Journal: Science Advances

Article Title: Hcn1-dependent engram neurons in the PVN encode gastric inflammatory sensitization

doi: 10.1126/sciadv.aeb6961

Figure Lengend Snippet: ( A ) Schematic of the HCl/EtOH-induced gastritis model. h, hours. ( B ) Gross morphology of gastric tissues. ( C and D ) Histopathological analysis (C: H&E staining; D: mucosal injury score). ( E ) Elevated IL-1β and TNF-α levels in gastric tissues of gastritis mice. ( F ) TdTomato (TdT) expression in activated neurons post–4-OHT treatment. ( G ) Experimental workflow for PRV retrograde tracing in Fos-CreER T2 × Rosa-TdT mice. ( H ) Whole-brain mapping of PRV-EGFP + neurons in the saline group and the gastritis group in Fos-CreER T2 × Rosa-TdT mice. ( I ) Quantification of c-Fos/PRV-EGFP colocalization across brain regions in the saline group and the gastritis group. ( J ) Representative c-Fos immunofluorescence images of the saline group and the gastritis group. ( K ) c-Fos + neuron counts in gastritis versus control [ n = 6 mice; F (5,55) = 123.4, two-way ANOVA].

Article Snippet: Fos-CreER T2 mice (the Jackson Laboratory, strain no. 030323) were crossed with Rosa-TdTomato reporter mice (the Jackson Laboratory, strain no. 007914) to generate Fos-CreER T2 × Rosa-TdT mice for neuronal labeling.

Techniques: Staining, Expressing, Retrograde Tracing, Saline, Immunofluorescence, Control

Journal: Science Advances

Article Title: Hcn1-dependent engram neurons in the PVN encode gastric inflammatory sensitization

doi: 10.1126/sciadv.aeb6961

Figure Lengend Snippet: ( A ) Schematic of the water-immersion RS-induced gastritis model. ( B ) Gross morphological appearance of gastric tissues in mice. ( C and D ) Gastric mucosal injury scores and representative H&E-stained sections ( n = 6 mice; two-tailed unpaired t test). ( E ) Stress significantly elevated levels of inflammatory cytokines IL-1β and TNF-α in gastric tissues compared to controls ( n = 6; two-tailed t test). ( F ) Representative Fos immunofluorescence images in PVN from control and stressed mice. ( G ) Increased Fos expression in the PVN of stressed mice versus controls ( n = 6; two-tailed t test). ( H ) Elevated serum corticosterone levels in stressed mice ( n = 7; two-tailed t test). ( I and J ) Enhanced gastric nerve firing frequency following stress exposure ( n = 5; two-tailed t test). ( K ) Experimental timeline for PRV retrograde tracing in Fos-CreER T2 × Rosa-TdT mice subjected to RS. ( L ) Representative images showing PRV-EGFP + neurons colocalized with Fos + cells across brain regions. ( M ) Quantification of Fos/PRV colocalization rates in different brain areas.

Article Snippet: Fos-CreER T2 mice (the Jackson Laboratory, strain no. 030323) were crossed with Rosa-TdTomato reporter mice (the Jackson Laboratory, strain no. 007914) to generate Fos-CreER T2 × Rosa-TdT mice for neuronal labeling.

Techniques: Staining, Two Tailed Test, Immunofluorescence, Control, Expressing, Retrograde Tracing

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: LRP1 knockdown (LRP1 KD) impaired surfactant lipid metabolism. Human A549 cells were cultured at the ALI and transfected with lentiviral vectors for knocking down LRP1 expression. Gene and protein expression and surfactant lipids were analyzed. A: Schematic of the cell culture model on collagen-coated transwells and maintained at the air liquid interface (ALI), and comparison of gene expression for selected lipid and surfactant-relevant proteins in cells cultured in submerged conditions vs. ALI. B: Confocal microscopy image of fluorescent staining for surfactant protein C (SP-C, green) and nuclei (Hoechst, blue) of cells cultured at the ALI. C: Confirmation of LRP1 knockdown in cells after stable transfection with LRP1 shRNA by Western blot and D: by immunofluorescence. Cells transfected with scrambled shRNA were used as controls. E: Phospholipid (PL) classes collected in the apical wash (surfactant) and cellular lysate of control and LRP1 KD cells cultured at the ALI. F: Intracellular concentration of free fatty acids (FFA). G: Schematic representation of the Kennedy pathway for de novo synthesis of dipalmitoylphosphatidylcholine (DPPC). H: Gene expression of enzymes involved in surfactant PL synthesis. I: Gene expression of enzymes involved in de novo lipogenesis. J: Representative Western blot for protein detection of fatty acid synthase (FAS) and optical density quantification of two independent experiments. K: Fatty acid synthase specific activity in lysates of control and LRP1 KD cells. Mean ± SD is shown. N ≥ 5 for all groups. Significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. ABCA3, ATP-Binding Cassette Subfamily A Member 3; ACACA, Acetyl-CoA carboxylase 1; ACOX1, acyl-Co oxidase 1; ALI, air liquid interface; CCTα, CTP:phosphocholine cytidylyltransferase alpha; CK, choline kinase; DAG, diacylglycerol; FASN, fatty acid synthase; FFA, free fatty acids; LPC, lysophosphatidylcholine; PA, phosphatidic acid; PC, phosphatidylcholine; PLA 2 , Phospholipase A 2 ; SCD 1, stearoyl-CoA desaturase 1.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Knockdown, Cell Culture, Transfection, Expressing, Comparison, Gene Expression, Confocal Microscopy, Staining, Stable Transfection, shRNA, Western Blot, Immunofluorescence, Control, Concentration Assay, Activity Assay, Binding Assay

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: LRP1 knockdown increased intracellular neutral lipid storage. Control and LRP1 KD cells were cultured at the ALI and neutral lipid metabolism was analyzed. A: Representative images of Oil Red O staining for neutral lipids. B: Intracellular concentration of TG and CE. C: Gene expression of fatty acid oxidation-involved proteins PPARa, CPT1b and ACOX1. D: Concentration of intracellular acylcarnitines. E: Determination of fatty acid oxidation in cell lysates F: mRNA expression of PDK4. G: mRNA expression of TG synthesizing enzymes DGAT1 and DGTA2. H: Intracellular concentration of the TG precursors MAG, PA and DAG. I) Kinetics of cellular uptake of fluorescently labelled free fatty acid (FFA) by cultures at the ALI. J: Intracellular concentration of the most abundant cholesteryl esters CE 18:1 and CE 22:6. K) mRNA expression of the enzymes involved in regulating cholesterol synthesis HMG-CoA reductase, HMG-CoA synthase, SREBP1 and SREBP2. L-M: Representative western blots for SREBP1 and SREBP2 in their precursor and cleaved (active, nuclear) forms, with quantification of western blots from two independent experiments. N: Decay curve showing clearance from the media for fluorescently labelled Dil-LDL in control and LRP1 KD cultures. O: Gene expression of cholesterol exporters ABCA1 and ABCG1. P: Concentration of cholesterol ester in media after 16h of culture with control and LRP1 KD cells. Mean ± SD is shown. Significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. ABCA1, ATP Binding Cassette Subfamily A Member 1; ABCG1, ATP Binding Cassette Subfamily G Member 1; ACOX1, Acyl-CoA oxidase1; CE, cholesterol ester; CPT1b, carnitine palmitoyltransferase 1 beta; DAG, diacylglycerol; DGAT1, diacylglycerol O-acyltransferase 1; DGAT2, diacylglycerol O-acyltransferase 2; FFA, free fatty acid; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase; HMG-CoA, hydroxymethylglutaryl-CoA; LDL, Low Density Lipoprotein; MAG, monoacylglycerol; PA, phosphatidic acid, PDK4, Pyruvate dehydrogenase kinase 4; PPARa, peroxisome proliferator-activated receptor alpha; SREBP, sterol regulatory element-binding transcription factor; TG, triacylglycerol.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Knockdown, Control, Cell Culture, Staining, Concentration Assay, Gene Expression, Expressing, Western Blot, Binding Assay

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Generation of T2C-specific LRP1 knockout (SPC-LRP1−/−) mice. Mice floxed for LRP1 were crossed with mice expressing tamoxifen-inducible Cre recombinase under the control of SP-C promoter. Recombination was induced at 5–7 weeks of age and tissues were collected after a minimum of 4 weeks. Floxed mice without Cre expression were used as WT. A: Immunofluorescence for detection of LRP1 in alveoli. Cell nuclei were labelled with Hoechst (blue), LRP1 with Alexa-488-conjugated antibodies (green), and epithelial cells with antibodies against EpCam and Alexa-555-conjugated (red). Overlap and differential interference contrast images are shown too. B: Gene expression of bronchoalveolar epithelial and alveolar type 1 marker HOPX and T2C marker ABCA3 in lung homogenates and in primary T2C-enriched fractions isolated from mice. C: Western blot detection of LRP1 in isolated T2C and lung homogenates from WT and SPC-LRP1 −/− mice. D: Western blot detection of LRP1 in homogenates of liver, brain and adipose harvested from WT and SPC-LRP1 −/− mice. For all blots, equal amounts of protein were loaded in each lane and detection for the housekeeping proteins actin or GAPDH and Coomassie staining were used as loading controls. Optical density quantification is shown next to each blot. E: Representative images of H&E staining showing parenchymal areas from lungs of WT and SPC-LRP1 −/− mice.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Knock-Out, Expressing, Control, Immunofluorescence, Gene Expression, Marker, Isolation, Western Blot, Staining

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: SPC-LRP1 −/− showed lower amounts of surfactant lipid than WT mice. T2C, BAL and lung tissue from WT and SPC-LRP1 −/− mice were analyzed for surfactant biology. A: Concentration of the different lipid groups and classes detected in BAL fluid. B: Concentration of the most abundant PC acyl-species detected in BAL fluid. C: Western blot for surfactant proteins in BAL fluid. Optical density quantification for each blot is shown below. D: Concentration of the different intracellular lipid groups and classes detected in primary T2C. E: Concentration of the most abundant PC acyl-species detected in T2C. F: Concentration of the most abundant CE acyl-species in T2C. G: Representative images of lung sections co-stained for neutral lipid by Oil Red O and for immune cells by CD45 immunohistochemistry. Count of cells that stained positive for each marker alone or both is shown. H: Representative transmission electron microscopy images of T2C. Stereological parameters were quantified and are shown in the left panels: volume of T2C relative to parenchyma (Vv (T2C|par)), volume of lamellar bodies relative to T2C (Vv(LB |T2C), and surface/volume ratio of lamellar bodies (S/V (LB)). Mean ± SD is shown. Significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. BAL, bronchoalveolar lavage: CD45, cluster of differentiation 45; CE, cholesteryl ester; Cer, ceramide; FC, free cholesterol; ORO, oil red O; PA, phosphatidic acid; PC, phosphatidylcholine; PCe, ether phosphatidylcholine; PE, phosphatidylethanolamine; PEp, plasmalogen phosphatidylethanolamine; PG, phosphatidylglycerol; PI, phosphatidylinositol; PS, phosphatidylserine; TG, triglyceride; SM, sphingomyelin; SP-A, surfactant protein A; SP-B, surfactant protein B; SP-C, surfactant protein C; SP-D, surfactant protein D.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Concentration Assay, Western Blot, Staining, Immunohistochemistry, Marker, Transmission Assay, Electron Microscopy

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Female SPC-LRP1−/− mice showed less pulmonary compliance than WT mice. Pulmonary function, morphology and gene expression were analyzed in WT and SPC-LRP1 −/− mice. All data in this figure refer to female mice. A: Pressure-volume loops analyzed by forced oscillatory maneuvers (Flexivent, SciReq). Arrows indicate the direction of the loop for a given respiratory cycle. The bottom portion corresponds to the inspiratory phase, and the upper portion corresponds to the expiratory phase. B: Selected pulmonary function parameters: compliance, forced vital capacity (FVC) and forced expiratory volume in 0.1 s (FEV0.1). C: Representative transmission electron microscopy images highlighting collagen areas with the letters Col. Stereology-based quantification of the volume of collagen relative to parenchyma (Vv (Collagen|par)) is shown. D: Gene expression of the most common collagen components of the extracellular matrix, measured in lung homogenates. E: Gene expression of profibrotic markers in lung homogenates. F: Surface tension of BAL fluid, relative to the measurement in BAL from WT mice. G: Protein concentration in BAL fluid. H: Gene expression of proinflammatory markers in lung homogenates. Mean ± SD is shown. Significance: ∗ P < 0.05. CCL2, chemokine ligand 2; CD68, cluster of differentiation 68; Col1A1, Collagen, type I, alpha 1; Col1A2, Collagen, type I, alpha 2; Col3A1, Collagen, type III, alpha 1; IL1β, interleukin 1 beta; IL-6, interleukin 6; KC, keratinocyte-derived cytokine; TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Gene Expression, Transmission Assay, Electron Microscopy, Protein Concentration, Derivative Assay

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Detection of LRP1 in T2C in mice exposed to room air and smoke. Female WT mice were exposed to 6 months of room air or second-hand smoke, and lungs were collected, fixed, and processed for immunohistochemistry. A: Representative images obtained by confocal microscopy. Cell nuclei were labelled with Hoechst (blue), LRP1 with Alexa-488-conjugated antibodies (green), and epithelial cells with antibodies against EpCam and Alexa-555-conjugated (red). Images were acquired at 63X and alveolar epithelial cells with cuboidal morphology were selected as T2C as marked for some examples in the merged image. B: Green fluorescence, corresponding to LRP1, was quantified in the selected cells. Mean ± SD is shown. Significance: ∗ P < 0.05.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Immunohistochemistry, Confocal Microscopy, Fluorescence

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Female SPC-LRP1−/− mice had exacerbated smoke-induced fibrotic remodeling. WT and SPC-LRP1 −/− mice were exposed to second-hand smoke or room air for 6 months, starting at 2 months of age, and pulmonary function and morphology were evaluated. All data in this figure refer to female mice. A: Pressure-volume loops for WT and SPC-LRP1 −/− mice exposed to smoke (dashed line) or room air (solid line). B: Pulmonary compliance for WT and SPC-LRP1 −/− mice exposed to smoke or room air. C: Other relevant function testing parameters: inspiratory capacity, FVC, FEV0.1 and ratio FEV0.1/FVC for identification of disease pattern. D: Histological assessment of fibrosis and emphysema. Representative images of lung sections stained with Masson’s trichrome (left panels), fibrosis scoring using Ashcroft’s system, and chord length measurements. Mean ± SD is shown. Significance: ∗ P < 0.05, ∗∗ P < 0.01,∗∗∗ P < 0.001 for comparisons between room air and smoke groups, within the same genotype, and # P < 0.05, ### P < 0.001 for comparisons between WT and SPC-LRP1 −/− , within the same exposure.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Staining

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Transcriptomic analysis of T2C. Primary T2Cs were isolated from WT and SPC-LRP1 −/− mice and processed for RNA sequencing followed by pathway enrichment analysis. LRP1 KD and control cells were subjected to the same analysis. A: Vulcano plot showing all transcripts detected in mouse primary cells. Each dot represents a transcript. Red color indicates upregulation and blue color indicates downregulation in SPC-LRP1 −/− relative to WT mice. B: Ridgeline plot of KEGG pathways enriched in T2C from SPC-LRP1 −/− relative to WT mice analyzed by GSEA. Each dot represents a transcript in a specific pathway, and its log-fold change relative to WT mice is shown. Red color indicates upregulation and blue color indicates downregulation in SPC-LRP1 −/− mice. Peaks displaced to the right indicate upregulation of the overall pathway, and peaks displaced to the left indicate downregulation. Pathway regulation significance is indicated by darker shading of the peak’s area and the reference shading is shown on the right side. C: Vulcano plot showing all transcripts detected in LRP1 KD and control cell lines, using the same color-coding criteria as above. D: Ridgeline plot of KEGG pathways enriched in LRP1 KD cells, using the same color-coding criteria as above. E: Expression of LRP1 and enzymes involved in surfactant lipid synthesis, fatty acid oxidation and cholesterol metabolism in T2C populations of human samples from patients with COPD and control subjects in the publicly available dataset GSE136831 . ABCA1, ATP Binding Cassette Subfamily A Member 1; ABCA3, ATP Binding Cassette Subfamily A Member 3; ABCG1, ATP Binding Cassette Subfamily G Member 1; ACC1, Acetyl-CoA carboxylase 1; ACOX1, acyl-Co oxidase 1; CHKA, choline kinase A; CHKA, choline kinase B; CPT1A, carnitine palmitoyltransferase 1 alpha; CPT1B, carnitine palmitoyltransferase 1 beta; FASN, fatty acid synthase; HMGCS1, hydroxymethylglutaryl-CoA synthase 1; HMGCR, hydroxymethylglutaryl-CoA reductase; PCYT1A, CTP:phosphocholine cytidylyltransferase alpha; PPARA, peroxisome proliferator-activated receptor alpha; SCD 1, stearoyl-CoA desaturase; SREBF, sterol regulatory element-binding factor.

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Isolation, RNA Sequencing, Control, Expressing, Binding Assay

Journal: Journal of Lipid Research

Article Title: Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice

doi: 10.1016/j.jlr.2026.101042

Figure Lengend Snippet: Summary of the findings in this study. Left side: in WT mice, T2Cs maintain tightly regulated metabolism, including surfactant PL synthesis and secretion, cholesterol export and maintenance of extracellular matrix, to ensure optimal surfactant and pulmonary function. Smoke exposure triggers alveolar tissue emphysematous destruction, increased ECM deposition and impairments in pulmonary function. Right side: in mice with decreased LRP1 expression in T2C (SPC-LRP1 −/− mice), lipid metabolism is suppressed, surfactant synthesis is compromised, and metabolic pathways involved in inflammation and xenobiotic detoxification are activated. With smoke exposure, such baseline results in exacerbated collagen deposition, and pulmonary fibrotic remodeling. Created in BioRender. Garcia, I. (2026) https://BioRender.com/xya5fb0 .

Article Snippet: Tamoxifen-inducible T2C-specific Lrp1 knockout mice (SPC-LRP1 −/− ) were generated by crossing commercially available Lrp1 flox/flox mice (Jackson Labs, ME) with Sftpc-CreER T2 mice generously donated by Dr Brigid Hogan (Duke University) to generate Sftpc-CreER T2 -Lrp1 flox/WT (hemizygous) mice, which were crossed again with Lrp1 flox/flox mice to generate Sftpc-CreER T2 -Lrp1 flox/flox mice (SPC-LRP1 −/− ).

Techniques: Expressing

Journal: eLife

Article Title: Control of innate olfactory valence by segregated cortical amygdala circuits

doi: 10.7554/eLife.104677

Figure Lengend Snippet: Related to . The Arc-creER T2 mouse in combination with a cre-dependent AAV was used to express ChR2-eYFP in either aplCoA or pplCoA. Mice were administered tamoxifen and exposed to TMT. ( A ) Representative images of ChR2-eYFP in the aplCoA (top) or pplCoA (bottom). ( B ) Optogenetic stimulation-induced change in performance index for aplCoA- (left) or pplCoA-injected (right) mice. Photostimulation induces aversive responses in aplCoA and approach responses in pplCoA. * p<0.05; ** p<0.01; Additional specific details of statistical tests can be found in .

Article Snippet: Strain, strain background ( Mouse ) , Arc-CreER T2 , Jackson labs , RRID: IMSR_JAX:022357 , .

Techniques: Injection

Journal: iScience

Article Title: In vivo reprogramming of NG2 glia improves bladder function after spinal cord injury

doi: 10.1016/j.isci.2026.114850

Figure Lengend Snippet: SOX2-mediated glial reprogramming in the adult mouse spinal cord (A) Experimental scheme. SOX2-expressing lentiviruses were injected into the adult spinal cord, and tissues were analyzed 4 weeks (wk) later using immunohistochemistry (IHC). (B) Quantification of SOX2-induced DCX + immature neurons (mean ± SEM, n = 3–4 mice per group). Notably, DCX + cells were nearly absent in the p75-2-only condition. (C) Confocal images of DCX + cells induced by either wild-type SOX2 (SOX2 WT ) or the phospho-mimetic mutant SOX2 (SOX2 S251E ). Scale bars, 20 μm (D) Experimental scheme for tracing the cellular origin of mutant SOX2-reprogrammed cells. Adult transgenic mice were treated with tamoxifen (Tam), followed by intraspinal viral injections, and analyzed 4 weeks later. (E) Confocal images and quantifications (mean ± SEM, n = 3 mice per group) showing that NG2 glia are the cellular origin of mutant SOX2-reprogrammed cells in the adult spinal cord. NG2 glia and astrocytes were lineage-traced using Pdgfra-CreER T2 ;R26R-tdT and Aldh1l1-CreER T2 ;R26R-tdT mice, respectively. Scale bar, 20 μm (F) Experimental scheme for a time-course analysis of mutant SOX2-mediated reprogramming. dpv, days post virus injection. (G) Quantification of mutant SOX2-induced ASCL1 + neural progenitors (mean ± SEM, n = 3 mice per group). (H) Confocal images showing induction of ASCL1 + neural progenitors by mutant SOX2. Scale bar, 20 μm (I) Experimental scheme for tracing the progeny of mutant SOX2-induced ASCL1 + progenitors in the adult spinal cord. wpv, weeks post virus injection. (J) Quantification of mutant SOX2-induced tdT + cells at 4 wpv (mean ± SEM, n = 5 mice). (K) Confocal images showing robust detection of DCX + tdT + cells in mutant SOX2-expressing spinal cord. Scale bar, 20 μm.

Article Snippet: Mouse: Pdgfra-CreER T2 , The Jackson Laboratory , JAX: 032770; RRID: IMSR_JAX: 032770.

Techniques: Expressing, Injection, Immunohistochemistry, Mutagenesis, Transgenic Assay, Virus

Journal: iScience

Article Title: In vivo reprogramming of NG2 glia improves bladder function after spinal cord injury

doi: 10.1016/j.isci.2026.114850

Figure Lengend Snippet: SOX2-mediated glial reprogramming in the adult mouse spinal cord (A) Experimental scheme. SOX2-expressing lentiviruses were injected into the adult spinal cord, and tissues were analyzed 4 weeks (wk) later using immunohistochemistry (IHC). (B) Quantification of SOX2-induced DCX + immature neurons (mean ± SEM, n = 3–4 mice per group). Notably, DCX + cells were nearly absent in the p75-2-only condition. (C) Confocal images of DCX + cells induced by either wild-type SOX2 (SOX2 WT ) or the phospho-mimetic mutant SOX2 (SOX2 S251E ). Scale bars, 20 μm (D) Experimental scheme for tracing the cellular origin of mutant SOX2-reprogrammed cells. Adult transgenic mice were treated with tamoxifen (Tam), followed by intraspinal viral injections, and analyzed 4 weeks later. (E) Confocal images and quantifications (mean ± SEM, n = 3 mice per group) showing that NG2 glia are the cellular origin of mutant SOX2-reprogrammed cells in the adult spinal cord. NG2 glia and astrocytes were lineage-traced using Pdgfra-CreER T2 ;R26R-tdT and Aldh1l1-CreER T2 ;R26R-tdT mice, respectively. Scale bar, 20 μm (F) Experimental scheme for a time-course analysis of mutant SOX2-mediated reprogramming. dpv, days post virus injection. (G) Quantification of mutant SOX2-induced ASCL1 + neural progenitors (mean ± SEM, n = 3 mice per group). (H) Confocal images showing induction of ASCL1 + neural progenitors by mutant SOX2. Scale bar, 20 μm (I) Experimental scheme for tracing the progeny of mutant SOX2-induced ASCL1 + progenitors in the adult spinal cord. wpv, weeks post virus injection. (J) Quantification of mutant SOX2-induced tdT + cells at 4 wpv (mean ± SEM, n = 5 mice). (K) Confocal images showing robust detection of DCX + tdT + cells in mutant SOX2-expressing spinal cord. Scale bar, 20 μm.

Article Snippet: Mouse: Aldh1l1-CreER T2 , The Jackson Laboratory , JAX: 031008; RRID: IMSR_JAX: 031008.

Techniques: Expressing, Injection, Immunohistochemistry, Mutagenesis, Transgenic Assay, Virus