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Image Search Results
Journal: Frontiers in Cardiovascular Medicine
Article Title: Serotonin transporter downregulation is associated with aortic stenosis, and early profibrotic remodeling is mitigated by pharmacological inhibition of HTR2B receptor
doi: 10.3389/fcvm.2026.1729078
Figure Lengend Snippet: Effects of AngII on human AVICs with SERT knockdown. (A) Gene expression of SERT, HTR2B, HTR2A in AngII-treated compared to Nontreated (NT) Ctrl AVICs. (B) SERT KD by siRNA lead to increased expression of HTR2A gene expression. (C) HTR2A and HTR2B expression with siSERT or siSERT combined with AngII treatment. (D) COL1A1, SPP1, RUNX2, TGFβ1 expression in response to AngII treatment in human AVICs compared to Nontreated group. (E) COL1A1, RUNX2, TGFβ1 expression treated with siSERT alone or siSERT combined with AngII treatment. All gene expression results were calculated by the 2 −ΔΔCT method, n ≥ 4 per group. Error bars indicate SEM. P-value vs. NT. *indicates p-value <0.1, **indicates p-value <0.05, and ***indicates p -value <0.01 by Student's t -test or one-way ANOVA with post-hoc Dunnett's test.
Article Snippet: SPP1 ,
Techniques: Knockdown, Gene Expression, Expressing
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Microglial Spp1 deficiency led to age‐dependent memory deficits. (A) Western blot analysis of Spp1 protein in the hippocampus of young (31–43 years; mean 38.3) and old humans (88–95 years; mean 90.6) ( n = 3 per group). (B) Representative images showing the co‐localization of Spp1 and the microglial marker (IBA1) in brain sections from young and aged humans. Dashed white boxes indicate magnified images of individual cells, and donut chart point to IBA1 + Spp1 +/− cells, Scale bars = 10 μm ( n = 3 per group). (C) Representative images showing the co‐localization of Spp1 mRNA and the microglial marker (IBA1) in brain sections from young (3 M) and aged (22 M) mice. Dashed white boxes indicate magnified images of individual cells, and donut chart indicate the proportion IBA1 + Spp1 mRNA +/− cells, Scale bars = 10 μm ( n = 3 per group). (D) Representative images showing the co‐localization of Spp1 and the microglial marker (IBA1) in brain sections from young (3 M), and aged (22 M) mice. Dashed white boxes indicate magnified images of individual cells, and donut chart point to IBA1 + Spp1 +/− cells, Scale bars = 10 μm ( n = 3 per group). (E) Schematic diagram of the experimental design. (F) Percentage of correct alternations in the Y‐maze test of adult ( n = 12) and aged ( n = 13) Spp1 fl/fl mice and Spp1‐cKO mice. (G/J) Learning curves during Morris Water Maze (MWM) training for adult (G) ( n = 12) and aged (J) ( n = 13) Spp1 fl/fl and Spp1‐cKO mice, measured by latency to find the platform. (H/K) Representative path plots showing the search patterns of adult (H) and aged (K) Spp1 fl/fl and Spp1‐cKO mice during the MWM probe trial. (I) Number of platform crossings during the MWM probe trial of adult ( n = 12) and aged ( n = 13) Spp1 fl/fl mice and Spp1‐cKO mice. (L) Time spent in the target quadrant during the MWM probe trial of adult ( n = 12) and aged ( n = 13) Spp1 fl/fl mice and Spp1‐cKO mice. Data are presented as the mean ± standard error of the mean (SEM). Two‐way repeated measures ANOVA was used to compare the latency to platform acquisition during the learning curves (G/J). Other data were analyzed using unpaired two‐tailed t ‐tests. * p < 0.05, ** p < 0.01, *** p < 0.001, ns = no significant difference. Figure was created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Western Blot, Marker, Two Tailed Test
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Deficiency of Spp1 impaired microglial phagocytic function. (A) Heatmap showing differentially expressed genes (DEGs) between two groups of aged MG with high ( n = 3) and low ( n = 4) phagocytic activity. Red indicates upregulated genes, while blue indicates downregulated genes. (B) Representative images of microglial uptake of myelin‐555 in aged mice. Yellow arrows indicate Spp1‐positive microglia phagocytosing myelin‐555; blue arrows indicate Spp1‐negative microglia phagocytosing myelin‐555. Scale bars = 15 μm ( n = 6 mice per group). (C, D) Representative images showing phagocytosis of myelin‐555 by primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice; white dashed lines indicating magnified images of individual MG. Scale bars = 15 μm. (E) %Myelin + cell (of cell population) = number of phagocytic cells/total cell count ( n = 3 per group). (F) Relative myelin‐555 intensity of phagocytic cells = total fluorescence intensity/total number of phagocytic cells ( n = 3 per group). (G, H) Myelin‐555 was stereotactically injected into the hippocampus of aged Spp1 fl/fl and Spp1‐cKO mice to assess MG phagocytosis. Scale bars, 10 μm (low magnification) and 5 μm (high magnification). (I) Proportion of myelin + MG ( n = 4 per group). (J) Analysis of myelin volume within MG ( n = 4 per group). Data are presented as the mean ± standard error of the mean (SEM). Data were analyzed by unpaired two‐tailed t ‐tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Mouse/Cell pattern was created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Activity Assay, Isolation, Cell Characterization, Fluorescence, Injection, Two Tailed Test
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Deficiency of Spp1 disrupted microglia oxidative phosphorylation. (A) Heatmap of GSVA analysis comparing gene set enrichment between primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice; blue indicates downregulation, and red indicates upregulation. (B) Quantification of ATP levels in primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice ( n = 6 per group). (C) Measurement of Seahorse XF mitochondrial stress OCR in primary microglia from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice. (D) Basal OCR ( n = 3 per group). (E) Maximum OCR ( n = 3 per group). (F) Heatmap of GSVA pathway scores showing significant downregulation of Oxidative Phosphorylation in the microglial cluster of aged (18‐month‐old) Spp1‐cKO mice compared to controls. (G) Subsets of high SPP1‐expressing (SPP1 high MG) and low SPP1‐expressing (SPP1 low MG) in aged human brains ( GSE157827 ). (H) Oxidative phosphorylation pathway scores in SPP1 high and SPP1 low MG in aged human brains. (I) Violin plot showing AUCell scores for SPP1 high MG and SPP1 low MG cells. Data are presented as the mean ± standard error of the mean (SEM). Statistical significance was determined using unpaired two‐tailed t ‐tests for (B, D, E) and Wilcoxon rank‐sum test for (I). FCCP, Carbonyl cyanide 4‐trifluoromethoxyphenylhydrazone; Anti & Rot, Antimycin A and Rotenone; 2‐DG, 2‐Deoxy‐D‐glucose. * p < 0.05, ** p < 0.01, ns = no significant difference. Human/Mouse/Cell pattern was created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Phospho-proteomics, Isolation, Expressing, Two Tailed Test
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Deficiency of Spp1 in microglia disrupted mitochondrial complex I‐dependent oxidative phosphorylation. (A) Heatmap showing changes in key OXPHOS‐related genes in primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice. (B) Workflow diagram of the Oroboros O2k multi‐dimensional energy metabolism analysis system used to measure OCR in BV2 cell homogenates. (C) Basal OCR in BV2 cells ( n = 3 per group). (D‐F) Mitochondrial respiration states in BV2 cells: Complex I respiration (D), complex II respiration (E), and complex IV respiration (F) ( n = 3 per group). (G) Histogram showing the relative mitochondrial complex I enzyme activity ( n = 4 per group). (H) Western blot analysis showing changes in protein expression levels of Spp1 and Ndufs2 after Spp1 knockdown in BV2 cells ( n = 3 per group). (I) Workflow diagram of the Oroboros O2k multi‐dimensional energy metabolism analysis system used to measure OCR in hippocampal tissue from Spp1 fl/fl and Spp1‐cKO mice. (J) Basal OCR in hippocampal tissue from Spp1 fl/fl and Spp1‐cKO mice ( n = 4 per group). (K–M) Mitochondrial respiration states in hippocampal tissue from Spp1 fl/fl and Spp1‐cKO mice: Complex I respiration (K), complex II respiration (L), and complex IV respiration (M) ( n = 4 per group). (N) Schematic diagram showing Spp1 deficiency disrupting OXPHOS via compromised complex I activity. Data are presented as the mean ± standard error of the mean (SEM). Data were analyzed by unpaired two‐tailed t ‐tests. * p < 0.05, ** p < 0.01, *** p < 0.001, ns = no significant difference. Mouse patterns and experimental apparatus were created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Phospho-proteomics, Isolation, Activity Assay, Western Blot, Expressing, Knockdown, Two Tailed Test
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Spp1 deficiency inhibited AKT signaling pathway and administration of AKT agonist reversed manifestation. (A) KEGG pathway analysis of differentially expressed genes from sequencing data of primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice. (B) Heatmap showing GSVA enrichment scores for the “PI3K‐Akt signaling” pathway in primary microglia isolated from postnatal day 3 (P3) Spp1 fl/fl and Spp1‐cKO mice. Each column represents one RNA‐seq sample (red indicating up‐regulation, and blue indicating down‐regulation). (C) scRNA‐seq analysis showing the downregulation of PI3K–Akt signaling pathway in the microglial cluster of 18‐month‐old Spp1‐cKO mice compared to controls. (D) Western blot analysis showing the changes in protein expression levels of p‐AKT, AKT after Spp1 knockdown in BV2 cells ( n = 3 per group). (E) ATP levels ( n = 4 per group). (F) Mitochondrial complex I‐dependent oxygen consumption rate (OCR) ( n = 3 per group). (G) Histogram showing the relative mitochondrial complex I enzyme activity ( n = 4 per group). (H) %Myelin + cell (of cell population) = number of phagocytic cells/total cell count ( n = 4 per group). (I) ATP levels in the hippocampus of Spp1 fl/fl + solvent, Spp1‐cKO + solvent, and Spp1‐cKO + SC79 mice ( n = 3 per group). (J) Western blot analysis showing the changes in protein expression levels of p‐AKT, AKT, and Ndufs2 ( n = 3 per group). (K) Percentage of correct alternations in the Y‐maze test. (L) Learning curves during MWM training, measured by latency to find the platform. (M) Time spent in the target quadrant during the probe phase of the MWM. Data are presented as the mean ± standard error of the mean (SEM). Two‐way repeated measures ANOVA was used to compare the latency to find the platform in the learning curves (L). Figure D was analyzed using two‐tailed t ‐tests. Other data were analyzed using one‐way ANOVA and LSD post hoc test. * p < 0.05, ** p < 0.01, ns = no significant difference. Mouse pattern was created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Sequencing, Isolation, RNA Sequencing, Western Blot, Expressing, Knockdown, Activity Assay, Cell Characterization, Solvent, Two Tailed Test
Journal: Aging Cell
Article Title: Deficiency of Microglial‐Derived Spp1 Exacerbates Age‐Related Memory Decline by Impairing Mitochondrial Complex I Function
doi: 10.1111/acel.70378
Figure Lengend Snippet: Microglia‐specific Spp1 overexpression restores ATP production, phagocytosis, and memory in Spp1‐deficient models. (A) Representative confocal images of Spp1 immunofluorescence in BV2 cells: Control (NC), Spp1 knockdown (sh‐Spp1), and sh‐Spp1 rescued by AAV‐Spp1. Scale bars = 10 μm. (B) Quantification of relative Spp1 fluorescence intensity ( n = 3 per group). (C) Representative bright‐field/fluorescence overlays of myelin‐555 uptake (red) by BV2 cells under the three conditions. Scale bars = 10 μm. (D) %Myelin + cell (of cell population) = number of phagocytic cells/total cell count ( n = 3 per group). (E) ATP levels normalized to total protein in control (NC), Spp1 knockdown (sh‐Spp1), and sh‐Spp1 cells rescued by AAV‐Spp1 ( n = 3 per group). (F) Mitochondrial complex I activity in control (NC), Spp1 knockdown (sh‐Spp1), and sh‐Spp1 cells rescued by AAV‐Spp1 ( n = 3 per group). (G) Top: Schematic diagram illustrating the experimental strategy for microglia‐specific Spp1 overexpression. Bottom: Relative fluorescence intensity of Spp1 immunostaining in IBA1 + microglia ( n = 3 mice per group). (H) Representative immunofluorescence images showing the expression of AAV‐driven EGFP in IBA1 + microglia in the hippocampus. Scale bars = 10 μm. (I) Y‐maze spontaneous alternation rate ( n = 8 mice per group). (J) Learning curves during MWM training, measured by latency to find the platform ( n = 8 mice per group). (K) Representative path plots showing the search patterns during the MWM probe trial. (L) Time spent in the target quadrant during the probe phase of the MWM. Data are presented as the mean ± standard error of the mean (SEM). Two‐way repeated measures ANOVA was used to compare the latency to find the platform in the learning curves (J). Other data were analyzed using one‐way ANOVA and LSD post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001. Brain pattern was created using BioRender.
Article Snippet: The Cx3cr1 ‐CreERT2 (Stock No. C001247) and
Techniques: Over Expression, Immunofluorescence, Control, Knockdown, Fluorescence, Cell Characterization, Activity Assay, Immunostaining, Expressing
Journal: Developmental cell
Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice
doi: 10.1016/j.devcel.2024.05.019
Figure Lengend Snippet: (A) Diagram of experimental design, representative FACS plots and quantification of CD9+CD26+ dermal fibroblasts percentage from Lin- Thy1+SCA1+ dorsal skin cells after three daily CNO intradermal injections from TRPV1 activated mice and their controls (****p<0.0001). (B) UMAP projection demonstrating the clustering of sorted Thy1+SCA1+ fibroblasts based on scRNAseq data, and the overlay of the Hashtag signal differentiating the subcutis and dermal clusters. (C) Normalized fold change (FC) calculation comparing cell numbers in dermal clusters between TRPV1 activated mice and their controls. (D) UMAP projection of sorted fibroblast scRNAseq data demonstrating cell distribution between clusters in the TRPV1 activated sample and control. (E-H) UMAP projection of sorted fibroblasts demonstrating the expression of (E) Col23A1 (F) Prdm1 (G) Crabp1 and (H) Lef1 as well as the list of top five velocity driver genes for cluster #3. (I) UMAP projection demonstrating calculated DP-core enrichment score and (J) Lepr expression. (K) UMAP projection of scRNASeq from Li et al. demonstrating its calculated DP-score (left) and cluster #3 enrichment score (right). (L) UMAP projection of sorted fibroblasts demonstrating the expression of Spp1. (M) Representative FACS histograms of anti-Spp1 staining of Lin- Thy1+SCA-1+ dermal cells (red) or CD9+CD26+ subset (orange) from the back skin of TRPV1 activated mouse. Secondary only staining control in blue. (N) Quantification of Spp1+CD9+CD26+ dermal fibroblasts from TRPV1 activated mice and controls (*p=0.017). (O) Representative images of RNAscope staining for Spp1 (green) and the Lepr (red) on dorsal skin collected from TRPV1 activated mice and controls. Scale bar, 100um. White arrows point out DP; yellow arrows point out Spp1 expression out of DP. DP images scale bar, 25um.
Article Snippet:
Techniques: Control, Expressing, Staining, RNAscope
Journal: Developmental cell
Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice
doi: 10.1016/j.devcel.2024.05.019
Figure Lengend Snippet: (A) Diagram of experimental design and representative images from shaved TRPV1 activated mice and controls. Mice monitored for hair coat growth for 12 days after the last TRPV1 activation with CNO (postnatal day 63). (B) Enlarged dashed rectangle from panel A depicting hair growth in a TRPV1 activated mouse. (C) HF length quantification of dorsal skin from mice treated as in A. Data combined from 6 to 8 HF per mouse, taken from 6 mice per group (****p<0.0001). (D) Representative immunofluorescent images of dorsal skin from mice treated as in A. Staining with anti-keratin14 (KRT14; green) marking epidermal layer and Ki67 (purple) marking the HF bulb. DAPI stain in blue. Scale bar 100μm. (E) Quantification of normalized Ki67 MFI signal in the peri-follicular area of dorsal skin from mice treated as in A. Data combined from 4 regions of interest (ROI) per mouse taken from 5 TRPV1 activated mice and 9 controls (****p<0.0001). (F) Diagram of experimental design and representative images from TRPV1 activated mice and controls treated with CNO on half of their back skin (marked with dashed rectangle). Anti-Spp1 neutralizing antibody or IgG control were injected intradermally to the same skin area. Data are combined from 4 HFs per mouse collected from 6 controls, 3 TRPV1 activated + IgG treated and 4 TRPV1 activated + anti-Spp1 treated mice (****p<0.0001). (G-H) Percentage of CD9+CD26+ dermal fibroblasts from TRPV1 activated mice and their controls intradermally injected with (G) QWF (SubP antagonist) or vehicle (**p=0.005, ***p=0.0004), (H) CGRP8–37 (CGRP antagonist) or vehicle (***p=0.0001, ****p<0.0001). (I) Diagram of experimental design and representative images from TRPV1 activated mice and controls pre-treated intradermally with CGRP8–37 or vehicle and monitored for hair coat growth for 14 days. Quantification of HF length from 6 to 8 HFs per mouse, taken from 3–6 mice per group (****p<0.0001). (J) Representative immunofluorescent images of dorsal skin from mice treated as in I. Stained with anti-KRT14 (green), Ki67 (pink), and DAPI (blue). Scale bar, 100μm.
Article Snippet:
Techniques: Activation Assay, Staining, Control, Injection
Journal: Developmental cell
Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice
doi: 10.1016/j.devcel.2024.05.019
Figure Lengend Snippet: (A) Representative immunofluorescent images and quantification of DRGs collected from mice with naïve back skin or 90 minutes after tape stripping. Stained with anti-c-Fos (red), anti-TRPV1 (green) and DAPI (blue). White arrowheads indicate neuron cell bodies that are TRPV1+ only. Data combined from 6–7 fields of view taken from 4 mice per group (****p<0.0001). Scale bar 50μm. (B) Percentage of CD9+CD26+ dermal fibroblasts from naïve back skin and 18 hours after tape stripping 6 or 12 times (***p=0.0004,****p<0.0001). (C) Diagram of experimental design and quantification of CD9+CD26+ dermal cell percentage 18 hours after tape stripping from the back skin of TRPV1Cre DTR+ treated with DTx or TRPV1Cre DTA+ mice and their controls (****p<0.0001). (D) Representative FACS histogram of anti-Spp1 staining. Dorsal skin treated as in C and gated on total Lin- Thy1+SCA-1+ cells (red) and the CD9+CD26+ cell subset (orange). Secondary only staining control in blue. (E) Quantification of Spp1+CD9+CD26+ dermal fibroblasts from TRPV1 ablated and control mice treated as in C (**p=0.005). (F) TRPV1 ablated mice and controls treated as in C and monitored for hair coat recovery for 12 days (postnatal day 61). (G) Representative bright field images of samples described in F. Data for HF length quantification collected from 8 HFs per mouse taken from 6 control and 5 TRPV1 ablated mice (****p<0.0001). (H) Ramp1 KO mice and controls treated as in F. HF length quantification from 4 HFs per mouse taken from 4 control and 5 Ramp1 KO mice (****p<0.0001). (I) Mice treated as in F and intradermally injected with anti-Spp1 or isotype control while being monitored for hair coat recovery for 16 days (postnatal day 65). HF length quantification from 4 HFs per mouse taken from 6 isotype control and 5 anti-Spp1 injected mice (**p=0.005).
Article Snippet:
Techniques: Stripping Membranes, Staining, Control, Injection
Journal: Developmental cell
Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice
doi: 10.1016/j.devcel.2024.05.019
Figure Lengend Snippet: Key resources table
Article Snippet:
Techniques: Recombinant, RNAscope, Multiplex Assay, In Situ, Software
Journal: Scientific Reports
Article Title: Propolis nanoemulsion and mesenchymal stem cell conditioned medium promote osteoblastogenesis against lipopolysaccharide-induced osteolysis in hyperglycemic rats
doi: 10.1038/s41598-026-46778-2
Figure Lengend Snippet: Serum concentrations of (a) ALP, (b) Coll1a1, and (c) osteopontin across treatment groups. Significant differences between groups are indicated above the bars. Abbreviations: ALP, alkaline phosphatase; Coll1a1, collagen type I alpha 1; LPS, lipopolysaccharide; NEP, nanoemulsion propolis; HUCMSCs-CM, human umbilical cord mesenchymal stem cells conditioned medium. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Article Snippet: This was performed following the instructions of the rat Coll1a1, ALP, and
Techniques: