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miR-130b inhibits macrophage expression of <t>PGC-1α</t> and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).
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miR-130b inhibits macrophage expression <t>of</t> <t>PGC-1α</t> and <t>PPARγ</t> protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).
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miR-130b inhibits macrophage expression <t>of</t> <t>PGC-1α</t> and <t>PPARγ</t> protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).
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miR-130b inhibits macrophage expression <t>of</t> <t>PGC-1α</t> and <t>PPARγ</t> protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).
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Cell Signaling Technology Inc anti pparγ
miR-130b inhibits macrophage expression <t>of</t> <t>PGC-1α</t> and <t>PPARγ</t> protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).
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Image Search Results


miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Journal: iScience

Article Title: Deletion of miR-130b/301b cluster promotes macrophage efferocytosis and resolution of adipose tissue inflammation

doi: 10.1016/j.isci.2026.115307

Figure Lengend Snippet: miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Article Snippet: The blots were incubated with antibodies specific for PPARγ (Cell Signaling Technology, #2435), PGC-1α (Cell Signaling Technology, #4259), β-actin (Cell Signaling Technology, #5125), CX3CR1 (Abcam, ab308613), and GAPDH (Proteintech, 60004), and detected by enhanced chemiluminescence (Pierce).

Techniques: Expressing, Derivative Assay, Transfection, Negative Control, Isolation, Knock-Out, Incubation, Cell Culture

miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Journal: iScience

Article Title: Deletion of miR-130b/301b cluster promotes macrophage efferocytosis and resolution of adipose tissue inflammation

doi: 10.1016/j.isci.2026.115307

Figure Lengend Snippet: miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Article Snippet: The blots were incubated with antibodies specific for PPARγ (Cell Signaling Technology, #2435), PGC-1α (Cell Signaling Technology, #4259), β-actin (Cell Signaling Technology, #5125), CX3CR1 (Abcam, ab308613), and GAPDH (Proteintech, 60004), and detected by enhanced chemiluminescence (Pierce).

Techniques: Expressing, Derivative Assay, Transfection, Negative Control, Isolation, Knock-Out, Incubation, Cell Culture