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Jackson Laboratory conditional trem2 knockout mice

<t>Trem2</t> is induced in PDGFR-α + adipocyte progenitors post high-fat diet feeding and associates with a lipid-handling gene signature. (A) t-distributed stochastic neighbor embedding (t-SNE) plot of ASC from eWAT of lean (18 weeks ND) and obese (12 weeks HFD) mice from Gene Expression Omnibus number GSE237143 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (B) Uniform Manifold Approximation and Projection (UMAP) plot of FAP from eWAT of lean (18 weeks ND) and obese (18 weeks HFD) mice from Gene Expression Omnibus number GSE160729 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (C) Violin plots showing scaled expression levels of the indicated genes ( Cd36, Tyrobp, Apoe, Fabp4, and Plin2 ). Cells were stratified into Trem2 -positive and Trem2 -negative subsets based on expression profiles shown in (A) .

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1) Product Images from "TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity"

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2026.1738472

Trem2 is induced in PDGFR-α + adipocyte progenitors post high-fat diet feeding and associates with a lipid-handling gene signature. (A) t-distributed stochastic neighbor embedding (t-SNE) plot of ASC from eWAT of lean (18 weeks ND) and obese (12 weeks HFD) mice from Gene Expression Omnibus number GSE237143 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (B) Uniform Manifold Approximation and Projection (UMAP) plot of FAP from eWAT of lean (18 weeks ND) and obese (18 weeks HFD) mice from Gene Expression Omnibus number GSE160729 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (C) Violin plots showing scaled expression levels of the indicated genes ( Cd36, Tyrobp, Apoe, Fabp4, and Plin2 ). Cells were stratified into Trem2 -positive and Trem2 -negative subsets based on expression profiles shown in (A) .

Figure Legend Snippet: Trem2 is induced in PDGFR-α + adipocyte progenitors post high-fat diet feeding and associates with a lipid-handling gene signature. (A) t-distributed stochastic neighbor embedding (t-SNE) plot of ASC from eWAT of lean (18 weeks ND) and obese (12 weeks HFD) mice from Gene Expression Omnibus number GSE237143 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (B) Uniform Manifold Approximation and Projection (UMAP) plot of FAP from eWAT of lean (18 weeks ND) and obese (18 weeks HFD) mice from Gene Expression Omnibus number GSE160729 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (C) Violin plots showing scaled expression levels of the indicated genes ( Cd36, Tyrobp, Apoe, Fabp4, and Plin2 ). Cells were stratified into Trem2 -positive and Trem2 -negative subsets based on expression profiles shown in (A) .

Techniques Used: Gene Expression, Expressing

$TREM2 promotes adipocyte differentiation. (A) Mouse Trem2 and Pparg expression during adipocyte differentiation of stromal vascular fraction cells derived from epididymal white adipose (eWAT), n = 4 per genotype. (B) Representative oil red O staining of adipocytes derived from eWAT 14 days post-differentiation. Magnification is 50 x (C) Pparg , Adipoq and Oil Red O quantification in adipocytes derived from eWAT 14 days post-differentiation, n = 6–7 per genotype. (D) AKT signaling in WT and Trem2 -/- 14-day differentiated adipocytes derived from eWAT, post 20-minute insulin treatment (E) Trem2 , Pparg and Oil Red O levels in adipocytes derived from mouse embryonic fibroblasts (MEF), n = 4 per genotype. (F) Representative oil Red O staining from (E) . Magnification is 5 x. Results in (A, C, E) represent mean ± SEM. All data is representative of 2 independent experiments except data in (C) which is pooled from 2 experiments. Statistical analysis was performed with one-way ANOVA followed by Tukey post-test (A, E) or Student’s T-test (C) . *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.$
Figure Legend Snippet: TREM2 promotes adipocyte differentiation. (A) Mouse Trem2 and Pparg expression during adipocyte differentiation of stromal vascular fraction cells derived from epididymal white adipose (eWAT), n = 4 per genotype. (B) Representative oil red O staining of adipocytes derived from eWAT 14 days post-differentiation. Magnification is 50 x (C) Pparg , Adipoq and Oil Red O quantification in adipocytes derived from eWAT 14 days post-differentiation, n = 6–7 per genotype. (D) AKT signaling in WT and Trem2 -/- 14-day differentiated adipocytes derived from eWAT, post 20-minute insulin treatment (E) Trem2 , Pparg and Oil Red O levels in adipocytes derived from mouse embryonic fibroblasts (MEF), n = 4 per genotype. (F) Representative oil Red O staining from (E) . Magnification is 5 x. Results in (A, C, E) represent mean ± SEM. All data is representative of 2 independent experiments except data in (C) which is pooled from 2 experiments. Statistical analysis was performed with one-way ANOVA followed by Tukey post-test (A, E) or Student’s T-test (C) . *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Techniques Used: Expressing, Derivative Assay, Staining

TREM2 deletion in PDGFR-α + pre-adipocytes promotes early adipocyte differentiation. (A) Schematic representation of the Trem2 floxed allele used to generate Trem2 ΔPdgrfα animals. LoxP sites flank exons 2 and 3 of the Trem2 gene. The locations of the forward and reverse primers used to confirm Trem2 deletion are indicated and result in the loss of a 151bp PCR product. (B) Sorting strategy for PDGFR-α+ ASC. ASC are gated as single cells, viable, Lin - (CD45 - CD31 - Ter119 - CD11b - ) cells. Cells were further gated as CD29 + Sca1 + PDGFR-α + . (C) Gel depicting deletion efficiency as determined using PCR on genomic DNA isolated from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals. (D, E) Trem2 and Pdgfra levels in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals for the indicated time points, n = 3–4 per genotype. (F) Pparg levels during early adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (G) Adipoq levels during late adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (H-J) Trem2 , Pparg and Adipoq expression in differentiated adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from Trem2 -/- mice, n = 3–6 per genotype. Data in (D–J) represent mean ± SEM and data in (H–J) is representative of 2 independent experiments. Statistical analysis was performed with Two-way ANOVA followed by Bonferroni post-test. *P < 0.05, ***P < 0.001, ****P < 0.0001.

Figure Legend Snippet: TREM2 deletion in PDGFR-α + pre-adipocytes promotes early adipocyte differentiation. (A) Schematic representation of the Trem2 floxed allele used to generate Trem2 ΔPdgrfα animals. LoxP sites flank exons 2 and 3 of the Trem2 gene. The locations of the forward and reverse primers used to confirm Trem2 deletion are indicated and result in the loss of a 151bp PCR product. (B) Sorting strategy for PDGFR-α+ ASC. ASC are gated as single cells, viable, Lin - (CD45 - CD31 - Ter119 - CD11b - ) cells. Cells were further gated as CD29 + Sca1 + PDGFR-α + . (C) Gel depicting deletion efficiency as determined using PCR on genomic DNA isolated from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals. (D, E) Trem2 and Pdgfra levels in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals for the indicated time points, n = 3–4 per genotype. (F) Pparg levels during early adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (G) Adipoq levels during late adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (H-J) Trem2 , Pparg and Adipoq expression in differentiated adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from Trem2 -/- mice, n = 3–6 per genotype. Data in (D–J) represent mean ± SEM and data in (H–J) is representative of 2 independent experiments. Statistical analysis was performed with Two-way ANOVA followed by Bonferroni post-test. *P < 0.05, ***P < 0.001, ****P < 0.0001.

Techniques Used: Isolation, Derivative Assay, Expressing

TREM2 expression in PDGFR-α + pre-adipocytes moderately restrains pre-adipocyte hyperplasia but has no effect on adipose remodeling in obesity. (A) Percentage of PDGFR-α + CD24 + ASC within the lineage-negative pool of eWAT at the indicated times of HFD feeding. n=5-8. (B) Percentage of Ki67 + PDGFR-α + CD24 + ASC three days post HFD. n = 3-4. (C) Percentage of PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT (left), absolute numbers (middle) and percentage Ki67 + (right) therein in both genotypes 3 days post HFD. n=5-6. (D) Body and eWAT weight of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (E) Percentage of PDGFR-α + or PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT of Trem2 ΔPdgrfα and littermate control animals 15 weeks post HFD. n=6-9 (F) Representative H&E staining of eWAT in both groups of animals post 15 weeks HFD. (G) Quantification of adipocyte frequency from (F) . n = 13–16 mice per genotype. All data represent mean ± SEM and are representative of 2 independent experiments. Data in A and G is pooled data from 2 independent experiments. Statistical analysis was performed with one-way ANOVA followed by Dunnett post-test (A) or Student’s T-test (B–G) . *P < 0.05, ***P < 0.001, ****P < 0.0001.

Figure Legend Snippet: TREM2 expression in PDGFR-α + pre-adipocytes moderately restrains pre-adipocyte hyperplasia but has no effect on adipose remodeling in obesity. (A) Percentage of PDGFR-α + CD24 + ASC within the lineage-negative pool of eWAT at the indicated times of HFD feeding. n=5-8. (B) Percentage of Ki67 + PDGFR-α + CD24 + ASC three days post HFD. n = 3-4. (C) Percentage of PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT (left), absolute numbers (middle) and percentage Ki67 + (right) therein in both genotypes 3 days post HFD. n=5-6. (D) Body and eWAT weight of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (E) Percentage of PDGFR-α + or PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT of Trem2 ΔPdgrfα and littermate control animals 15 weeks post HFD. n=6-9 (F) Representative H&E staining of eWAT in both groups of animals post 15 weeks HFD. (G) Quantification of adipocyte frequency from (F) . n = 13–16 mice per genotype. All data represent mean ± SEM and are representative of 2 independent experiments. Data in A and G is pooled data from 2 independent experiments. Statistical analysis was performed with one-way ANOVA followed by Dunnett post-test (A) or Student’s T-test (B–G) . *P < 0.05, ***P < 0.001, ****P < 0.0001.

Techniques Used: Expressing, Control, Staining

No influence of TREM2 deletion in PDGFR-α + cells on metabolic health and ATMs. (A) Fasted blood glucose of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (B, C) Insulin tolerance (ITT) (B) or oral glucose tolerance test (oGTT) (C) of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (D) Serum non-esterified fatty acids (NEFA), triglyceride (TAG), and total cholesterol (T-CHOL) in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=5-8. (E) Gating strategy used to identify ATM populations. ATMs are gated as single cells, viable, CD45 + CD11b + F4/80 + cells. Within the ATM pool the cells were further gated as CD11c + CD206 - or CD9 + or BODIPY + . (F) Percentage of CD11b + F4/80 + ATMs within the CD45 + immune cell pool and absolute macrophage amounts in both genotypes of obese animals, 15 weeks post HFD. n=6-9. (G) Percentage of CD11c + , CD9 + or BODIPY + macrophages within the CD11b + F4/80 + ATM pool in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. All data represent mean ± SEM and are representative of 2 independent experiments.

Figure Legend Snippet: No influence of TREM2 deletion in PDGFR-α + cells on metabolic health and ATMs. (A) Fasted blood glucose of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (B, C) Insulin tolerance (ITT) (B) or oral glucose tolerance test (oGTT) (C) of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (D) Serum non-esterified fatty acids (NEFA), triglyceride (TAG), and total cholesterol (T-CHOL) in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=5-8. (E) Gating strategy used to identify ATM populations. ATMs are gated as single cells, viable, CD45 + CD11b + F4/80 + cells. Within the ATM pool the cells were further gated as CD11c + CD206 - or CD9 + or BODIPY + . (F) Percentage of CD11b + F4/80 + ATMs within the CD45 + immune cell pool and absolute macrophage amounts in both genotypes of obese animals, 15 weeks post HFD. n=6-9. (G) Percentage of CD11c + , CD9 + or BODIPY + macrophages within the CD11b + F4/80 + ATM pool in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. All data represent mean ± SEM and are representative of 2 independent experiments.

Techniques Used:

Image Search Results

Journal: Frontiers in Endocrinology

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

doi: 10.3389/fendo.2026.1738472

Figure Lengend Snippet: Trem2 is induced in PDGFR-α + adipocyte progenitors post high-fat diet feeding and associates with a lipid-handling gene signature. (A) t-distributed stochastic neighbor embedding (t-SNE) plot of ASC from eWAT of lean (18 weeks ND) and obese (12 weeks HFD) mice from Gene Expression Omnibus number GSE237143 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (B) Uniform Manifold Approximation and Projection (UMAP) plot of FAP from eWAT of lean (18 weeks ND) and obese (18 weeks HFD) mice from Gene Expression Omnibus number GSE160729 . The original clustering and cell annotations were retained. Color intensity represents normalized expression levels of Pdgfra (top) and Trem2 (bottom). (C) Violin plots showing scaled expression levels of the indicated genes ( Cd36, Tyrobp, Apoe, Fabp4, and Plin2 ). Cells were stratified into Trem2 -positive and Trem2 -negative subsets based on expression profiles shown in (A) .

Article Snippet: For the generation of conditional TREM2 knockout mice, Trem2^tm1c(EUCOMM)Wtsi mice (#029853, Jackson Laboratory) carrying floxed alleles of Trem2 were crossed with C57BL/6-Tg(Pdgfrα-cre)1Clc/J mice (#013148, Jackson Laboratory), which express Cre recombinase under the control of the Pdgfrα promoter to achieve adipocyte progenitor–specific Trem2 deletion.

Techniques: Gene Expression, Expressing

Journal: Frontiers in Endocrinology

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

doi: 10.3389/fendo.2026.1738472

Figure Lengend Snippet: TREM2 promotes adipocyte differentiation. (A) Mouse Trem2 and Pparg expression during adipocyte differentiation of stromal vascular fraction cells derived from epididymal white adipose (eWAT), n = 4 per genotype. (B) Representative oil red O staining of adipocytes derived from eWAT 14 days post-differentiation. Magnification is 50 x (C) Pparg , Adipoq and Oil Red O quantification in adipocytes derived from eWAT 14 days post-differentiation, n = 6–7 per genotype. (D) AKT signaling in WT and Trem2 -/- 14-day differentiated adipocytes derived from eWAT, post 20-minute insulin treatment (E) Trem2 , Pparg and Oil Red O levels in adipocytes derived from mouse embryonic fibroblasts (MEF), n = 4 per genotype. (F) Representative oil Red O staining from (E) . Magnification is 5 x. Results in (A, C, E) represent mean ± SEM. All data is representative of 2 independent experiments except data in (C) which is pooled from 2 experiments. Statistical analysis was performed with one-way ANOVA followed by Tukey post-test (A, E) or Student’s T-test (C) . *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Techniques: Expressing, Derivative Assay, Staining

Journal: Frontiers in Endocrinology

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

doi: 10.3389/fendo.2026.1738472

Figure Lengend Snippet: TREM2 deletion in PDGFR-α + pre-adipocytes promotes early adipocyte differentiation. (A) Schematic representation of the Trem2 floxed allele used to generate Trem2 ΔPdgrfα animals. LoxP sites flank exons 2 and 3 of the Trem2 gene. The locations of the forward and reverse primers used to confirm Trem2 deletion are indicated and result in the loss of a 151bp PCR product. (B) Sorting strategy for PDGFR-α+ ASC. ASC are gated as single cells, viable, Lin - (CD45 - CD31 - Ter119 - CD11b - ) cells. Cells were further gated as CD29 + Sca1 + PDGFR-α + . (C) Gel depicting deletion efficiency as determined using PCR on genomic DNA isolated from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals. (D, E) Trem2 and Pdgfra levels in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals for the indicated time points, n = 3–4 per genotype. (F) Pparg levels during early adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (G) Adipoq levels during late adipocyte differentiation in adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from both genotypes of animals, n = 3–4 per genotype. (H-J) Trem2 , Pparg and Adipoq expression in differentiated adipocytes derived from sorted Lin - CD29 + Sca-1 + PDGFR-α + eWAT ASC from Trem2 -/- mice, n = 3–6 per genotype. Data in (D–J) represent mean ± SEM and data in (H–J) is representative of 2 independent experiments. Statistical analysis was performed with Two-way ANOVA followed by Bonferroni post-test. *P < 0.05, ***P < 0.001, ****P < 0.0001.

Techniques: Isolation, Derivative Assay, Expressing

Journal: Frontiers in Endocrinology

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

doi: 10.3389/fendo.2026.1738472

Figure Lengend Snippet: TREM2 expression in PDGFR-α + pre-adipocytes moderately restrains pre-adipocyte hyperplasia but has no effect on adipose remodeling in obesity. (A) Percentage of PDGFR-α + CD24 + ASC within the lineage-negative pool of eWAT at the indicated times of HFD feeding. n=5-8. (B) Percentage of Ki67 + PDGFR-α + CD24 + ASC three days post HFD. n = 3-4. (C) Percentage of PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT (left), absolute numbers (middle) and percentage Ki67 + (right) therein in both genotypes 3 days post HFD. n=5-6. (D) Body and eWAT weight of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (E) Percentage of PDGFR-α + or PDGFR-α + CD24 + ASC within the lineage negative pool of eWAT of Trem2 ΔPdgrfα and littermate control animals 15 weeks post HFD. n=6-9 (F) Representative H&E staining of eWAT in both groups of animals post 15 weeks HFD. (G) Quantification of adipocyte frequency from (F) . n = 13–16 mice per genotype. All data represent mean ± SEM and are representative of 2 independent experiments. Data in A and G is pooled data from 2 independent experiments. Statistical analysis was performed with one-way ANOVA followed by Dunnett post-test (A) or Student’s T-test (B–G) . *P < 0.05, ***P < 0.001, ****P < 0.0001.

Techniques: Expressing, Control, Staining

Journal: Frontiers in Endocrinology

Article Title: TREM2 promotes adipogenesis of PDGFR-α + adipose stem cells but is dispensable for adipose remodeling and metabolic health during diet-induced obesity

doi: 10.3389/fendo.2026.1738472

Figure Lengend Snippet: No influence of TREM2 deletion in PDGFR-α + cells on metabolic health and ATMs. (A) Fasted blood glucose of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (B, C) Insulin tolerance (ITT) (B) or oral glucose tolerance test (oGTT) (C) of Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. (D) Serum non-esterified fatty acids (NEFA), triglyceride (TAG), and total cholesterol (T-CHOL) in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=5-8. (E) Gating strategy used to identify ATM populations. ATMs are gated as single cells, viable, CD45 + CD11b + F4/80 + cells. Within the ATM pool the cells were further gated as CD11c + CD206 - or CD9 + or BODIPY + . (F) Percentage of CD11b + F4/80 + ATMs within the CD45 + immune cell pool and absolute macrophage amounts in both genotypes of obese animals, 15 weeks post HFD. n=6-9. (G) Percentage of CD11c + , CD9 + or BODIPY + macrophages within the CD11b + F4/80 + ATM pool in Trem2 ΔPdgrfα animals and controls 15 weeks post HFD. n=6-9. All data represent mean ± SEM and are representative of 2 independent experiments.

Techniques:

TREM2 deletion aggravates cognitive impairment and promotes Aβ accumulation in the prefrontal cortex of T1D mice. a , b Blood glucose ( a ) and body weight ( b ) of mice in each group. n = 13. c Escape latency of each group for days 1 to 8 by Morris water maze (MWM). n = 12. d , e Time percent in the target quadrant ( d ) and representative path maps ( e ) of each group following removal of the platform. n = 12. f Swimming speeds of each group. n = 6. g Escape latency of each group in the MWM visible platform test on day 9. n = 7. h Recognition index in the novel object recognition test. n = 6. i) Grooming duration in the splash test. n = 9. j , k Mean percentage of conditioned freezing in the context test ( j ) and in the cued test ( k ). Ctrl, n = 6; T1D, n = 6; TREM2 cKO, n = 6 and T1D + TREM2 cKO, n = 5. l Representative images of Western blot showed the TREM2 expression in the prefrontal cortex. m Representative images of immunofluorescent staining of Iba1 (red), 6E10 (green) and DAPI (blue) in the prefrontal cortex. Scale bar = 20 μm. n , o , p Relative number of Iba1 positive cells (n), relative fluorescent area of 6E10 ( o ) and percentage of 6E10 area per micoglia ( p ) in the prefrontal cortex. n = 6. q The level of Aβ1–42 in the prefrontal cortex by ELISA. n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For a-d, f-k, n-q, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01, ### p < 0.001, compared with Ctrl group. & p < 0.05, compared with T1D group.

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: TREM2 deletion aggravates cognitive impairment and promotes Aβ accumulation in the prefrontal cortex of T1D mice. a , b Blood glucose ( a ) and body weight ( b ) of mice in each group. n = 13. c Escape latency of each group for days 1 to 8 by Morris water maze (MWM). n = 12. d , e Time percent in the target quadrant ( d ) and representative path maps ( e ) of each group following removal of the platform. n = 12. f Swimming speeds of each group. n = 6. g Escape latency of each group in the MWM visible platform test on day 9. n = 7. h Recognition index in the novel object recognition test. n = 6. i) Grooming duration in the splash test. n = 9. j , k Mean percentage of conditioned freezing in the context test ( j ) and in the cued test ( k ). Ctrl, n = 6; T1D, n = 6; TREM2 cKO, n = 6 and T1D + TREM2 cKO, n = 5. l Representative images of Western blot showed the TREM2 expression in the prefrontal cortex. m Representative images of immunofluorescent staining of Iba1 (red), 6E10 (green) and DAPI (blue) in the prefrontal cortex. Scale bar = 20 μm. n , o , p Relative number of Iba1 positive cells (n), relative fluorescent area of 6E10 ( o ) and percentage of 6E10 area per micoglia ( p ) in the prefrontal cortex. n = 6. q The level of Aβ1–42 in the prefrontal cortex by ELISA. n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For a-d, f-k, n-q, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. ## p < 0.01, ### p < 0.001, compared with Ctrl group. & p < 0.05, compared with T1D group.

Article Snippet: The C57BL/6J mice were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd., while TREM2 conditional knockout (TREM2 cKO) mice on a C57BL/6J background were obtained from Cyagen Biosciences Inc.

Techniques: Western Blot, Expressing, Staining, Enzyme-linked Immunosorbent Assay, Knock-Out, In Vivo

The impact of TREM2 on microglial phagocytosis of Aβ under T1D and high glucose condition. a-c Representative images of immunofluorescent staining ( a ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( b ) and CD68/Iba-1 ratio ( c ) in the prefrontal cortex. Scale bar = 10 μm. n = 6. d-f Representative images of immunofluorescent staining ( d ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( e ) and CD68/Iba-1 ratio ( f ) in primary cultured microglia. n = 5. g Representative images of Western blot showed the TREM2 expression in BV2 cells from different treatment groups. h, i Representative images ( h ) and mean intensity ( i ) of fluorescent Aβ (green) in BV2 cells at different time points. Scale bar = 7.8 μm. n = 3. j, k The percentage of fluorescent Aβ + BV2 cells ( j ) and representative flow cytometry dot plots ( k ). n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. NG: Normal glucose group. HG: High glucose group. HG + TREM2 cKO: TREM2 knockout high-glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. HG + Vector: High-glucose group with empty-vector. HG + TREM2-OE: High-glucose group with TREM2 overexpression. NG + Aβ: Normal glucose group with Aβ. HG + TREM2-si + Aβ: High-glucose group with TREM2 knockdown and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For b, c, e, f, i, j, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. # p < 0.05, ## p < 0.01, compared with NG + Aβ group. &&& p < 0.001, compared with HG + Vector + Aβ group.

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The impact of TREM2 on microglial phagocytosis of Aβ under T1D and high glucose condition. a-c Representative images of immunofluorescent staining ( a ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( b ) and CD68/Iba-1 ratio ( c ) in the prefrontal cortex. Scale bar = 10 μm. n = 6. d-f Representative images of immunofluorescent staining ( d ) of Iba1 (red), CD68 (green) and DAPI (blue), CD68 mean intensity ( e ) and CD68/Iba-1 ratio ( f ) in primary cultured microglia. n = 5. g Representative images of Western blot showed the TREM2 expression in BV2 cells from different treatment groups. h, i Representative images ( h ) and mean intensity ( i ) of fluorescent Aβ (green) in BV2 cells at different time points. Scale bar = 7.8 μm. n = 3. j, k The percentage of fluorescent Aβ + BV2 cells ( j ) and representative flow cytometry dot plots ( k ). n = 5. WT: Wild-type. TREM2 cKO: TREM2 knockout. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. NG: Normal glucose group. HG: High glucose group. HG + TREM2 cKO: TREM2 knockout high-glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. HG + Vector: High-glucose group with empty-vector. HG + TREM2-OE: High-glucose group with TREM2 overexpression. NG + Aβ: Normal glucose group with Aβ. HG + TREM2-si + Aβ: High-glucose group with TREM2 knockdown and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For b, c, e, f, i, j, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001. # p < 0.05, ## p < 0.01, compared with NG + Aβ group. &&& p < 0.001, compared with HG + Vector + Aβ group.

Techniques: Staining, Cell Culture, Western Blot, Expressing, Flow Cytometry, Knock-Out, Plasmid Preparation, Over Expression, Knockdown, In Vivo, In Vitro

The impact of TREM2 on microglial cell migration towards different forms of Aβ. a Flow chart of cell experiments. b , c Representative images ( b ) and quantitative analysis of western blot ( c ) showed the expression of TREM2 in BV2 cells. n = 3. d , e Representative images ( d ) and migration index of BV2 cells ( e ) at different time points post scratch. n = 3. f Representative images of cell migration in BV2 cells analyzed by Transwell assay. g , h Migration ratio of BV2 cells towards fAβ ( f ) and oAβ ( g ). n = 3. NG: Normal glucose group. HG: High glucose group. TREM2-si: TREM2 knockdown group. HG + Vector: High-glucose group with empty vector. HG + TREM2-si: TREM2 knockdown high-glucose group. fAβ: Aβ fibril. oAβ: Aβ oligomer. Data were presented as mean ± SEM. For in vitro studies, n represents the number of biologically independent experiments performed. For c, two-tailed unpaired t test. For e, g, h, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The impact of TREM2 on microglial cell migration towards different forms of Aβ. a Flow chart of cell experiments. b , c Representative images ( b ) and quantitative analysis of western blot ( c ) showed the expression of TREM2 in BV2 cells. n = 3. d , e Representative images ( d ) and migration index of BV2 cells ( e ) at different time points post scratch. n = 3. f Representative images of cell migration in BV2 cells analyzed by Transwell assay. g , h Migration ratio of BV2 cells towards fAβ ( f ) and oAβ ( g ). n = 3. NG: Normal glucose group. HG: High glucose group. TREM2-si: TREM2 knockdown group. HG + Vector: High-glucose group with empty vector. HG + TREM2-si: TREM2 knockdown high-glucose group. fAβ: Aβ fibril. oAβ: Aβ oligomer. Data were presented as mean ± SEM. For in vitro studies, n represents the number of biologically independent experiments performed. For c, two-tailed unpaired t test. For e, g, h, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Migration, Western Blot, Expressing, Transwell Assay, Knockdown, Plasmid Preparation, In Vitro, Two Tailed Test

Distribution and expression dynamics of Aβ-related genes in microglial subpopulations of T1D mice. a, b Bubble plot ( a ) and violin plots ( b ) showing the expression of Aβ-related genes for each microglia subpopulation. c , e , g Violin plots showing the expression of Cx3cr1 ( c ), Ccr5 ( e ) and Trem2 ( g ) in the microglial subpopulations. d , f , h Violin plots comparing the levels of Cx3cr1 ( d ), Ccr5 ( f ) and Trem2 ( h ) in microglia between the Ctrl and T1D groups. i Violin plot showing the levels of Trem2 among microglia subpopulations. j-l Smoothed expression curves of Trem2 ( j ), Cx3cr1 ( k ) and Ccr5 ( l ) along the trajectory in microglia subpopulations. M: Microglia, Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. n = 3. For in vivo studies, n represents the number of animals per group. For c-i, unpaired t test. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Distribution and expression dynamics of Aβ-related genes in microglial subpopulations of T1D mice. a, b Bubble plot ( a ) and violin plots ( b ) showing the expression of Aβ-related genes for each microglia subpopulation. c , e , g Violin plots showing the expression of Cx3cr1 ( c ), Ccr5 ( e ) and Trem2 ( g ) in the microglial subpopulations. d , f , h Violin plots comparing the levels of Cx3cr1 ( d ), Ccr5 ( f ) and Trem2 ( h ) in microglia between the Ctrl and T1D groups. i Violin plot showing the levels of Trem2 among microglia subpopulations. j-l Smoothed expression curves of Trem2 ( j ), Cx3cr1 ( k ) and Ccr5 ( l ) along the trajectory in microglia subpopulations. M: Microglia, Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. n = 3. For in vivo studies, n represents the number of animals per group. For c-i, unpaired t test. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group

Techniques: Expressing, In Vivo

Microglial activation and TREM2 expression in the prefrontal cortex and hippocampus of T1D mice. a , b Representative images of immunofluorescent staining of Iba1 (red), TREM2 (green) and DAPI (blue) in the prefrontal cortex ( a ) and hippocampus ( b ). Scale bar = 5 μm. c , j Schematic diagrams of prefrontal cortex ( c ) and hippocampus ( j ). d The relative number of Iba1-positive cells in the prefrontal cortex normalized to the control group. e The soma size of Iba1-positive cells in the prefrontal cortex. f , m The relative mRNA levels of LPL, CST7 and TREM2 in the prefrontal cortex ( f ) and hippocampus ( m ). n = 6. g , h , i Representative images ( g ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( h ), and the TREM2/Iba1 ratio ( i ) in the prefrontal cortex. n = 6. k The relative number of Iba1-positive cells in the hippocampus normalized to the control group. n = 6. l The soma size of Iba1-positive cells in the hippocampus. n = 6. n , o , p Representative images ( n ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( o ), and the TREM2/Iba1 ratio ( p ) in the hippocampus. n = 6. Ctrl: Wild-type nondiabetic group. 8 W, 15 W: T1D mice at 8 and 15 weeks post-STZ injection, respectively. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For d-f, h-i, k-m, o-p, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group.

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Microglial activation and TREM2 expression in the prefrontal cortex and hippocampus of T1D mice. a , b Representative images of immunofluorescent staining of Iba1 (red), TREM2 (green) and DAPI (blue) in the prefrontal cortex ( a ) and hippocampus ( b ). Scale bar = 5 μm. c , j Schematic diagrams of prefrontal cortex ( c ) and hippocampus ( j ). d The relative number of Iba1-positive cells in the prefrontal cortex normalized to the control group. e The soma size of Iba1-positive cells in the prefrontal cortex. f , m The relative mRNA levels of LPL, CST7 and TREM2 in the prefrontal cortex ( f ) and hippocampus ( m ). n = 6. g , h , i Representative images ( g ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( h ), and the TREM2/Iba1 ratio ( i ) in the prefrontal cortex. n = 6. k The relative number of Iba1-positive cells in the hippocampus normalized to the control group. n = 6. l The soma size of Iba1-positive cells in the hippocampus. n = 6. n , o , p Representative images ( n ) and quantitative analysis of Western blot showed the protein levels of Iba1 and TREM2 ( o ), and the TREM2/Iba1 ratio ( p ) in the hippocampus. n = 6. Ctrl: Wild-type nondiabetic group. 8 W, 15 W: T1D mice at 8 and 15 weeks post-STZ injection, respectively. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For d-f, h-i, k-m, o-p, One-way ANOVA. * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Ctrl group.

Techniques: Activation Assay, Expressing, Staining, Control, Western Blot, Injection, In Vivo

Identification and functional validation of differentially expressed genes related to TREM2 in the brain of T1D mice. a Volcano plot of differential gene expression profiles in the prefrontal cortex between T1D mice and T1D + TREM2 cKO mice. b Chord plot displaying the top 10 GO terms of differentially expressed genes. c , d Representative images of immunofluorescent staining ( c ) of TOM20 (green) and DAPI (blue), and the mitochondrial fragmentation index in BV2 cells, calculated as punctate/(punctate + rod-shaped + reticular) ( d ). Scale bar = 10 μm. n = 3. e) Representative electron microscopy images of mitochondria in BV2 cells. f Top 10 ranked hub gene networks generated by Cytohubba. g The relative mRNA levels of Ccr5, Cx3cr1, and Cxcl10 in the prefrontal cortex. n = 5. h GSEA showed significant enrichment in the PI3K/AKT/MTOR signaling pathway. i , k , l Representative images of immunofluorescent staining ( i ) of P-mTOR (green), Iba1 (red), and DAPI (blue), the intensity of P-mTOR in microglia ( k ), and normalized intensity of P-mTOR in microglia ( l ) in the prefrontal cortex. Scale bar = 10 μm. n = 8. j , m-o Representative images ( j ) and quantitative analysis of Western blot showed the levels of P-mTOR/mTOR ( m ), P-Erk1/2/Erk1/2 ( n ), and P-GSK3β/GSK3β ( o ) in BV2 cells. n = 3. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. DEGs: Differentially expressed genes. GO: Gene ontology. GSEA: Gene set enrichment analysis. NG: Normal glucose group. HG: High glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For d, g, k-o, One-way ANOVA. * p < 0.05, ** p < 0.01

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: Identification and functional validation of differentially expressed genes related to TREM2 in the brain of T1D mice. a Volcano plot of differential gene expression profiles in the prefrontal cortex between T1D mice and T1D + TREM2 cKO mice. b Chord plot displaying the top 10 GO terms of differentially expressed genes. c , d Representative images of immunofluorescent staining ( c ) of TOM20 (green) and DAPI (blue), and the mitochondrial fragmentation index in BV2 cells, calculated as punctate/(punctate + rod-shaped + reticular) ( d ). Scale bar = 10 μm. n = 3. e) Representative electron microscopy images of mitochondria in BV2 cells. f Top 10 ranked hub gene networks generated by Cytohubba. g The relative mRNA levels of Ccr5, Cx3cr1, and Cxcl10 in the prefrontal cortex. n = 5. h GSEA showed significant enrichment in the PI3K/AKT/MTOR signaling pathway. i , k , l Representative images of immunofluorescent staining ( i ) of P-mTOR (green), Iba1 (red), and DAPI (blue), the intensity of P-mTOR in microglia ( k ), and normalized intensity of P-mTOR in microglia ( l ) in the prefrontal cortex. Scale bar = 10 μm. n = 8. j , m-o Representative images ( j ) and quantitative analysis of Western blot showed the levels of P-mTOR/mTOR ( m ), P-Erk1/2/Erk1/2 ( n ), and P-GSK3β/GSK3β ( o ) in BV2 cells. n = 3. Ctrl: Wild-type nondiabetic group. T1D: Wild-type diabetic group. T1D + TREM2 cKO: TREM2 knockout diabetic group. DEGs: Differentially expressed genes. GO: Gene ontology. GSEA: Gene set enrichment analysis. NG: Normal glucose group. HG: High glucose group. HG + Aβ: High-glucose group with Aβ. HG + Vector + Aβ: High-glucose group with empty vector and Aβ. HG + TREM2-OE + Aβ: High-glucose group with TREM2 overexpression and Aβ. Data were presented as mean ± SEM. For in vivo studies, n represents the number of animals per group. For in vitro studies, n represents the number of biologically independent experiments performed. For d, g, k-o, One-way ANOVA. * p < 0.05, ** p < 0.01

Techniques: Functional Assay, Biomarker Discovery, Gene Expression, Staining, Electron Microscopy, Generated, Western Blot, Knock-Out, Plasmid Preparation, Over Expression, In Vivo, In Vitro

The TREM2-mTOR Axis Drives Microglial Clearance of Aβ in the Diabetic Brain. Accumulation of Aβ oligomers and upregulated TREM2 expression were observed in the prefrontal cortex of T1D mice. Under hyperglycemic conditions, Aβ activates TREM2, which phosphorylates its adaptor DAP12 and recruits Syk kinase. Syk then initiates the downstream PI3K-Akt-mTOR signaling pathway. This cascade enhances mitochondrial function and upregulates chemokines including Cxcl10, thereby enabling microglia to migrate toward, phagocytose, and clear Aβ oligomers efficiently. Collectively, these findings demonstrate that TREM2 plays a critical role in maintaining microglial homeostasis and countering Aβ pathology in T1D

Journal: Journal of Neuroinflammation

Article Title: Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology

doi: 10.1186/s12974-025-03611-3

Figure Lengend Snippet: The TREM2-mTOR Axis Drives Microglial Clearance of Aβ in the Diabetic Brain. Accumulation of Aβ oligomers and upregulated TREM2 expression were observed in the prefrontal cortex of T1D mice. Under hyperglycemic conditions, Aβ activates TREM2, which phosphorylates its adaptor DAP12 and recruits Syk kinase. Syk then initiates the downstream PI3K-Akt-mTOR signaling pathway. This cascade enhances mitochondrial function and upregulates chemokines including Cxcl10, thereby enabling microglia to migrate toward, phagocytose, and clear Aβ oligomers efficiently. Collectively, these findings demonstrate that TREM2 plays a critical role in maintaining microglial homeostasis and countering Aβ pathology in T1D

Techniques: Expressing

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