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BioVendor Instruments resource source identifier antibodies anti fgf21 biovendor
Resource Source Identifier Antibodies Anti Fgf21 Biovendor, supplied by BioVendor Instruments, used in various techniques. Bioz Stars score: 94/100, based on 134 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 134 article reviews

resource source identifier antibodies anti fgf21 biovendor - by Bioz Stars, 2026-07

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β-Klotho and FGF21 immunoreactivity in hepatic lesions of a 40-week-old TSOD mouse. ( A – C ) Representative views of CCF on H&E. ( D ) Serial section of the same regions as ( A ), stained for β-Klotho, revealing strong immunoreactivity corresponding to the CCF. ( E ) Serial section of the same regions as ( B ), stained for FGF21, revealing weak immunoreactivity corresponding to the CCF. ( F ) Serial section of the same regions as ( C ), stained for FGF21, revealing no immunoreactivity corresponding to the CCF. Arrows indicate CCF.

Journal: Acta Histochemica et Cytochemica

Article Title: Clear Cell Foci as Precursors of Hepatocyte Nuclear Factor 1-alpha–inactivated Hepatocellular Adenoma in a Metabolic Syndrome Mouse Model

doi: 10.1267/ahc.25-00053

Figure Lengend Snippet: β-Klotho and FGF21 immunoreactivity in hepatic lesions of a 40-week-old TSOD mouse. ( A – C ) Representative views of CCF on H&E. ( D ) Serial section of the same regions as ( A ), stained for β-Klotho, revealing strong immunoreactivity corresponding to the CCF. ( E ) Serial section of the same regions as ( B ), stained for FGF21, revealing weak immunoreactivity corresponding to the CCF. ( F ) Serial section of the same regions as ( C ), stained for FGF21, revealing no immunoreactivity corresponding to the CCF. Arrows indicate CCF.

Article Snippet: FGF21 (Bioss Antibodies bs-2318R) , Rabbit polyclonal , 1:100.

Techniques: Staining

Liver-specific inhibition of Rab2A increases FGF21 expression and secretion . A , serum FGF21 levels in shNC and shRab2A mice (male, n = 5 per group; samples from PMID: 35061665 ). B , serum FGF21 levels in Flox and LCK mice under “Random feed” and “Fasted” conditions (male, n = 5 per group). C , serum FGF21 levels in Flox and LCK mice after 12 weeks of HFHCD feeding (male, n = 6 versus 5). D , hepatic Fgf21 mRNA levels in “Random feed” Flox and LCK mice at 10 weeks of age (male, n = 5 per group). E , hepatic Fgf21 mRNA levels in “Fasted” Flox and LCK mice at 16 weeks of age (male, n = 5 per group). F , hepatic Fgf21 mRNA levels in Flox and LCK mice after 12 weeks of HFHCD feeding (male, n = 6 versus 5). G , representative immunoblots of hepatic FGF21 protein in “Fasted” Flox and LCK mice at 16 weeks of age. H , quantification of the immunoblots in ( G ). I , representative immunoblots of hepatic FGF21 protein in Flox and LCK mice after 12 weeks of HFHCD feeding. J , quantification of the immunoblots in ( I ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. FGF21, fibroblast growth factor 21; HFHCD, high-fat–high-cholesterol diet; LCK, liver-specific Rab2A knockout.

Journal: The Journal of Biological Chemistry

Article Title: Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B–CREBH signaling

doi: 10.1016/j.jbc.2025.110977

Figure Lengend Snippet: Liver-specific inhibition of Rab2A increases FGF21 expression and secretion . A , serum FGF21 levels in shNC and shRab2A mice (male, n = 5 per group; samples from PMID: 35061665 ). B , serum FGF21 levels in Flox and LCK mice under “Random feed” and “Fasted” conditions (male, n = 5 per group). C , serum FGF21 levels in Flox and LCK mice after 12 weeks of HFHCD feeding (male, n = 6 versus 5). D , hepatic Fgf21 mRNA levels in “Random feed” Flox and LCK mice at 10 weeks of age (male, n = 5 per group). E , hepatic Fgf21 mRNA levels in “Fasted” Flox and LCK mice at 16 weeks of age (male, n = 5 per group). F , hepatic Fgf21 mRNA levels in Flox and LCK mice after 12 weeks of HFHCD feeding (male, n = 6 versus 5). G , representative immunoblots of hepatic FGF21 protein in “Fasted” Flox and LCK mice at 16 weeks of age. H , quantification of the immunoblots in ( G ). I , representative immunoblots of hepatic FGF21 protein in Flox and LCK mice after 12 weeks of HFHCD feeding. J , quantification of the immunoblots in ( I ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. FGF21, fibroblast growth factor 21; HFHCD, high-fat–high-cholesterol diet; LCK, liver-specific Rab2A knockout.

Article Snippet: The following primary and secondary antibodies were used: goat anti FGF21 (R&D Systems; AF3057), mouse anti-Rab2A (Proteintech; 67501-1-Ig), mouse anti-tubulin (DUONENG-BIO; AB0178801), mouse anti-actin (Zen-Bioscience; 200068-8F10), rabbit anti-CREBH (Kerafast; EWS101), rabbit anti-GAPDH (Proteintech; 10494-1-AP), rabbit anti-APOB (Proteintech; 20578-1-AP), mouse anti-CHC (Santa Cruz; sc-12734), rabbit anti-GRP94 (Proteintech; 14700-1-AP), mouse anti-GRASP55 (Santa Cruz; sc-271840), HRP-conjugated goat anti-mouse IgG (Jackson ImmunoResearch; 115-035-003), HRP-conjugated goat anti-rabbit IgG (Jackson ImmunoResearch; 111-035-003), and HRP-conjugated rabbit anti-goat IgG (Jackson ImmunoResearch; 305-035-003).

Techniques: Inhibition, Expressing, Western Blot, Two Tailed Test, Knock-Out

CREBH knockdown rescues FGF21 expression and the metabolic phenotypes of LCK mice . A , schematic of the experimental timeline for adeno-associated virus (AAV) injection in Flox and LCK mice. B and C , representative immunoblots and quantification of hepatic CREBH protein levels after AAV-mediated knockdown. D – M , analyses performed after 7 weeks of AAV injection and subsequent euthanasia (male, n = 6 versus 6 versus 6): Hepatic mRNA levels of Creb3l3 , Fgf21 , Apoa4 , and Fsp27β ( D ). Representative immunoblots and quantification of hepatic FGF21 protein levels ( E and F ). Serum FGF21 levels ( G ). mRNA expression of thermogenic-related genes in epWAT ( H ) and scWAT ( I ). Representative H&E-stained sections of epWAT ( J ) and quantitative results ( K ). The weights of adipose tissues and the whole body ( L and M ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. ns indicates no significant difference ( p > 0.05). CREBH, cAMP-responsive element–binding protein H; epWAT, epididymal white adipose tissue; FGF21, fibroblast growth factor 21; LCK, liver-specific Rab2A knockout; scWAT, subcutaneous white adipose tissue.

Journal: The Journal of Biological Chemistry

Article Title: Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B–CREBH signaling

doi: 10.1016/j.jbc.2025.110977

Figure Lengend Snippet: CREBH knockdown rescues FGF21 expression and the metabolic phenotypes of LCK mice . A , schematic of the experimental timeline for adeno-associated virus (AAV) injection in Flox and LCK mice. B and C , representative immunoblots and quantification of hepatic CREBH protein levels after AAV-mediated knockdown. D – M , analyses performed after 7 weeks of AAV injection and subsequent euthanasia (male, n = 6 versus 6 versus 6): Hepatic mRNA levels of Creb3l3 , Fgf21 , Apoa4 , and Fsp27β ( D ). Representative immunoblots and quantification of hepatic FGF21 protein levels ( E and F ). Serum FGF21 levels ( G ). mRNA expression of thermogenic-related genes in epWAT ( H ) and scWAT ( I ). Representative H&E-stained sections of epWAT ( J ) and quantitative results ( K ). The weights of adipose tissues and the whole body ( L and M ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. ns indicates no significant difference ( p > 0.05). CREBH, cAMP-responsive element–binding protein H; epWAT, epididymal white adipose tissue; FGF21, fibroblast growth factor 21; LCK, liver-specific Rab2A knockout; scWAT, subcutaneous white adipose tissue.

Techniques: Knockdown, Expressing, Virus, Injection, Western Blot, Staining, Two Tailed Test, Binding Assay, Knock-Out

APOB knockdown rescues CREBH activation, FGF21 expression, and the metabolic phenotypes of LCK mice . A , schematic of the experimental timeline for adeno-associated virus (AAV) injection in Flox and LCK mice. B , representative immunoblots of hepatic APOB protein levels after AAV-mediated knockdown. C and D , representative immunoblots and quantification of hepatic CREBH cleavage levels after APOB knockdown. E – M , analyses performed after 8 weeks of AAV injection and subsequent euthanasia (male, n = 5 versus 5 versus 5): hepatic mRNA levels of Creb3l3 , Fgf21 , Apoa4 , Fsp27β , and Apoc2 ( E ). Representative immunoblots and quantification of hepatic FGF21 protein levels ( F and G ). Serum FGF21 levels ( H ). mRNA expression of thermogenic-related genes in scWAT ( I ). Representative H&E-stained sections of epWAT ( J ) and quantitative results ( K ). The weights of adipose tissues and the whole body ( L and M ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. ns indicates no significant difference ( p > 0.05). AAV, adeno-associated virus; APOB, apolipoprotein B; CREBH, cAMP-responsive element–binding protein H; epWAT, epididymal white adipose tissue; FGF21, fibroblast growth factor 21; LCK, liver-specific Rab2A knockout; scWAT, subcutaneous white adipose tissue.

Journal: The Journal of Biological Chemistry

Article Title: Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B–CREBH signaling

doi: 10.1016/j.jbc.2025.110977

Figure Lengend Snippet: APOB knockdown rescues CREBH activation, FGF21 expression, and the metabolic phenotypes of LCK mice . A , schematic of the experimental timeline for adeno-associated virus (AAV) injection in Flox and LCK mice. B , representative immunoblots of hepatic APOB protein levels after AAV-mediated knockdown. C and D , representative immunoblots and quantification of hepatic CREBH cleavage levels after APOB knockdown. E – M , analyses performed after 8 weeks of AAV injection and subsequent euthanasia (male, n = 5 versus 5 versus 5): hepatic mRNA levels of Creb3l3 , Fgf21 , Apoa4 , Fsp27β , and Apoc2 ( E ). Representative immunoblots and quantification of hepatic FGF21 protein levels ( F and G ). Serum FGF21 levels ( H ). mRNA expression of thermogenic-related genes in scWAT ( I ). Representative H&E-stained sections of epWAT ( J ) and quantitative results ( K ). The weights of adipose tissues and the whole body ( L and M ). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. ns indicates no significant difference ( p > 0.05). AAV, adeno-associated virus; APOB, apolipoprotein B; CREBH, cAMP-responsive element–binding protein H; epWAT, epididymal white adipose tissue; FGF21, fibroblast growth factor 21; LCK, liver-specific Rab2A knockout; scWAT, subcutaneous white adipose tissue.

Techniques: Knockdown, Activation Assay, Expressing, Virus, Injection, Western Blot, Staining, Two Tailed Test, Binding Assay, Knock-Out

$Starvation-induced APOB trafficking defects activate the CREBH–FGF21 axis . Wildtype C57BL/6J mice were fasted for 16 h or not prior to analysis. A , hepatic triglyceride (TG) levels (n = 6 per group). B , VLDL–TG secretion rates (n = 5 per group). C , representative immunoblots of total hepatic APOB. D , quantification of APOB protein levels from ( C ). E , representative immunoblots of APOB distribution in the endoplasmic reticulum (ER) and Golgi apparatus fractions. F , quantification of APOB levels in subcellular fractions from ( E ). G , representative immunoblots of CREBH cleavage. H , quantification of cleaved CREBH from ( G ). I , hepatic mRNA levels of Fgf21 , Fsp27β , and Apoa4 (n = 4 per group). J , representative immunoblots of hepatic FGF21 proteins. K , quantification of FGF21 protein levels from ( J ). L , serum FGF21 levels (n = 5 per group). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. APOB, apolipoprotein B; CREBH, cAMP-responsive element–binding protein H; FGF21, fibroblast growth factor 21; TG, triglyceride; VLDL, very low–density lipoprotein.$

Journal: The Journal of Biological Chemistry

Article Title: Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B–CREBH signaling

doi: 10.1016/j.jbc.2025.110977

Figure Lengend Snippet: Starvation-induced APOB trafficking defects activate the CREBH–FGF21 axis . Wildtype C57BL/6J mice were fasted for 16 h or not prior to analysis. A , hepatic triglyceride (TG) levels (n = 6 per group). B , VLDL–TG secretion rates (n = 5 per group). C , representative immunoblots of total hepatic APOB. D , quantification of APOB protein levels from ( C ). E , representative immunoblots of APOB distribution in the endoplasmic reticulum (ER) and Golgi apparatus fractions. F , quantification of APOB levels in subcellular fractions from ( E ). G , representative immunoblots of CREBH cleavage. H , quantification of cleaved CREBH from ( G ). I , hepatic mRNA levels of Fgf21 , Fsp27β , and Apoa4 (n = 4 per group). J , representative immunoblots of hepatic FGF21 proteins. K , quantification of FGF21 protein levels from ( J ). L , serum FGF21 levels (n = 5 per group). Data are presented as mean ± SD. p Values were determined using the unpaired two-tailed Student’s t test. APOB, apolipoprotein B; CREBH, cAMP-responsive element–binding protein H; FGF21, fibroblast growth factor 21; TG, triglyceride; VLDL, very low–density lipoprotein.

Techniques: Western Blot, Two Tailed Test, Binding Assay

Summary of results and work model . A graphical abstract was created to summarize the key findings of this study, outlining a multistep regulatory pathway. VLDL assembly and maturation (steps 1–3): newly assembled VLDL 2 particles are transported from the ER to the Golgi via COPII vesicles. At the Golgi, the Rab2A–HSD17B13 complex mediates lipid droplet–Golgi contacts, facilitating lipid transfer to support VLDL 1 maturation. CREBH activation and signaling (steps 4–6): full-length CREBH resides in the ER and is transported to the Golgi under specific conditions, where its proteolytic cleavage—partially dependent on APOB availability—generates the active N-terminal fragment. This fragment translocates to the nucleus and drives transcription of Fsp27β , Fgf21 , and Apoa4 . Systemic metabolic regulation (steps 7–9): secreted FGF21 promotes adipose tissue lipolysis; ApoA-IV enhances VLDL lipidation and expansion in the Golgi; and lipid droplet–localized FSP27β facilitates hepatic lipid storage. Pathophysiological perturbations: in Rab2A-deficient hepatocytes, disrupted lipid droplet–Golgi contacts reduce lipid flux to the Golgi, impairing VLDL maturation. This leads to APOB accumulation in the Golgi, which promotes CREBH cleavage and elevates FGF21 expression. During fasting, AMPK-mediated suppression of Rab2A activity, combined with partial inhibition of APOB ER-to-Golgi transport, further reduces VLDL secretion. These changes are sensed by CREBH, enhancing its activation and driving a transcriptional program that adaptively regulates systemic lipid homeostasis. Graphical abstract created with BioRender (Chen, 2025; https://BioRender.com/7gyj0x2 ). AMPK, AMP-activated protein kinase; APOB, apolipoprotein B; COPII, coat protein complex II; CREBH, cAMP-responsive element–binding protein H; ER, endoplasmic reticulum; VLDL, very low–density lipoprotein.

Journal: The Journal of Biological Chemistry

Article Title: Rab2A modulates liver fibroblast growth factor 21 (FGF21) expression and systemic metabolism via apolipoprotein B–CREBH signaling

doi: 10.1016/j.jbc.2025.110977

Figure Lengend Snippet: Summary of results and work model . A graphical abstract was created to summarize the key findings of this study, outlining a multistep regulatory pathway. VLDL assembly and maturation (steps 1–3): newly assembled VLDL 2 particles are transported from the ER to the Golgi via COPII vesicles. At the Golgi, the Rab2A–HSD17B13 complex mediates lipid droplet–Golgi contacts, facilitating lipid transfer to support VLDL 1 maturation. CREBH activation and signaling (steps 4–6): full-length CREBH resides in the ER and is transported to the Golgi under specific conditions, where its proteolytic cleavage—partially dependent on APOB availability—generates the active N-terminal fragment. This fragment translocates to the nucleus and drives transcription of Fsp27β , Fgf21 , and Apoa4 . Systemic metabolic regulation (steps 7–9): secreted FGF21 promotes adipose tissue lipolysis; ApoA-IV enhances VLDL lipidation and expansion in the Golgi; and lipid droplet–localized FSP27β facilitates hepatic lipid storage. Pathophysiological perturbations: in Rab2A-deficient hepatocytes, disrupted lipid droplet–Golgi contacts reduce lipid flux to the Golgi, impairing VLDL maturation. This leads to APOB accumulation in the Golgi, which promotes CREBH cleavage and elevates FGF21 expression. During fasting, AMPK-mediated suppression of Rab2A activity, combined with partial inhibition of APOB ER-to-Golgi transport, further reduces VLDL secretion. These changes are sensed by CREBH, enhancing its activation and driving a transcriptional program that adaptively regulates systemic lipid homeostasis. Graphical abstract created with BioRender (Chen, 2025; https://BioRender.com/7gyj0x2 ). AMPK, AMP-activated protein kinase; APOB, apolipoprotein B; COPII, coat protein complex II; CREBH, cAMP-responsive element–binding protein H; ER, endoplasmic reticulum; VLDL, very low–density lipoprotein.

Techniques: Activation Assay, Expressing, Activity Assay, Inhibition, Binding Assay

A RNA sequencing pre-processing flowchart. B Signaling pathways up-regulated in rPTX3-treated MC3T3-E1. C Volcano map of differential genes between rPTX3 treatment and Dex groups. D Heat map of differential genes of the cytokines and growth factors between rPTX3 treatment and Dex groups based on RNA sequencing. E qPCR analysis of Fgf21, Gdf15, Hgf, Ereg, Tgfb2 , and Fgf10 in Dex stimulated MC3T3-E1 treated with or without rPTX3 and quantification, normalized to Gapdh (internal control). F WB analysis and relative quantification of FGF21 in Dex stimulated MC3T3-E1 treated with or without rPTX3. Actin was used as an internal control. G qPCR analysis of Fgf21 in shFGF21 infected MC3T3-E1. H WB analysis and quantification of FGF21 in shFGF21 infected MC3T3-E1. Actin was used as an internal control. I WB analysis and quantification of osteogenesis markers (ALP, Runx2 and COL1 at day 7, OCN and OPN at day 14) and apoptosis markers (Bcl-2 and Bax at 24 h) in five groups of MC3T3-E1. Actin was used as an internal control. J Cell death/live analysis in five groups and quantification. K Flow cytometry analysis in five groups and quantification. (Apoptotic cells: Q2 + Q3) L , M ALP staining and ARS staining in five groups and quantification. N , O Immunofluorescence staining and quantitative analysis of relative FI of osteogenesis markers OCN (day 14), Runx2 (day 7) in five groups. Control: MC3T3 cells cultured with standard OIM, n = 3; shFGF21: shFGF21-MC3T3 cells cultured with standard OIM, n = 3; Dex: MC3T3 cells cultured with standard OIM and dexamethasone (10 μM), n = 3; shFGF21+Dex: shFGF21-MC3T3 cells cultured with standard OIM and dexamethasone (10 μM). Dex+rFGF21: MC3T3 cells cultured with standard OIM co-cultured with dexamethasone (10 μM) and rFGF21 (200 ng/mL), n = 3. Statistical analysis: Dunnett’s post-hoc tests (n = 3 independent experiments). Error bars: standard deviation, SD. The images provided in all figures represent typical examples from each experimental group. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Communications Biology

Article Title: Pentraxin 3 ameliorates glucocorticoid-induced osteonecrosis of the femoral head via TLR4/NF-κB/FGF21 signaling axis

doi: 10.1038/s42003-025-09282-3

Figure Lengend Snippet: A RNA sequencing pre-processing flowchart. B Signaling pathways up-regulated in rPTX3-treated MC3T3-E1. C Volcano map of differential genes between rPTX3 treatment and Dex groups. D Heat map of differential genes of the cytokines and growth factors between rPTX3 treatment and Dex groups based on RNA sequencing. E qPCR analysis of Fgf21, Gdf15, Hgf, Ereg, Tgfb2 , and Fgf10 in Dex stimulated MC3T3-E1 treated with or without rPTX3 and quantification, normalized to Gapdh (internal control). F WB analysis and relative quantification of FGF21 in Dex stimulated MC3T3-E1 treated with or without rPTX3. Actin was used as an internal control. G qPCR analysis of Fgf21 in shFGF21 infected MC3T3-E1. H WB analysis and quantification of FGF21 in shFGF21 infected MC3T3-E1. Actin was used as an internal control. I WB analysis and quantification of osteogenesis markers (ALP, Runx2 and COL1 at day 7, OCN and OPN at day 14) and apoptosis markers (Bcl-2 and Bax at 24 h) in five groups of MC3T3-E1. Actin was used as an internal control. J Cell death/live analysis in five groups and quantification. K Flow cytometry analysis in five groups and quantification. (Apoptotic cells: Q2 + Q3) L , M ALP staining and ARS staining in five groups and quantification. N , O Immunofluorescence staining and quantitative analysis of relative FI of osteogenesis markers OCN (day 14), Runx2 (day 7) in five groups. Control: MC3T3 cells cultured with standard OIM, n = 3; shFGF21: shFGF21-MC3T3 cells cultured with standard OIM, n = 3; Dex: MC3T3 cells cultured with standard OIM and dexamethasone (10 μM), n = 3; shFGF21+Dex: shFGF21-MC3T3 cells cultured with standard OIM and dexamethasone (10 μM). Dex+rFGF21: MC3T3 cells cultured with standard OIM co-cultured with dexamethasone (10 μM) and rFGF21 (200 ng/mL), n = 3. Statistical analysis: Dunnett’s post-hoc tests (n = 3 independent experiments). Error bars: standard deviation, SD. The images provided in all figures represent typical examples from each experimental group. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The sections were then incubated overnight at 4 °C with primary antibodies targeting PTX3 (1:200 dilution, 13797-1-AP, Proteintech), osteocalcin (OCN, 1:200 dilution, DF12303, Affinity), alkaline phosphatase (ALP, 1:200 dilution, DF6225, Affinity), Collagen I (COL1, 1:500 dilution, A24112, ABclonal), phosphorylated p65 (p-p65,1:200 dilution, AF2006, Affinity), phosphorylated IκB (p-IκB, 1:1000 dilution, 82349-1-RR, Proteintech) and FGF21 (1:200 dilution, TC52978S, Abmart).

Techniques: RNA Sequencing, Protein-Protein interactions, Control, Quantitative Proteomics, Infection, Flow Cytometry, Staining, Immunofluorescence, Cell Culture, Standard Deviation

A , B FGF2 and FGF21 exhibit certain structural similarities at the protein level. C Co-Immunoprecipitation analysis of FGF21 and PTX3 interaction. D KEGG enrichment analysis and heatmap visualization of TLR/NF-κB pathway-associated differentially expressed genes. E WB analysis and quantification of FGF21 and TLR4/NF-κB pathway-associated markers TLR4, MyD88, p-p65/p65 and p-IκB/IκB in five groups of MC3T3-E1. Actin was used as an internal control. F Cell death/live analysis in five groups. G Flow cytometry analysis in five groups. (Apoptotic cells: Q2 + Q3). H , I ALP staining and ARS staining in five groups. J , K Immunofluorescence staining of osteogenesis markers OCN (Day 14), Runx2 (Day 7) in five groups. L The appearance of femoral heads in five groups. M HE staining of femoral heads in five groups. N IHC staining of ALP, OCN, and COL1 in five groups. (n = 3 independent experiments) Statistical analysis: Dunnett’s post-hoc tests. Error bars: standard deviation, SD. Control: Standard OIM, n = 3/ vehicle-treated, n = 5; Dex: Standard OIM co-cultured with dexamethasone (10 μM), n = 3/ glucocorticoid-induced osteonecrosis model, n = 5; Dex+rPTX3: Standard OIM co-cultured with dexamethasone (10 uM) and rPTX3 (200 ng/mL), n = 3/ model + 200 ng/g recombinant PTX3, n = 5; Dex+rPTX3+TAK-242: Standard OIM co-cultured with dexamethasone (10 uM), rPTX3 (200 ng/mL) and TAK-242 (50 nM), n = 3/ model + rPTX3 + TAK-242, n = 5; Dex+rPTX3 + SN50: Standard OIM co-cultured with dexamethasone (10 μM), rPTX3 (200 ng/mL) and SN50 (50 μg/mL), n = 3/ model + rPTX3 + SN50, n = 5. Red arrows: empty lacunae; Black arrows: trabecular bone disruption; Star symbol: necrotic bone marrow; White arrows: positive cells. The images provided in all figures represent typical examples from each experimental group. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Communications Biology

Article Title: Pentraxin 3 ameliorates glucocorticoid-induced osteonecrosis of the femoral head via TLR4/NF-κB/FGF21 signaling axis

doi: 10.1038/s42003-025-09282-3

Figure Lengend Snippet: A , B FGF2 and FGF21 exhibit certain structural similarities at the protein level. C Co-Immunoprecipitation analysis of FGF21 and PTX3 interaction. D KEGG enrichment analysis and heatmap visualization of TLR/NF-κB pathway-associated differentially expressed genes. E WB analysis and quantification of FGF21 and TLR4/NF-κB pathway-associated markers TLR4, MyD88, p-p65/p65 and p-IκB/IκB in five groups of MC3T3-E1. Actin was used as an internal control. F Cell death/live analysis in five groups. G Flow cytometry analysis in five groups. (Apoptotic cells: Q2 + Q3). H , I ALP staining and ARS staining in five groups. J , K Immunofluorescence staining of osteogenesis markers OCN (Day 14), Runx2 (Day 7) in five groups. L The appearance of femoral heads in five groups. M HE staining of femoral heads in five groups. N IHC staining of ALP, OCN, and COL1 in five groups. (n = 3 independent experiments) Statistical analysis: Dunnett’s post-hoc tests. Error bars: standard deviation, SD. Control: Standard OIM, n = 3/ vehicle-treated, n = 5; Dex: Standard OIM co-cultured with dexamethasone (10 μM), n = 3/ glucocorticoid-induced osteonecrosis model, n = 5; Dex+rPTX3: Standard OIM co-cultured with dexamethasone (10 uM) and rPTX3 (200 ng/mL), n = 3/ model + 200 ng/g recombinant PTX3, n = 5; Dex+rPTX3+TAK-242: Standard OIM co-cultured with dexamethasone (10 uM), rPTX3 (200 ng/mL) and TAK-242 (50 nM), n = 3/ model + rPTX3 + TAK-242, n = 5; Dex+rPTX3 + SN50: Standard OIM co-cultured with dexamethasone (10 μM), rPTX3 (200 ng/mL) and SN50 (50 μg/mL), n = 3/ model + rPTX3 + SN50, n = 5. Red arrows: empty lacunae; Black arrows: trabecular bone disruption; Star symbol: necrotic bone marrow; White arrows: positive cells. The images provided in all figures represent typical examples from each experimental group. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques: Immunoprecipitation, Control, Flow Cytometry, Staining, Immunofluorescence, Immunohistochemistry, Standard Deviation, Cell Culture, Recombinant, Disruption

Schematic diagram of PTX3-mediated amelioration of glucocorticoid-induced osteonecrosis in the femoral head via TLR4/NF-κB/FGF21 signaling axis.

Journal: Communications Biology

Article Title: Pentraxin 3 ameliorates glucocorticoid-induced osteonecrosis of the femoral head via TLR4/NF-κB/FGF21 signaling axis

doi: 10.1038/s42003-025-09282-3

Figure Lengend Snippet: Schematic diagram of PTX3-mediated amelioration of glucocorticoid-induced osteonecrosis in the femoral head via TLR4/NF-κB/FGF21 signaling axis.

Techniques:

( A ) Mice were locally injected at the iBAT with AAV8-shLamp2A (shRNA-Lamp2A) or control AAV8 (shRNA-scrambled). Lamp2A mRNA, representative immunoblot image, and quantification of L2A protein levels in BAT ( n = 3 to 6). ITR, inverted terminal repeat. GFP, green fluorescent protein. ( B ) Top: Representative histology images of BAT. Bottom: Average lipid droplet size and percentage of microscopy area occupied by lipid droplets ( n = 9). ( C ) Left: Representative oxygen consumption graph. Right: Average oxygen consumption during the day and night periods in mice ( n = 5 to 6). AUC, area under the curve. ( D ) Blood glucose and triglyceride levels in L2A-KD and control mice after cold exposure (4°C, 24 hours) ( n = 5 to 6). ( E ) Representative immunoblot images and quantification of Ucp1 protein levels (left) ( n = 4) and Fgf21 protein levels (right, n = 5) in the BAT of L2A-KD and control mice after cold exposure (4°C, 24 hours). ( F ) Representative immunoblot images and quantification of Pdgfrb protein levels (top, n = 5) and Aebp1 (bottom, n = 5) in the BAT of L2A-KD and control mice after cold exposure (4°C, 24 hours). Results are shown as means ± SEM, * P < 0.05 and *** P < 0.001 in statistical comparisons between L2A-KD and control mice.

Journal: Science Advances

Article Title: Chaperone-mediated autophagy controls brown adipose tissue thermogenic activity

doi: 10.1126/sciadv.ady0415

Figure Lengend Snippet: ( A ) Mice were locally injected at the iBAT with AAV8-shLamp2A (shRNA-Lamp2A) or control AAV8 (shRNA-scrambled). Lamp2A mRNA, representative immunoblot image, and quantification of L2A protein levels in BAT ( n = 3 to 6). ITR, inverted terminal repeat. GFP, green fluorescent protein. ( B ) Top: Representative histology images of BAT. Bottom: Average lipid droplet size and percentage of microscopy area occupied by lipid droplets ( n = 9). ( C ) Left: Representative oxygen consumption graph. Right: Average oxygen consumption during the day and night periods in mice ( n = 5 to 6). AUC, area under the curve. ( D ) Blood glucose and triglyceride levels in L2A-KD and control mice after cold exposure (4°C, 24 hours) ( n = 5 to 6). ( E ) Representative immunoblot images and quantification of Ucp1 protein levels (left) ( n = 4) and Fgf21 protein levels (right, n = 5) in the BAT of L2A-KD and control mice after cold exposure (4°C, 24 hours). ( F ) Representative immunoblot images and quantification of Pdgfrb protein levels (top, n = 5) and Aebp1 (bottom, n = 5) in the BAT of L2A-KD and control mice after cold exposure (4°C, 24 hours). Results are shown as means ± SEM, * P < 0.05 and *** P < 0.001 in statistical comparisons between L2A-KD and control mice.

Article Snippet: The membranes were incubated with primary antibodies specific for L2A (51-2200, Life Technologies), UCP1 (ab10983, Abcam), FGF21 (sc-81946, Santa Cruz), AEBP1 (sc-271374, Santa Cruz), PDGFRB (MA5-15143, Invitrogen), β-tubulin (T8660, Sigma-Aldrich), and then with horseradish peroxidase (HRP)–conjugated anti-mouse immunoglobulin G (IgG; 1721011, Bio-Rad), or anti-rabbit IgG (ab6721, Abcam), as appropriate.

Techniques: Injection, shRNA, Control, Western Blot, Microscopy

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