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Proteintech pparγ
Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression <t>of</t> <t>PPARα</t> and <t>PPARγ,</t> which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
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1) Product Images from "A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques"

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.041

Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
Figure Legend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Techniques Used: Binding Assay, Construct, Expressing

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Article Snippet: .. Next, 4.5 μl anti-PPARg (Cat#16,643–1-AP, Proteintech, USA) or IgG (Cat#2729S, Cell Signaling Technology, USA) of the same species was added to the supernatant of output or IgG groups, respectively; then, 30 μl prewashed protein G-agarose was added to each tube, which was incubated overnight at 4 °C. ..

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Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression <t>of</t> <t>PPARα</t> and <t>PPARγ,</t> which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
Pparγ, supplied by Proteintech, 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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Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression <t>of</t> <t>PPARα</t> and <t>PPARγ,</t> which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
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Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression <t>of</t> <t>PPARα</t> and <t>PPARγ,</t> which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
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Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression <t>of</t> <t>PPARα</t> and <t>PPARγ,</t> which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.
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A Graphic scheme of adipogenic transdifferentiation induction protocol and microphotographs of control and transdifferentiated AsPC-1 cells at day 0, 3, 7, and 10; Rectangle dialog boxes magnify the field of view from the two groups. B Visualization of accumulated lipid droplets by oil red O staining in control and transdifferentiated AsPC-1 cells on day 10 after induction. Five random fields of view were used for quantification, values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. C Relative mRNA expression levels (normalized to ACTB expression from the same individual sample) of adipocyte markers adiponectin, CEBPA, <t>PPARG</t> , and FABP4 in eight human pancreatic cell lines. Values were presented as the mean ± SD ( n = 3 per group) and compared by Student’s t -test. Abbreviation: SD Standard deviation.
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A Graphic scheme of adipogenic transdifferentiation induction protocol and microphotographs of control and transdifferentiated AsPC-1 cells at day 0, 3, 7, and 10; Rectangle dialog boxes magnify the field of view from the two groups. B Visualization of accumulated lipid droplets by oil red O staining in control and transdifferentiated AsPC-1 cells on day 10 after induction. Five random fields of view were used for quantification, values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. C Relative mRNA expression levels (normalized to ACTB expression from the same individual sample) of adipocyte markers adiponectin, CEBPA, <t>PPARG</t> , and FABP4 in eight human pancreatic cell lines. Values were presented as the mean ± SD ( n = 3 per group) and compared by Student’s t -test. Abbreviation: SD Standard deviation.
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Image Search Results


Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Article Snippet: To block nonspecific binding, membranes were incubated with 5% skim milk for 1 h. Thereafter, membranes were incubated overnight at 4 °C with primary antibodies against ABCA1, ABCG1, ACOX1, CPT1A, LC3 (ab192890, 1:2000, abcam), LAMP1 (84658-5-RR, 1:8000, Proteintech), PPARα (66826-1-Ig, 1:3000, Proteintech), PPARγ (66936-1-Ig, 1:10000, Proteintech), P62 (18420-1-AP, 1:10000, Proteintech), MCAD (55210-1-AP, 1:3000, Proteintech), LCAD (17526-1-AP, 1:10000, Proteintech), tubulin (80762-1-RR, 1:10000, Proteintech), GAPDH (60004-1-Ig, 1:50000, Proteintech), and β-actin (66009-1-Ig, 1:20000, Proteintech).

Techniques: Binding Assay, Construct, Expressing

A Graphic scheme of adipogenic transdifferentiation induction protocol and microphotographs of control and transdifferentiated AsPC-1 cells at day 0, 3, 7, and 10; Rectangle dialog boxes magnify the field of view from the two groups. B Visualization of accumulated lipid droplets by oil red O staining in control and transdifferentiated AsPC-1 cells on day 10 after induction. Five random fields of view were used for quantification, values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. C Relative mRNA expression levels (normalized to ACTB expression from the same individual sample) of adipocyte markers adiponectin, CEBPA, PPARG , and FABP4 in eight human pancreatic cell lines. Values were presented as the mean ± SD ( n = 3 per group) and compared by Student’s t -test. Abbreviation: SD Standard deviation.

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: A Graphic scheme of adipogenic transdifferentiation induction protocol and microphotographs of control and transdifferentiated AsPC-1 cells at day 0, 3, 7, and 10; Rectangle dialog boxes magnify the field of view from the two groups. B Visualization of accumulated lipid droplets by oil red O staining in control and transdifferentiated AsPC-1 cells on day 10 after induction. Five random fields of view were used for quantification, values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. C Relative mRNA expression levels (normalized to ACTB expression from the same individual sample) of adipocyte markers adiponectin, CEBPA, PPARG , and FABP4 in eight human pancreatic cell lines. Values were presented as the mean ± SD ( n = 3 per group) and compared by Student’s t -test. Abbreviation: SD Standard deviation.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Control, Staining, Expressing, Standard Deviation

Visualization and quantification of immunostaining of CEBPA ( A ), PPARG ( B ), and FABP4 ( C ) in control and transdifferentiated AsPC-1 cells on day 10. The protein expression levels were quantified by integrated intensity and positive area of five random fields of view. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. D The protein expression levels of CEBPA and PPARG as adipogenesis markers and GAPDH as reference marker in AsPC-1. Abbreviation: SD standard deviation.

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: Visualization and quantification of immunostaining of CEBPA ( A ), PPARG ( B ), and FABP4 ( C ) in control and transdifferentiated AsPC-1 cells on day 10. The protein expression levels were quantified by integrated intensity and positive area of five random fields of view. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. D The protein expression levels of CEBPA and PPARG as adipogenesis markers and GAPDH as reference marker in AsPC-1. Abbreviation: SD standard deviation.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Immunostaining, Control, Expressing, Marker, Standard Deviation

A Schematic illustration of orthotopic PDAC models workflow. B , C Orthotopic PDAC samples collected from control and transdifferentiated groups. Tumors were outlined with yellow dashes. Tumor weight and tumor volume were presented as mean ± SD ( n = 5 per group) and compared by Student’s t -test. D Relative mRNA expression levels of adipogenesis markers (CEBPA, PPARG, FABP4, and adiponectin), EMT markers (E-cadherin and vimentin), and EMT-TFs (Snail1, Snail2, Twist1, Twist2, ZEB1, and ZEB2) in control and transdifferentiated groups. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. E Volcano map of differentially expressed genes (DEGs) between control and transdifferentiated group ( n = 5 per group). F GO term analysis of DEGs based on gene counts showed significantly downregulated pathways in transdifferentiated group, indicating reduced angiogenesis, cellular response to cytokines, extracellular matrix organization, and cell migration. G BODIPY detection of lipid droplets in control and transdifferentiated groups from orthotopic PDAC samples. Tumors were outlined with white dashes; a representative view of fields was magnified and displayed in Fig. . Abbreviation: PDAC Pancreatic ductal adenocarcinoma, SD Standard deviation, EMT epithelial-mesenchymal transition, TF transcription factor; DEG differentially expressed genes, GO Gene ontology.

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: A Schematic illustration of orthotopic PDAC models workflow. B , C Orthotopic PDAC samples collected from control and transdifferentiated groups. Tumors were outlined with yellow dashes. Tumor weight and tumor volume were presented as mean ± SD ( n = 5 per group) and compared by Student’s t -test. D Relative mRNA expression levels of adipogenesis markers (CEBPA, PPARG, FABP4, and adiponectin), EMT markers (E-cadherin and vimentin), and EMT-TFs (Snail1, Snail2, Twist1, Twist2, ZEB1, and ZEB2) in control and transdifferentiated groups. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. E Volcano map of differentially expressed genes (DEGs) between control and transdifferentiated group ( n = 5 per group). F GO term analysis of DEGs based on gene counts showed significantly downregulated pathways in transdifferentiated group, indicating reduced angiogenesis, cellular response to cytokines, extracellular matrix organization, and cell migration. G BODIPY detection of lipid droplets in control and transdifferentiated groups from orthotopic PDAC samples. Tumors were outlined with white dashes; a representative view of fields was magnified and displayed in Fig. . Abbreviation: PDAC Pancreatic ductal adenocarcinoma, SD Standard deviation, EMT epithelial-mesenchymal transition, TF transcription factor; DEG differentially expressed genes, GO Gene ontology.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Control, Expressing, Migration, Standard Deviation