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MedChemExpress pim1 protein

Figure 1. <t>PIM1</t> is significantly elevated in human unstable carotid atherosclerosis plaques and mouse advanced atherosclerosis plaques. (A) Uniform manifold approximation and projection (UMAP) visualization of vascular cells. (B) Dot plot overview of expression of key marker genes identified for the cell types. (C) Volcano plot showing differential expression genes of endothelial cells in 0 weeks and 26 weeks. (D) Volcano plot showing differential expression genes of HUVECs in normal status and EndMT status. (E) Venn diagram showing 13 overlapping genes between genes differentially expressed in mouse atherosclerotic plaques and genes identified in HUVECs. (F) The expression level of PIM1 in endothelial cells of atherosclerotic plaques at different time points. (G) Representative Western blot images and quantification of PIM1 levels in arcus aortae and thoracic aorta from normal diet (ND) and high fat diet (HFD) mice. (H) Representative immunohistochemical and immunofluorescence images of PIM1 in sections of carotid artery of ApoE–/– mice fed a normal diet (ND) and high fat diet (HFD) mice (n = 5). Scale bar of immunohistochemical = 100 μm, Scale bar of immunofluorescence = 50 μm. (I) The PIM1 expression levels analysis based on RNA-seq data from GSE43292. (J) Representative H&E, Masson and immunohistochemical, immunofluorescence images of PIM1 on stable and unstable plaques sections from human carotid artery (n = 10). Scale bar of H&E, Masson and immunohistochemical = 100 μm, Scale bar of immunofluorescence = 500 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Pim1 Protein, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis."

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

Journal: Theranostics

doi: 10.7150/thno.102597

Figure 1. PIM1 is significantly elevated in human unstable carotid atherosclerosis plaques and mouse advanced atherosclerosis plaques. (A) Uniform manifold approximation and projection (UMAP) visualization of vascular cells. (B) Dot plot overview of expression of key marker genes identified for the cell types. (C) Volcano plot showing differential expression genes of endothelial cells in 0 weeks and 26 weeks. (D) Volcano plot showing differential expression genes of HUVECs in normal status and EndMT status. (E) Venn diagram showing 13 overlapping genes between genes differentially expressed in mouse atherosclerotic plaques and genes identified in HUVECs. (F) The expression level of PIM1 in endothelial cells of atherosclerotic plaques at different time points. (G) Representative Western blot images and quantification of PIM1 levels in arcus aortae and thoracic aorta from normal diet (ND) and high fat diet (HFD) mice. (H) Representative immunohistochemical and immunofluorescence images of PIM1 in sections of carotid artery of ApoE–/– mice fed a normal diet (ND) and high fat diet (HFD) mice (n = 5). Scale bar of immunohistochemical = 100 μm, Scale bar of immunofluorescence = 50 μm. (I) The PIM1 expression levels analysis based on RNA-seq data from GSE43292. (J) Representative H&E, Masson and immunohistochemical, immunofluorescence images of PIM1 on stable and unstable plaques sections from human carotid artery (n = 10). Scale bar of H&E, Masson and immunohistochemical = 100 μm, Scale bar of immunofluorescence = 500 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Figure Legend Snippet: Figure 1. PIM1 is significantly elevated in human unstable carotid atherosclerosis plaques and mouse advanced atherosclerosis plaques. (A) Uniform manifold approximation and projection (UMAP) visualization of vascular cells. (B) Dot plot overview of expression of key marker genes identified for the cell types. (C) Volcano plot showing differential expression genes of endothelial cells in 0 weeks and 26 weeks. (D) Volcano plot showing differential expression genes of HUVECs in normal status and EndMT status. (E) Venn diagram showing 13 overlapping genes between genes differentially expressed in mouse atherosclerotic plaques and genes identified in HUVECs. (F) The expression level of PIM1 in endothelial cells of atherosclerotic plaques at different time points. (G) Representative Western blot images and quantification of PIM1 levels in arcus aortae and thoracic aorta from normal diet (ND) and high fat diet (HFD) mice. (H) Representative immunohistochemical and immunofluorescence images of PIM1 in sections of carotid artery of ApoE–/– mice fed a normal diet (ND) and high fat diet (HFD) mice (n = 5). Scale bar of immunohistochemical = 100 μm, Scale bar of immunofluorescence = 50 μm. (I) The PIM1 expression levels analysis based on RNA-seq data from GSE43292. (J) Representative H&E, Masson and immunohistochemical, immunofluorescence images of PIM1 on stable and unstable plaques sections from human carotid artery (n = 10). Scale bar of H&E, Masson and immunohistochemical = 100 μm, Scale bar of immunofluorescence = 500 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques Used: Expressing, Marker, Quantitative Proteomics, Western Blot, Immunohistochemical staining, Immunofluorescence, RNA Sequencing

Figure 2. PIM1 is upregulated in endothelial cells under the conditions of ox-LDL stimulation. (A-C) qRT-PCR showing the transcript levels of ZEB1, ZO-1, VE-Cadherin. N-Cadherin, CD31, α-SMA, Slug, Snail and TAGLN in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (D) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (E) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (F) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (G) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (H) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated HUVEC. Scale bar = 20 μm. (I) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated MAEC. Scale bar = 20 μm. qRT-PCR Graph is representative of fold change relative to vehicle-treated control cells normalized to 1 (dashed line). Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Figure Legend Snippet: Figure 2. PIM1 is upregulated in endothelial cells under the conditions of ox-LDL stimulation. (A-C) qRT-PCR showing the transcript levels of ZEB1, ZO-1, VE-Cadherin. N-Cadherin, CD31, α-SMA, Slug, Snail and TAGLN in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (D) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (E) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (F) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (G) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (H) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated HUVEC. Scale bar = 20 μm. (I) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated MAEC. Scale bar = 20 μm. qRT-PCR Graph is representative of fold change relative to vehicle-treated control cells normalized to 1 (dashed line). Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques Used: Quantitative RT-PCR, Western Blot, Immunofluorescence, Expressing, Control

Figure 3. PIM1 silence attenuates the process of EndMT. (A) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail mRNA levels in HUVEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (B) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail

Figure Legend Snippet: Figure 3. PIM1 silence attenuates the process of EndMT. (A) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail mRNA levels in HUVEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (B) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail

Techniques Used: Quantitative RT-PCR

Figure 5. Endothelial cell–specific PIM1 knockdown reduces EndMT and attenuates atherosclerotic plaque progress. (A) Representative photographs and plaques area quantification of atherosclerotic plaques in the aortic arches and carotid artery in the 2 groups (n = 10). (B) Representative oil red O staining images and quantification of the atherosclerotic lesions in the whole aorta in the 2 groups (n = 10). (C) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the aortic root in the 2 groups (n = 10). Scale bar=500 μm. (D) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the carotid artery bifurcation in the 2 groups (n = 10). Scale bar=100 μm. (E) Representative immunohistochemical staining images of PIM1 protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500μm. Scale bar of carotid artery bifurcation =100 μm. (F) Representative immunohistochemical staining images of VE-Cadherin protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (G) Representative immunohistochemical staining images of Slug protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (H) Representative immunohistochemical staining images of Snail protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Figure Legend Snippet: Figure 5. Endothelial cell–specific PIM1 knockdown reduces EndMT and attenuates atherosclerotic plaque progress. (A) Representative photographs and plaques area quantification of atherosclerotic plaques in the aortic arches and carotid artery in the 2 groups (n = 10). (B) Representative oil red O staining images and quantification of the atherosclerotic lesions in the whole aorta in the 2 groups (n = 10). (C) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the aortic root in the 2 groups (n = 10). Scale bar=500 μm. (D) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the carotid artery bifurcation in the 2 groups (n = 10). Scale bar=100 μm. (E) Representative immunohistochemical staining images of PIM1 protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500μm. Scale bar of carotid artery bifurcation =100 μm. (F) Representative immunohistochemical staining images of VE-Cadherin protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (G) Representative immunohistochemical staining images of Slug protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (H) Representative immunohistochemical staining images of Snail protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques Used: Knockdown, Staining, Immunohistochemical staining

$Figure 6. PIM1 promotes the EndMT of endothelial cell through phosphorylation of NDRG1 at Ser-330. (A) The proteins of input, IgG and anti-PIM1 were purified and size fractionated on 10% SDS-PAGE. The gel was stained by coomassie brilliant blue staining. (B) Venn diagram showing 1 overlapping protein (NDRG1) between protein mass spectrometry and already reported PIM1 phosphorylated substrates. (C) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (D) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC and MAEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (E) Molecular simulations and protein docking of PIM1 and NDRG1. (F) Schematic diagrams of 6*His-Tagged full-length (WT) NDRG1, and their various deletion mutants (180-294aa, and 326-394aa) (Top). HEK 293T cells were co-transfected with His-Tagged NDRG1 or its deletion mutants or vectors, and whole cell lysates were assessed by immunoprecipitation followed by immunoblotting with anti-His-Tag and anti-PIM1 (bottom). (G) Schematic diagrams of Myc-Tagged wildtype (WT) PIM1, and Myc-Tagged mutant (Mut) PIM1. (H) HEK 293T cells were co-transfected with Myc-Tagged wildtype (WT) PIM1, Myc-Tagged mutant (Mut) PIM1 and whole cell lysates were assessed by immunoprecipitation followed by$
Figure Legend Snippet: Figure 6. PIM1 promotes the EndMT of endothelial cell through phosphorylation of NDRG1 at Ser-330. (A) The proteins of input, IgG and anti-PIM1 were purified and size fractionated on 10% SDS-PAGE. The gel was stained by coomassie brilliant blue staining. (B) Venn diagram showing 1 overlapping protein (NDRG1) between protein mass spectrometry and already reported PIM1 phosphorylated substrates. (C) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (D) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC and MAEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (E) Molecular simulations and protein docking of PIM1 and NDRG1. (F) Schematic diagrams of 6*His-Tagged full-length (WT) NDRG1, and their various deletion mutants (180-294aa, and 326-394aa) (Top). HEK 293T cells were co-transfected with His-Tagged NDRG1 or its deletion mutants or vectors, and whole cell lysates were assessed by immunoprecipitation followed by immunoblotting with anti-His-Tag and anti-PIM1 (bottom). (G) Schematic diagrams of Myc-Tagged wildtype (WT) PIM1, and Myc-Tagged mutant (Mut) PIM1. (H) HEK 293T cells were co-transfected with Myc-Tagged wildtype (WT) PIM1, Myc-Tagged mutant (Mut) PIM1 and whole cell lysates were assessed by immunoprecipitation followed by

Techniques Used: Phospho-proteomics, Purification, SDS Page, Staining, Mass Spectrometry, Western Blot, Transfection, Immunoprecipitation, Mutagenesis

Figure 7. NDRG1 is Required for PIM1-Induced EndMT. (A) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC pretreated with shNC or shNDRG1-1, shNDRG1-2 and stimulated with H2O2 (200 μM)

Figure Legend Snippet: Figure 7. NDRG1 is Required for PIM1-Induced EndMT. (A) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC pretreated with shNC or shNDRG1-1, shNDRG1-2 and stimulated with H2O2 (200 μM)

Techniques Used: Western Blot

Image Search Results

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 1. PIM1 is significantly elevated in human unstable carotid atherosclerosis plaques and mouse advanced atherosclerosis plaques. (A) Uniform manifold approximation and projection (UMAP) visualization of vascular cells. (B) Dot plot overview of expression of key marker genes identified for the cell types. (C) Volcano plot showing differential expression genes of endothelial cells in 0 weeks and 26 weeks. (D) Volcano plot showing differential expression genes of HUVECs in normal status and EndMT status. (E) Venn diagram showing 13 overlapping genes between genes differentially expressed in mouse atherosclerotic plaques and genes identified in HUVECs. (F) The expression level of PIM1 in endothelial cells of atherosclerotic plaques at different time points. (G) Representative Western blot images and quantification of PIM1 levels in arcus aortae and thoracic aorta from normal diet (ND) and high fat diet (HFD) mice. (H) Representative immunohistochemical and immunofluorescence images of PIM1 in sections of carotid artery of ApoE–/– mice fed a normal diet (ND) and high fat diet (HFD) mice (n = 5). Scale bar of immunohistochemical = 100 μm, Scale bar of immunofluorescence = 50 μm. (I) The PIM1 expression levels analysis based on RNA-seq data from GSE43292. (J) Representative H&E, Masson and immunohistochemical, immunofluorescence images of PIM1 on stable and unstable plaques sections from human carotid artery (n = 10). Scale bar of H&E, Masson and immunohistochemical = 100 μm, Scale bar of immunofluorescence = 500 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: PIM1 protein (HY-P701745, MCE), PTBP1 protein (Ag28404, Proteintech), and small molecule Max-40279 (HY-145723, MCE; 500 nM) binding activities were generated with the SPR system, and the binding signal was exhibited by the response (RU) value.

Techniques: Expressing, Marker, Quantitative Proteomics, Western Blot, Immunohistochemical staining, Immunofluorescence, RNA Sequencing

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 2. PIM1 is upregulated in endothelial cells under the conditions of ox-LDL stimulation. (A-C) qRT-PCR showing the transcript levels of ZEB1, ZO-1, VE-Cadherin. N-Cadherin, CD31, α-SMA, Slug, Snail and TAGLN in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (D) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (E) qRT-PCR showing the transcript levels of PIM1 in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (F) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with ox-LDL (100 μg/mL, 48 h). (G) Representative Western blot images and quantification of PIM1, PIM1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (H) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated HUVEC. Scale bar = 20 μm. (I) Representative immunofluorescence images to detect PIM1 expression in 100 μg/mL ox-LDL-stimulated MAEC. Scale bar = 20 μm. qRT-PCR Graph is representative of fold change relative to vehicle-treated control cells normalized to 1 (dashed line). Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques: Quantitative RT-PCR, Western Blot, Immunofluorescence, Expressing, Control

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 3. PIM1 silence attenuates the process of EndMT. (A) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail mRNA levels in HUVEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (B) qRT-PCR analysis of PIM1, CD31, VE-Cadherin, α-SMA, Slug and Snail

Techniques: Quantitative RT-PCR

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 5. Endothelial cell–specific PIM1 knockdown reduces EndMT and attenuates atherosclerotic plaque progress. (A) Representative photographs and plaques area quantification of atherosclerotic plaques in the aortic arches and carotid artery in the 2 groups (n = 10). (B) Representative oil red O staining images and quantification of the atherosclerotic lesions in the whole aorta in the 2 groups (n = 10). (C) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the aortic root in the 2 groups (n = 10). Scale bar=500 μm. (D) Representative H&E staining images (top), oil red O staining images (middle), Masson staining images (bottom) and quantification of the atherosclerotic lesion area, oil red O positive percentage, collagen positive percentage in the carotid artery bifurcation in the 2 groups (n = 10). Scale bar=100 μm. (E) Representative immunohistochemical staining images of PIM1 protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500μm. Scale bar of carotid artery bifurcation =100 μm. (F) Representative immunohistochemical staining images of VE-Cadherin protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (G) Representative immunohistochemical staining images of Slug protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. (H) Representative immunohistochemical staining images of Snail protein levels in aortic root and carotid artery bifurcation sections in the 2 groups (n = 10). Scale bar of aortic root =500 μm. Scale bar of carotid artery bifurcation =100 μm. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

Techniques: Knockdown, Staining, Immunohistochemical staining

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 6. PIM1 promotes the EndMT of endothelial cell through phosphorylation of NDRG1 at Ser-330. (A) The proteins of input, IgG and anti-PIM1 were purified and size fractionated on 10% SDS-PAGE. The gel was stained by coomassie brilliant blue staining. (B) Venn diagram showing 1 overlapping protein (NDRG1) between protein mass spectrometry and already reported PIM1 phosphorylated substrates. (C) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC, MAEC and MPLEC treated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (D) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1 protein levels in HUVEC and MAEC pretreated with siNC or siPIM1-1, siPIM1-2 and stimulated with H2O2 (200 μM) and TGF-β (50 ng/mL, 48 h). (E) Molecular simulations and protein docking of PIM1 and NDRG1. (F) Schematic diagrams of 6*His-Tagged full-length (WT) NDRG1, and their various deletion mutants (180-294aa, and 326-394aa) (Top). HEK 293T cells were co-transfected with His-Tagged NDRG1 or its deletion mutants or vectors, and whole cell lysates were assessed by immunoprecipitation followed by immunoblotting with anti-His-Tag and anti-PIM1 (bottom). (G) Schematic diagrams of Myc-Tagged wildtype (WT) PIM1, and Myc-Tagged mutant (Mut) PIM1. (H) HEK 293T cells were co-transfected with Myc-Tagged wildtype (WT) PIM1, Myc-Tagged mutant (Mut) PIM1 and whole cell lysates were assessed by immunoprecipitation followed by

Techniques: Phospho-proteomics, Purification, SDS Page, Staining, Mass Spectrometry, Western Blot, Transfection, Immunoprecipitation, Mutagenesis

Journal: Theranostics

Article Title: PIM1 instigates endothelial-to-mesenchymal transition to aggravate atherosclerosis.

doi: 10.7150/thno.102597

Figure Lengend Snippet: Figure 7. NDRG1 is Required for PIM1-Induced EndMT. (A) Representative Western blot images and quantification of P-NDRG1(S330), NDRG1, ZO-1, ZEB1, CD31, N-Cadherin, VE-Cadherin, Vimentin, α-SMA, Slug, Snail and TAGLN levels in HUVEC pretreated with shNC or shNDRG1-1, shNDRG1-2 and stimulated with H2O2 (200 μM)

Techniques: Western Blot

Schematic illustration of A) bioinformatic analysis and B) clinical research guided novel target PIM1, C) regulatory mechanism of PIM1 for sepsis‐induced coagulopathy both in vivo and in vitro, and D) the preparation of multifunctional co‐delivery systems of PIM1 inhibitors and the antisepsis process in vivo.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: Schematic illustration of A) bioinformatic analysis and B) clinical research guided novel target PIM1, C) regulatory mechanism of PIM1 for sepsis‐induced coagulopathy both in vivo and in vitro, and D) the preparation of multifunctional co‐delivery systems of PIM1 inhibitors and the antisepsis process in vivo.

Article Snippet: The concentrations of PIM1 (CSB‐ E11825 h, Cusabio, China) in human plasma and TAT (CSB‐ E08433 m, Cusabio, China), Fbg (CSB‐ E08202 m, Cusabio, China), and D2D (CSB‐ E13584 m, Cusabio, China) in mouse plasma were assessed using ELISA kits according to the guidelines outlined in the respective ELISA kits.

Techniques: In Vivo, In Vitro

Identification and screening of key prognosis‐related genes. A) Forest plots illustrate the findings of a multivariate Cox regression analysis examining the relationship between the PRGs and 28‐day survival in patients with sepsis. B) Forest plot of the associations between the six prognostic molecules and 28‐day survival in patients with sepsis. C) Venn diagram of PRGs from Cox regression analysis and LASSO‐Cox regression analysis. D) Expression of two key PRGs (PIM1 and PILRA) in patients with sepsis and healthy controls. E) Expression of PIM1 and PILRA in dead group and alive group among patients with sepsis. F) Kaplan‐Meier curve of 28‐day survival for patients with sepsis and high and low expression of PIM1. G) ROC curves of PIM1 for the prediction of sepsis. Each bar represents the mean ± SD. The comparison between the two groups was performed using unpaired Student t‐tests (D and E).

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: Identification and screening of key prognosis‐related genes. A) Forest plots illustrate the findings of a multivariate Cox regression analysis examining the relationship between the PRGs and 28‐day survival in patients with sepsis. B) Forest plot of the associations between the six prognostic molecules and 28‐day survival in patients with sepsis. C) Venn diagram of PRGs from Cox regression analysis and LASSO‐Cox regression analysis. D) Expression of two key PRGs (PIM1 and PILRA) in patients with sepsis and healthy controls. E) Expression of PIM1 and PILRA in dead group and alive group among patients with sepsis. F) Kaplan‐Meier curve of 28‐day survival for patients with sepsis and high and low expression of PIM1. G) ROC curves of PIM1 for the prediction of sepsis. Each bar represents the mean ± SD. The comparison between the two groups was performed using unpaired Student t‐tests (D and E).

Techniques: Expressing, Comparison

Elevated expression of PIM1 correlates with disordered coagulation in patients with sepsis. A,B) Scatter plot and linear regression analysis between PIM1 and coagulation factors (F2 and F3) in the GSE65682 dataset. C) Plasma PIM1 levels by ELISA between healthy control and patients with sepsis. D) Plasma PIM1 levels by ELISA between patients with sepsis with and without DIC. E) Plasma PIM1 levels by ELISA between patients with sepsis with and without SIC. F) ROC curve for plasma PIM1 to discriminate between patients with sepsis and healthy volunteers, patients with DIC and non‐DIC sepsis, and patients with SIC and non‐SIC sepsis. G–J) Scatter plot and linear regression analysis between ELISA PIM1 and laboratory measurements of (G) PT, (H) INR, (I) APTT, and (J) platelet count. K) Plasma PIM1 levels by ELISA in patients with sepsis between survivors and non‐survivors. L) ROC curves for PIM1, APTT, SOFA score, and APACHEII score to predict 28‐day mortality in patients with sepsis. ELISA, enzyme‐linked immunosorbent assay; DIC, disseminated intravascular coagulation; SIC, sepsis‐induced coagulation; SOFA, sequential organ failure assessment; APACHE, acute physiology and chronic health evaluation. Each bar represents the mean ± SD. The comparison between the two groups was performed using an unpaired Student's t ‐test (C‐E and K). * p < 0.05, ** p < 0.01, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: Elevated expression of PIM1 correlates with disordered coagulation in patients with sepsis. A,B) Scatter plot and linear regression analysis between PIM1 and coagulation factors (F2 and F3) in the GSE65682 dataset. C) Plasma PIM1 levels by ELISA between healthy control and patients with sepsis. D) Plasma PIM1 levels by ELISA between patients with sepsis with and without DIC. E) Plasma PIM1 levels by ELISA between patients with sepsis with and without SIC. F) ROC curve for plasma PIM1 to discriminate between patients with sepsis and healthy volunteers, patients with DIC and non‐DIC sepsis, and patients with SIC and non‐SIC sepsis. G–J) Scatter plot and linear regression analysis between ELISA PIM1 and laboratory measurements of (G) PT, (H) INR, (I) APTT, and (J) platelet count. K) Plasma PIM1 levels by ELISA in patients with sepsis between survivors and non‐survivors. L) ROC curves for PIM1, APTT, SOFA score, and APACHEII score to predict 28‐day mortality in patients with sepsis. ELISA, enzyme‐linked immunosorbent assay; DIC, disseminated intravascular coagulation; SIC, sepsis‐induced coagulation; SOFA, sequential organ failure assessment; APACHE, acute physiology and chronic health evaluation. Each bar represents the mean ± SD. The comparison between the two groups was performed using an unpaired Student's t ‐test (C‐E and K). * p < 0.05, ** p < 0.01, **** p < 0.0001.

Techniques: Expressing, Coagulation, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Comparison

PIM1 inhibitor SMI‐4a protects septic mice against coagulation activation and sepsis‐induced acute lung injury. A) Schematic representation of animal experimental procedures. B) Representative western blot membranes and corresponding densitometric analyses of (C) PIM1 in lung tissue (n = 6/group). D) mRNA levels of PIM1 in murine lung tissues (n = 5/group). E) Platelet count in mice (n = 4/group). F–H) Plasma levels of coagulation‐related factors in mice plasma by ELISA, including (F) TAT, (G) D‐dimer, and (H) fibrinogen (n = 4/group). I) The lung sections were subjected to hematoxylin and eosin (HE) staining, F4/80, fibrin, and PIM1 immunohistochemical analysis (n = 4/group; scale bar:50 µm). J) Representative western blot membranes and corresponding densitometric analyses of (K) TF, (L) PAI‐1, (M) Thrombin in lung tissue (n = 6/group). N) mRNA levels of TF in murine lung tissues (n = 5/group). O–Q) mRNA levels of (O) IL‐1β, (P) IL‐6, and (Q) TNF‐ɑ in murine lung tissues (n = 5/group). R) Survival curves of mice in all groups (n = 10/group). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (C‐H and K‐Q). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: PIM1 inhibitor SMI‐4a protects septic mice against coagulation activation and sepsis‐induced acute lung injury. A) Schematic representation of animal experimental procedures. B) Representative western blot membranes and corresponding densitometric analyses of (C) PIM1 in lung tissue (n = 6/group). D) mRNA levels of PIM1 in murine lung tissues (n = 5/group). E) Platelet count in mice (n = 4/group). F–H) Plasma levels of coagulation‐related factors in mice plasma by ELISA, including (F) TAT, (G) D‐dimer, and (H) fibrinogen (n = 4/group). I) The lung sections were subjected to hematoxylin and eosin (HE) staining, F4/80, fibrin, and PIM1 immunohistochemical analysis (n = 4/group; scale bar:50 µm). J) Representative western blot membranes and corresponding densitometric analyses of (K) TF, (L) PAI‐1, (M) Thrombin in lung tissue (n = 6/group). N) mRNA levels of TF in murine lung tissues (n = 5/group). O–Q) mRNA levels of (O) IL‐1β, (P) IL‐6, and (Q) TNF‐ɑ in murine lung tissues (n = 5/group). R) Survival curves of mice in all groups (n = 10/group). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (C‐H and K‐Q). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Coagulation, Activation Assay, Western Blot, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Staining, Immunohistochemical staining

PIM1 inhibitor SMI‐4a reduces TF expression by downregulating mTOR phosphorylation via the AKT and MAPK pathways in vivo and in vitro. A) Representative western blot membranes and corresponding densitometric analyses of (B) PIM1 and (C) TF in RAW264.7 cells (n = 3/group). D) Representative images of immunofluorescence staining of PIM1 in RAW264.7 cells (400 ×, scale bar: 50 µm). E–I) mRNA levels of (E) TF, (F) PAI‐1, (G) IL‐1β, (H) IL‐6, and (I) TNF‐ɑ in RAW264.7 cells (n = 3/group). J) KEGG enrichment analysis of DEGs between RAW264.7 cells with and without SMI‐4a pretreated before stimulation of LPS. K) Schematic diagram of the potential signaling pathways involved between PIM1 and coagulation activation in sepsis. L) Representative western blot membranes and corresponding densitometric analyses of (M) p‐AKT, (N) p‐ERK, (O) p‐mTOR, and (P) p‐p70s6k in lung tissue (n = 6/group). Q) Representative western blot membranes of p‐AKT, p‐ERK, p‐mTOR, and p‐p70s6k in RAW264.7 cells (n = 3/group). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (B‐C, E‐I, and M‐P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: PIM1 inhibitor SMI‐4a reduces TF expression by downregulating mTOR phosphorylation via the AKT and MAPK pathways in vivo and in vitro. A) Representative western blot membranes and corresponding densitometric analyses of (B) PIM1 and (C) TF in RAW264.7 cells (n = 3/group). D) Representative images of immunofluorescence staining of PIM1 in RAW264.7 cells (400 ×, scale bar: 50 µm). E–I) mRNA levels of (E) TF, (F) PAI‐1, (G) IL‐1β, (H) IL‐6, and (I) TNF‐ɑ in RAW264.7 cells (n = 3/group). J) KEGG enrichment analysis of DEGs between RAW264.7 cells with and without SMI‐4a pretreated before stimulation of LPS. K) Schematic diagram of the potential signaling pathways involved between PIM1 and coagulation activation in sepsis. L) Representative western blot membranes and corresponding densitometric analyses of (M) p‐AKT, (N) p‐ERK, (O) p‐mTOR, and (P) p‐p70s6k in lung tissue (n = 6/group). Q) Representative western blot membranes of p‐AKT, p‐ERK, p‐mTOR, and p‐p70s6k in RAW264.7 cells (n = 3/group). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (B‐C, E‐I, and M‐P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Expressing, Phospho-proteomics, In Vivo, In Vitro, Western Blot, Immunofluorescence, Staining, Protein-Protein interactions, Coagulation, Activation Assay

PIM1 knockdown reduces the expression of TF in RAW264.7 cells stimulated with LPS by downregulating mTOR phosphorylation via the AKT and MAPK pathways. A) mRNA expression of PIM1 in RAW264.7 cells transfected with siNC or siPIM1. B) Western blot images and corresponding densitometric analyses of (C) PIM1 expression in RAW264.7 transfected with siNC or siPIM1. D, E) mRNA expression of (D) PIM1 and (E) TF in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. F) Western blot images and corresponding densitometric analyses of (G) PIM1 and (H) TF in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. I–L) mRNA expression of (I) PAI‐1, (J) IL‐1β, (K) IL‐6, and (L) TNF‐ɑ in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. M, P) Western blot images and corresponding densitometric analyses of N) p‐AKT, O) p‐ERK, Q) p‐mTOR, and R) p‐p70s6k in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (A, C–E, G–L, N,O, and Q,R). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: PIM1 knockdown reduces the expression of TF in RAW264.7 cells stimulated with LPS by downregulating mTOR phosphorylation via the AKT and MAPK pathways. A) mRNA expression of PIM1 in RAW264.7 cells transfected with siNC or siPIM1. B) Western blot images and corresponding densitometric analyses of (C) PIM1 expression in RAW264.7 transfected with siNC or siPIM1. D, E) mRNA expression of (D) PIM1 and (E) TF in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. F) Western blot images and corresponding densitometric analyses of (G) PIM1 and (H) TF in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. I–L) mRNA expression of (I) PAI‐1, (J) IL‐1β, (K) IL‐6, and (L) TNF‐ɑ in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. M, P) Western blot images and corresponding densitometric analyses of N) p‐AKT, O) p‐ERK, Q) p‐mTOR, and R) p‐p70s6k in RAW264.7 cells transfected with siNC or siPIM1 under stimulation of LPS. Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (A, C–E, G–L, N,O, and Q,R). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Knockdown, Expressing, Phospho-proteomics, Transfection, Western Blot

NPs knock down PIM1 expression and reduce the expression of TF in RAW264.7 cells. A) Western blot images and corresponding densitometric analyses of B) PIM1 expression in RAW264.7 pretreated with different NPs (n = 3). C) Western blot images and corresponding densitometric analyses of D) PIM1 and E) TF expression in RAW264.7 cells (n = 3). F–K) mRNA expression of F) PIM1, G) TF, H) PAI‐1, I) IL‐1β, J) IL‐6, and K) TNF‐ɑ measured by RT‐qPCR. Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (B and D–K). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: NPs knock down PIM1 expression and reduce the expression of TF in RAW264.7 cells. A) Western blot images and corresponding densitometric analyses of B) PIM1 expression in RAW264.7 pretreated with different NPs (n = 3). C) Western blot images and corresponding densitometric analyses of D) PIM1 and E) TF expression in RAW264.7 cells (n = 3). F–K) mRNA expression of F) PIM1, G) TF, H) PAI‐1, I) IL‐1β, J) IL‐6, and K) TNF‐ɑ measured by RT‐qPCR. Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (B and D–K). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Knockdown, Expressing, Western Blot, Quantitative RT-PCR

In vivo therapeutic effect of NPs in LPS‐induced septic mouse model. A) Ex vivo NIR imaging of major organs (heart, lung, kidneys, spleen, and liver) in mice. B) Survival rate of septic mice within 72 h after different treatments (n = 10/group). C) Western blot images and corresponding densitometric analyses of (D) PIM1 expression in the lung tissue (n = 6/group). E) mRNA expression of PIM1 in lung tissue measured by RT‐qPCR (n = 5). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (D and E). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Small (Weinheim an Der Bergstrasse, Germany)

Article Title: Multifunctional Co‐Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF‐Mediated Coagulopathy in Sepsis

doi: 10.1002/smll.202412688

Figure Lengend Snippet: In vivo therapeutic effect of NPs in LPS‐induced septic mouse model. A) Ex vivo NIR imaging of major organs (heart, lung, kidneys, spleen, and liver) in mice. B) Survival rate of septic mice within 72 h after different treatments (n = 10/group). C) Western blot images and corresponding densitometric analyses of (D) PIM1 expression in the lung tissue (n = 6/group). E) mRNA expression of PIM1 in lung tissue measured by RT‐qPCR (n = 5). Each bar represents the mean ± SD. Statistical analysis for three or more groups was carried out using one‐way ANOVA (D and E). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: In Vivo, Ex Vivo, Imaging, Western Blot, Expressing, Quantitative RT-PCR

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