exosomes from pleural effusion were obtained by ultracentrifugation of samples isolated from nine control individuals and nine patients with tuberculous pleurisy patients and processed by Novogene Co., Ltd (Beijing, China) for miRNA microarray analysis (lllumina SE50).

Techniques: Control, Sequencing, Expressing, RNA Sequencing, Quantitative RT-PCR

miR-503-5p regulated Smurf1/Smad7 signaling pathway. A , B Venn diagram showing overlap between differentially up-regulated miRNAs in TPE exosomes and miRNAs targeting Smurf1 or Smad7 predicted by the miRTarBase. The online analysis database “miRTarBase” ( https://miRTarBase.cuhk.edu.cn/ ) was used. C Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which miR-503-5p expression levels in cells were determined by qRT-PCR and normalized by the U6. D - E Human PMCs were transfected with miR-25-3p mimics or miR-503-5p mimics or miR-92a-3p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which intracellular mRNA levels of Smurf1 were measured by RT-qPCR and normalized to GAPDH ( D ). The protein expression of Smurf1 and TGF-β receptor (TGFBR) were detected by western blotting. Bar graphs revealed changes in relative ratio of Smurf1 and TGFBR to GAPDH. F Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which mRNA expression of Smurf1, TGFBR and COL1A1 were detected by qRT-PCR. G Human PMCs were incubated with miR-503-5p mimics. After 24 h, Smurf1 protein was detected by immunofluorescence staining and nuclei with DAPI staining. Bar scale: 50 μm. H - K Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h. miR-503-5p expression levels in cells were determined by qRT-PCR and normalized by the U6 ( H ). The protein expression of S Smurf1, TGFBR and COL1A1 were detected by western blotting ( I ). Bar graphs revealed changes in the relative ratio to GAPDH ( J ). mRNA levels of S Smurf1, TGFBR and COL1A1 were measured by RT-qPCR and normalized to GAPDH ( K ). Data are mean ± SEM. n = 3. * P < 0.05 (student’s t-test)

Journal: Respiratory Research

Article Title: Exosomal microRNAs of tuberculous pleural effusion orchestrating TGF-β signaling mediate pleural fibrosis

doi: 10.1186/s12931-026-03541-5

Figure Lengend Snippet: miR-503-5p regulated Smurf1/Smad7 signaling pathway. A , B Venn diagram showing overlap between differentially up-regulated miRNAs in TPE exosomes and miRNAs targeting Smurf1 or Smad7 predicted by the miRTarBase. The online analysis database “miRTarBase” ( https://miRTarBase.cuhk.edu.cn/ ) was used. C Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which miR-503-5p expression levels in cells were determined by qRT-PCR and normalized by the U6. D - E Human PMCs were transfected with miR-25-3p mimics or miR-503-5p mimics or miR-92a-3p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which intracellular mRNA levels of Smurf1 were measured by RT-qPCR and normalized to GAPDH ( D ). The protein expression of Smurf1 and TGF-β receptor (TGFBR) were detected by western blotting. Bar graphs revealed changes in relative ratio of Smurf1 and TGFBR to GAPDH. F Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h, after which mRNA expression of Smurf1, TGFBR and COL1A1 were detected by qRT-PCR. G Human PMCs were incubated with miR-503-5p mimics. After 24 h, Smurf1 protein was detected by immunofluorescence staining and nuclei with DAPI staining. Bar scale: 50 μm. H - K Human PMCs were transfected with miR-503-5p mimics (50 nmol/ml) or negative control (NC) for 24 h. miR-503-5p expression levels in cells were determined by qRT-PCR and normalized by the U6 ( H ). The protein expression of S Smurf1, TGFBR and COL1A1 were detected by western blotting ( I ). Bar graphs revealed changes in the relative ratio to GAPDH ( J ). mRNA levels of S Smurf1, TGFBR and COL1A1 were measured by RT-qPCR and normalized to GAPDH ( K ). Data are mean ± SEM. n = 3. * P < 0.05 (student’s t-test)

Article Snippet: Exosomes from pleural effusion were obtained by ultracentrifugation of samples isolated from nine control individuals and nine patients with tuberculous pleurisy patients and processed by Novogene Co., Ltd (Beijing, China) for miRNA microarray analysis (lllumina SE50).

Techniques: Transfection, Negative Control, Expressing, Quantitative RT-PCR, Western Blot, Incubation, Immunofluorescence, Staining

Triple miRNAs inhibitor attenuated TPE-Exo induced pleural fibrosis. C57BL/6 mice were intra-pleural injected by using PBS (100 µl/mouse), TPE-Exo (100 µl/mouse), TPE-Exo plus control inhibitor, or TPE-Exo plus triple miRNAs inhibitor with carbon particles (0.1 mg/mouse) as descriptions in the Methods. TPE-Exo from 50 ml TPE was administered at days 1, 5, 9. In TPE-Exo plus triple miRNAs inhibitor group, TPE-Exo was co-incubated with triple miRNAs inhibitor which restrained expressions of miR-150-3p, miR-424-3p and miR-503-5p. All mice were euthanized at day 21, and tissues were taken for analysis. A Representative Masson’s trichrome staining images of visceral pleura from lung sections, parietal pleura from chest wall and diaphragm sections. Original magnification, ×400. B Changes in pleural thickness. C Changes in collagen percentages of visceral and parietal pleura. Data are expressed as mean ± SEM. n = 6 mice. *** P < 0.001 (One-way ANOVA followed by the Bonferroni’s test)

Journal: Respiratory Research

Article Title: Exosomal microRNAs of tuberculous pleural effusion orchestrating TGF-β signaling mediate pleural fibrosis

doi: 10.1186/s12931-026-03541-5

Figure Lengend Snippet: Triple miRNAs inhibitor attenuated TPE-Exo induced pleural fibrosis. C57BL/6 mice were intra-pleural injected by using PBS (100 µl/mouse), TPE-Exo (100 µl/mouse), TPE-Exo plus control inhibitor, or TPE-Exo plus triple miRNAs inhibitor with carbon particles (0.1 mg/mouse) as descriptions in the Methods. TPE-Exo from 50 ml TPE was administered at days 1, 5, 9. In TPE-Exo plus triple miRNAs inhibitor group, TPE-Exo was co-incubated with triple miRNAs inhibitor which restrained expressions of miR-150-3p, miR-424-3p and miR-503-5p. All mice were euthanized at day 21, and tissues were taken for analysis. A Representative Masson’s trichrome staining images of visceral pleura from lung sections, parietal pleura from chest wall and diaphragm sections. Original magnification, ×400. B Changes in pleural thickness. C Changes in collagen percentages of visceral and parietal pleura. Data are expressed as mean ± SEM. n = 6 mice. *** P < 0.001 (One-way ANOVA followed by the Bonferroni’s test)

Article Snippet: Exosomes from pleural effusion were obtained by ultracentrifugation of samples isolated from nine control individuals and nine patients with tuberculous pleurisy patients and processed by Novogene Co., Ltd (Beijing, China) for miRNA microarray analysis (lllumina SE50).

Techniques: Injection, Control, Incubation, Staining

Results of a microarray analysis. Eight miRNAs were significantly downregulated in the patients with functional dyspepsia (FD) compared to those in healthy controls using method 1. However, six miRNAs were downregulated using method 2. Notably, five miRNAs were consistently downregulated between the two methods. Furthermore, five miRNAs and seven miRNAs were significantly upregulated using methods 1 and 2, respectively. Therefore, four miRNAs were consistently upregulated in patients with FD.

Journal: Internal Medicine

Article Title: Exosomal hsa-miR-3649 and hsa-miR-202-3p in Gastric Juice as Potential Biomarkers for Functional Dyspepsia with a Previous Helicobacter pylori Infection

doi: 10.2169/internalmedicine.6047-25

Figure Lengend Snippet: Results of a microarray analysis. Eight miRNAs were significantly downregulated in the patients with functional dyspepsia (FD) compared to those in healthy controls using method 1. However, six miRNAs were downregulated using method 2. Notably, five miRNAs were consistently downregulated between the two methods. Furthermore, five miRNAs and seven miRNAs were significantly upregulated using methods 1 and 2, respectively. Therefore, four miRNAs were consistently upregulated in patients with FD.

Article Snippet: An miRNA microarray analysis of the discovery cohort was performed using 3D-Gene R (Toray Industries, Tokyo, Japan), as described in our previous report ( ).

Techniques: Microarray, Functional Assay

The dataset GSE162794 has a total of 92 miRNAs upregulated and 79 miRNAs downregulated. The dataset GSE42716 has a total of 12 miRNAs upregulated and 1201 miRNAs downregulated.

Journal: Medicine

Article Title: Network pharmacology and bioinformatics study on the treatment of renal fibrosis with persicae semen-carthami flos drug pair

doi: 10.1097/MD.0000000000032946

Figure Lengend Snippet: The dataset GSE162794 has a total of 92 miRNAs upregulated and 79 miRNAs downregulated. The dataset GSE42716 has a total of 12 miRNAs upregulated and 1201 miRNAs downregulated.

Article Snippet: The dataset GSE42716 ( https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE42716 ) is a miRNA microarray analysis of UUO model mice studied by Keio University School of Medicine, which has a total of 8 samples, including 4 samples in the UUO group and 4 samples in the control group.

Techniques: