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goat anti mouse saa polyclonal antibody  (R&D Systems)


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    Structured Review

    R&D Systems goat anti mouse saa polyclonal antibody
    Goat Anti Mouse Saa Polyclonal Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+saa/pm41904943-180-10-18?v=R%26D+Systems
    Average 93 stars, based on 53 article reviews
    goat anti mouse saa polyclonal antibody - by Bioz Stars, 2026-07
    93/100 stars

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    a MA-plot comparing mammary glands from NP (MG NP ) and N (MG N ) mice. Red and blue dots indicate significantly upregulated and downregulated genes, respectively (adjusted p-value < 0.05); gray dots represent non-significant changes. b Box plots show eight upregulated and seven downregulated secretory genes with adjusted p-values < 0.05. Gene expression levels in MG NP are shown in red, and those in MG N are shown in cyan. c MTT assay results showing the effects of secretory peptides on HER2/neu+ mammary tumor cell proliferation. Cells were treated with either vehicle control, SAA1, <t>SAA2,</t> or THBS4 peptides, and cell viability was assessed at 1, 2, or 3 days post-treatment. All comparisons to the vehicle control yielded p < 0.05, except for the optical density measured 3 days after SAA2 treatment. d Representative images from Boyden chamber assays showing the migration of HER2/neu+ mammary tumor cells in response to secretory peptides, SAA1, SAA2, or THBS4. Ctrl, vehicle control. e Transcriptional expression of SAA1 and SAA2 in breast cancer samples from the TCGA and METABRIC databases, stratified by TP53 status (WT, wild-type vs. Mut, mutant).
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    a MA-plot comparing mammary glands from NP (MG NP ) and N (MG N ) mice. Red and blue dots indicate significantly upregulated and downregulated genes, respectively (adjusted p-value < 0.05); gray dots represent non-significant changes. b Box plots show eight upregulated and seven downregulated secretory genes with adjusted p-values < 0.05. Gene expression levels in MG NP are shown in red, and those in MG N are shown in cyan. c MTT assay results showing the effects of secretory peptides on HER2/neu+ mammary tumor cell proliferation. Cells were treated with either vehicle control, SAA1, <t>SAA2,</t> or THBS4 peptides, and cell viability was assessed at 1, 2, or 3 days post-treatment. All comparisons to the vehicle control yielded p < 0.05, except for the optical density measured 3 days after SAA2 treatment. d Representative images from Boyden chamber assays showing the migration of HER2/neu+ mammary tumor cells in response to secretory peptides, SAA1, SAA2, or THBS4. Ctrl, vehicle control. e Transcriptional expression of SAA1 and SAA2 in breast cancer samples from the TCGA and METABRIC databases, stratified by TP53 status (WT, wild-type vs. Mut, mutant).
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    Jackson Laboratory saa app ki mice
    a MA-plot comparing mammary glands from NP (MG NP ) and N (MG N ) mice. Red and blue dots indicate significantly upregulated and downregulated genes, respectively (adjusted p-value < 0.05); gray dots represent non-significant changes. b Box plots show eight upregulated and seven downregulated secretory genes with adjusted p-values < 0.05. Gene expression levels in MG NP are shown in red, and those in MG N are shown in cyan. c MTT assay results showing the effects of secretory peptides on HER2/neu+ mammary tumor cell proliferation. Cells were treated with either vehicle control, SAA1, <t>SAA2,</t> or THBS4 peptides, and cell viability was assessed at 1, 2, or 3 days post-treatment. All comparisons to the vehicle control yielded p < 0.05, except for the optical density measured 3 days after SAA2 treatment. d Representative images from Boyden chamber assays showing the migration of HER2/neu+ mammary tumor cells in response to secretory peptides, SAA1, SAA2, or THBS4. Ctrl, vehicle control. e Transcriptional expression of SAA1 and SAA2 in breast cancer samples from the TCGA and METABRIC databases, stratified by TP53 status (WT, wild-type vs. Mut, mutant).
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    Image Search Results


    NCAM1 overexpression in microglia/macrophages confers protection against neuroinflammation and apoptotic cell death after ischemic stroke in mouse tMCAO model. A Quantification for IL-1β, IL-6, TNF-α, CXCL1, and CCL2 mRNA expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice by qRT-PCR. n = 4. Results are represented as means ± SD. *** p < 0.001 vs. sham group and ## p < 0.01 and ### p < 0.001 vs. tMCAO plus Vector group. B Quantification for IL-1β, IL-6, TNF-α, CXCL1, and CCL2 protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice by ELISA. n = 4. Results are represented as means ± SD. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. C and D Western blotting images and quantitative analysis for iNOS, CD32, and CD86 protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice. n = 4. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. E and F Western blotting images and quantitative analysis for Bcl-xl, Bax, cleaved caspase-3, −9, and PARP protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice. n = 4. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. G and H Representative immunofluorescence images and quantitative analysis for TUNEL-positive cells in the peri-infarct hippocampus and cortex of CX3CR1 Cre/ERT2 mice by TUNEL staining. n = 4. Scale bar: 50 μm. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group

    Journal: Journal of Neuroinflammation

    Article Title: Microglial NCAM1 attenuates ischemic brain injury by inhibiting NF-κB-driven neuroinflammation through IκBα stabilization

    doi: 10.1186/s12974-026-03766-7

    Figure Lengend Snippet: NCAM1 overexpression in microglia/macrophages confers protection against neuroinflammation and apoptotic cell death after ischemic stroke in mouse tMCAO model. A Quantification for IL-1β, IL-6, TNF-α, CXCL1, and CCL2 mRNA expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice by qRT-PCR. n = 4. Results are represented as means ± SD. *** p < 0.001 vs. sham group and ## p < 0.01 and ### p < 0.001 vs. tMCAO plus Vector group. B Quantification for IL-1β, IL-6, TNF-α, CXCL1, and CCL2 protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice by ELISA. n = 4. Results are represented as means ± SD. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. C and D Western blotting images and quantitative analysis for iNOS, CD32, and CD86 protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice. n = 4. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. E and F Western blotting images and quantitative analysis for Bcl-xl, Bax, cleaved caspase-3, −9, and PARP protein expression in the peri-infarct region of CX3CR1 Cre/ERT2 mice. n = 4. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group. G and H Representative immunofluorescence images and quantitative analysis for TUNEL-positive cells in the peri-infarct hippocampus and cortex of CX3CR1 Cre/ERT2 mice by TUNEL staining. n = 4. Scale bar: 50 μm. *** p < 0.001 vs. sham group and ### p < 0.001 vs. tMCAO plus Vector group

    Article Snippet: The levels of IL-1β, IL-6, TNF-α, CXCL1, and CCL2 in tissue homogenates were quantified using commercial mouse ELISA kits (Multi Sciences, Hangzhou, China), and the results were expressed as picograms per milliliter (pg/mL).

    Techniques: Over Expression, Expressing, Quantitative RT-PCR, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Western Blot, Immunofluorescence, TUNEL Assay, Staining

    Brain tissue from human AD (A) and from 5xFAD, App SAA/SAA , App NLG/NLG , and App NLG/NLG :APOE4 mice (B-D) were stained for fibrin(ogen) (red), Aβ (blue), and the microglia marker Iba1 (green) primary antibodies (scale bar, 25 mm). ( A ) In AD brain tissue, fibrin(ogen) deposition was found within amyloid plaques (#), diffusely around some of the blood vessels (*), and decorating blood vessels (arrowheads). Representative images are shown from n = 3 samples. ( B ) 10-month-old 5xFAD mice showed robust fibrin(ogen) deposition within and around amyloid plaques and decorating blood vessels (arrowheads). Reactive microglia (green) accumulated around amyloid and fibrin(ogen) deposits. Representative images are shown from n = 10 samples. ( C, D ) Relative to 5xFAD mice (B), 21-month-old App NLG/NLG (C) and 15-month-old App NLG/NLG :APOE4 (D) mice showed more diffuse fibrin(ogen) deposition around amyloid plaques, with fibrin(ogen) forming an external halo around amyloid plaques. Reactive microglia cells (green) accumulated around amyloid and fibrin(ogen) deposits. Representative images are shown from n = 6–10 samples per genotype.

    Journal: bioRxiv

    Article Title: Therapeutic targeting of fibrin–microglia interactions ameliorates Alzheimer’s disease-related hyperexcitability and brain network dysfunction

    doi: 10.64898/2026.05.01.722324

    Figure Lengend Snippet: Brain tissue from human AD (A) and from 5xFAD, App SAA/SAA , App NLG/NLG , and App NLG/NLG :APOE4 mice (B-D) were stained for fibrin(ogen) (red), Aβ (blue), and the microglia marker Iba1 (green) primary antibodies (scale bar, 25 mm). ( A ) In AD brain tissue, fibrin(ogen) deposition was found within amyloid plaques (#), diffusely around some of the blood vessels (*), and decorating blood vessels (arrowheads). Representative images are shown from n = 3 samples. ( B ) 10-month-old 5xFAD mice showed robust fibrin(ogen) deposition within and around amyloid plaques and decorating blood vessels (arrowheads). Reactive microglia (green) accumulated around amyloid and fibrin(ogen) deposits. Representative images are shown from n = 10 samples. ( C, D ) Relative to 5xFAD mice (B), 21-month-old App NLG/NLG (C) and 15-month-old App NLG/NLG :APOE4 (D) mice showed more diffuse fibrin(ogen) deposition around amyloid plaques, with fibrin(ogen) forming an external halo around amyloid plaques. Reactive microglia cells (green) accumulated around amyloid and fibrin(ogen) deposits. Representative images are shown from n = 6–10 samples per genotype.

    Article Snippet: App SAA mice were obtained from The Jackson Laboratory (Jax 034711).

    Techniques: Staining, Marker

    SAA2 expression pattern in the mouse placenta. From embryonic (E) day 14–17, CD-1 dams received IL-1β (0.5 µg) by intraperitoneal injection daily. At E18, placentas were harvested. (A) Representative images of SAA2 expression in the PBS and IL-1β groups ( n = 3, 5 images per mouse examined). The right panels show high-magnification views of the areas outlined by white boxes in the corresponding left panels. Scale bar in the left panel, 1mm; in the right panel, 50 μm. (B) Fluorescent immune staining of SAA2 (red) and vimentin (green), an endothelial cell marker, or cytokeratin (green), a panel trophoblast marker, or F4/80 (green), a macrophage marker, in placentas. DAPI (blue) was used to label nuclei. Scale bar in left panel, 50 μm; in right panel, 10 μm.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation

    doi: 10.3389/fphar.2026.1749966

    Figure Lengend Snippet: SAA2 expression pattern in the mouse placenta. From embryonic (E) day 14–17, CD-1 dams received IL-1β (0.5 µg) by intraperitoneal injection daily. At E18, placentas were harvested. (A) Representative images of SAA2 expression in the PBS and IL-1β groups ( n = 3, 5 images per mouse examined). The right panels show high-magnification views of the areas outlined by white boxes in the corresponding left panels. Scale bar in the left panel, 1mm; in the right panel, 50 μm. (B) Fluorescent immune staining of SAA2 (red) and vimentin (green), an endothelial cell marker, or cytokeratin (green), a panel trophoblast marker, or F4/80 (green), a macrophage marker, in placentas. DAPI (blue) was used to label nuclei. Scale bar in left panel, 50 μm; in right panel, 10 μm.

    Article Snippet: Cells were cultured with the addition of mouse SAA2 protein (CUSABIO Technology, Houston, TX) at 100–1,000 ng/mL or LPS (1 μg/mL) based on published in vitro studies ( ; ; ) and pilot experiments showing macrophage activation within this range.

    Techniques: Expressing, Injection, Staining, Marker

    Maternal administration of si Saa2 reduces placental SAA2 expression and alleviates abnormal placental histology and fetal brain cortical changes following sub-chronic maternal inflammation. (A) A schematic diagram illustrating the study design for the mouse model of acute intrauterine injection using LPS. (B) A schematic diagram illustrating the study strategy for the mouse model of sub-chronic maternal inflammation using IL-1β intraperitoneal injection. SiRNA was infused using intravenous injections. (C) Placental concentrations of IL-1 β were measured by enzyme linked immunosorbent assay (ELISA). ( n = 4 per group). (D) Representative Western blotting of Saa2 expression in the placenta and statistical analysis normalized to the levels of β-actin as a loading control. PBS+PBS, n = 8; IL-1 β +PBS, n = 19; IL-1 β +si Saa2 , n = 9; PBS+si Saa2 , n = 3. (E) Representative fluorescence immunostaining for Saa2 (red) and DAPI (blue, nucleic staining) in the labyrinth of placentas. n = 3, 5 images per mouse examined. Scale bars, 50 μm. (F) Real-time quantitative polymerase chain reaction (RT‒qPCR) was performed to evaluate the effect of siRNA treatment, n = 6 for each group (G) Hematoxylin and eosin (H&E) staining was performed to compare placental thicknesses at ×5 magnification. The solid arrows crossing the central cut surface of the placentas indicate the location of measurements: fetal segments were identified as a compilation of the junctional zone and labyrinth. Scale bars, 200 μm (H) Statistical analysis shows the results of H&E staining measuring fetal placental length at the thickest location. PBS+PBS, n = 3; IL-1 β +PBS, n = 4; IL-1 β +si Saa2 , n = 3; PBS+si Saa2 , n = 3. (I) Nissl staining was performed to measure cortical thickness (upper red arrows) and ventricle area (lower red panels) in the fetal brain. Scale bars, 200 μm. (J,K) Nissl staining measuring cortical thickness and ventricle area. Quantitative data, with the median indicated by the solid line for each group, represents the average of these measurements from five random brain sections for each litter. PBS+PBS, n = 3; IL-1 β +PBS, n = 6; IL-1 β +si Saa2 , n = 4; PBS+si Saa2 , n = 3 (L) The fetal viability per litter. (M) Preterm birth rates. PBS+PBS, n = 18; IL-1 β +PBS, n = 34; IL-1 β +si Saa2 , n = 30; PBS+si Saa2 , n = 10. (N) Representative images of the placenta and its corresponding fetus between groups. (O,P) Placenta (O) and fetal weights (P) . PBS+PBS, n = 10; IL-1 β +PBS, n = 16; IL-1 β +si Saa2 , n = 8; PBS+si Saa2 , n = 8. IUI: intrauterine injection; IV: intravenous; IP: intraperitoneal. Values are expressed as the mean ± SEM, One-way ANOVA with Bonferroni post hoc tests for multiple comparisons of normally distributed data and Kruskal‒Wallis with Dunn’s multiple comparisons tests for nonparametric data (C,D,F,H,J,K,O,P) . Chi-square test (L,M) , * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation

    doi: 10.3389/fphar.2026.1749966

    Figure Lengend Snippet: Maternal administration of si Saa2 reduces placental SAA2 expression and alleviates abnormal placental histology and fetal brain cortical changes following sub-chronic maternal inflammation. (A) A schematic diagram illustrating the study design for the mouse model of acute intrauterine injection using LPS. (B) A schematic diagram illustrating the study strategy for the mouse model of sub-chronic maternal inflammation using IL-1β intraperitoneal injection. SiRNA was infused using intravenous injections. (C) Placental concentrations of IL-1 β were measured by enzyme linked immunosorbent assay (ELISA). ( n = 4 per group). (D) Representative Western blotting of Saa2 expression in the placenta and statistical analysis normalized to the levels of β-actin as a loading control. PBS+PBS, n = 8; IL-1 β +PBS, n = 19; IL-1 β +si Saa2 , n = 9; PBS+si Saa2 , n = 3. (E) Representative fluorescence immunostaining for Saa2 (red) and DAPI (blue, nucleic staining) in the labyrinth of placentas. n = 3, 5 images per mouse examined. Scale bars, 50 μm. (F) Real-time quantitative polymerase chain reaction (RT‒qPCR) was performed to evaluate the effect of siRNA treatment, n = 6 for each group (G) Hematoxylin and eosin (H&E) staining was performed to compare placental thicknesses at ×5 magnification. The solid arrows crossing the central cut surface of the placentas indicate the location of measurements: fetal segments were identified as a compilation of the junctional zone and labyrinth. Scale bars, 200 μm (H) Statistical analysis shows the results of H&E staining measuring fetal placental length at the thickest location. PBS+PBS, n = 3; IL-1 β +PBS, n = 4; IL-1 β +si Saa2 , n = 3; PBS+si Saa2 , n = 3. (I) Nissl staining was performed to measure cortical thickness (upper red arrows) and ventricle area (lower red panels) in the fetal brain. Scale bars, 200 μm. (J,K) Nissl staining measuring cortical thickness and ventricle area. Quantitative data, with the median indicated by the solid line for each group, represents the average of these measurements from five random brain sections for each litter. PBS+PBS, n = 3; IL-1 β +PBS, n = 6; IL-1 β +si Saa2 , n = 4; PBS+si Saa2 , n = 3 (L) The fetal viability per litter. (M) Preterm birth rates. PBS+PBS, n = 18; IL-1 β +PBS, n = 34; IL-1 β +si Saa2 , n = 30; PBS+si Saa2 , n = 10. (N) Representative images of the placenta and its corresponding fetus between groups. (O,P) Placenta (O) and fetal weights (P) . PBS+PBS, n = 10; IL-1 β +PBS, n = 16; IL-1 β +si Saa2 , n = 8; PBS+si Saa2 , n = 8. IUI: intrauterine injection; IV: intravenous; IP: intraperitoneal. Values are expressed as the mean ± SEM, One-way ANOVA with Bonferroni post hoc tests for multiple comparisons of normally distributed data and Kruskal‒Wallis with Dunn’s multiple comparisons tests for nonparametric data (C,D,F,H,J,K,O,P) . Chi-square test (L,M) , * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Cells were cultured with the addition of mouse SAA2 protein (CUSABIO Technology, Houston, TX) at 100–1,000 ng/mL or LPS (1 μg/mL) based on published in vitro studies ( ; ; ) and pilot experiments showing macrophage activation within this range.

    Techniques: Expressing, Injection, Enzyme-linked Immunosorbent Assay, Western Blot, Control, Fluorescence, Immunostaining, Staining, Real-time Polymerase Chain Reaction

    SAA2 induces inflammation in macrophage cells. (A) A schematic diagram illustrating our workflow involving recombinant mouse SAA2 (100 ng/mL, 500 ng/mL or 1 ug/mL) or PBS treatment of RAW264.7 macrophages for the indicated time periods (hpi = hours post-infection). (B,C) Cell phagocytosis and cytotoxicity as evaluated by flow cytometry and lactate dehydrogenase (LDH) assay, respectively. (D–G) Immune status as determined by flow cytometry (D,E) and their quantification (F,G) . (H) Concentrations of the indicated cytokines in the culture media and the time period at which they were measured by ELISA. Values are expressed as the mean ± SEM, n = 3 independent replicates performed at different time. One-way ANOVA One-way ANOVA with Bonferroni post hoc tests for multiple comparisons of normally distributed data, or Student’s t-test where appropriate. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation

    doi: 10.3389/fphar.2026.1749966

    Figure Lengend Snippet: SAA2 induces inflammation in macrophage cells. (A) A schematic diagram illustrating our workflow involving recombinant mouse SAA2 (100 ng/mL, 500 ng/mL or 1 ug/mL) or PBS treatment of RAW264.7 macrophages for the indicated time periods (hpi = hours post-infection). (B,C) Cell phagocytosis and cytotoxicity as evaluated by flow cytometry and lactate dehydrogenase (LDH) assay, respectively. (D–G) Immune status as determined by flow cytometry (D,E) and their quantification (F,G) . (H) Concentrations of the indicated cytokines in the culture media and the time period at which they were measured by ELISA. Values are expressed as the mean ± SEM, n = 3 independent replicates performed at different time. One-way ANOVA One-way ANOVA with Bonferroni post hoc tests for multiple comparisons of normally distributed data, or Student’s t-test where appropriate. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Cells were cultured with the addition of mouse SAA2 protein (CUSABIO Technology, Houston, TX) at 100–1,000 ng/mL or LPS (1 μg/mL) based on published in vitro studies ( ; ; ) and pilot experiments showing macrophage activation within this range.

    Techniques: Recombinant, Infection, Flow Cytometry, Lactate Dehydrogenase Assay, Enzyme-linked Immunosorbent Assay

    The P2X7 receptor is required for preterm birth induced by sub-chronic maternal inflammation. (A) A schematic diagram illustrating the study design. At E14-17, wild-type C57BJL (WT) and P2x7r knockout (P2X7R KO) mice underwent intraperitoneal injection (IP) with mouse recombinant IL-1 β or PBS for four consecutive days. Placenta was harvested from dams at embryonic (E) day 18. The Agarose gel at the bottom panel demonstrates multiplex PCR-based genotyping of genomic DNA samples for the detection of P2x7r (+/+) and P2x7r (−/−) genotypes. (B) At E18, fetal viability was determined as the percentage of fetuses that were viable. WT groups: PBS, n = 40 from 5 dam; IL-1 β , n = 78 from 11 dam; P2x7r −/− groups: PBS, n = 43 from 6 dam; IL-1 β , n = 43 from 7 dam. (C,D) Gel images of SAA2 expression in the placenta and statistical analysis normalized to the levels of actin as a loading control. WT groups: PBS, n = 5; IL-1 β , n = 7; P2X7R −/− groups: PBS, n = 4; IL-1 β , n = 6. One sample from the control P2X7R −/− group was excluded from analysis because the band was not fully resolved, as indicated by the vertical arrow. (E) Placental IL-1β expression following maternal inflammation as determined by ELISA. WT groups: PBS, n = 4; IL-1 β , n = 3; P2x7r −/− groups: PBS, n = 4; IL-1 β , n = 3. (F) Immunoprecipitation followed by Western blot analysis of RAW264.7 cells exposed to inflammatory conditions. IP: immunoprecipitation. Values are expressed as the mean ± SEM, Chi-square test (B) and Student’s t-test (D,E) , * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation

    doi: 10.3389/fphar.2026.1749966

    Figure Lengend Snippet: The P2X7 receptor is required for preterm birth induced by sub-chronic maternal inflammation. (A) A schematic diagram illustrating the study design. At E14-17, wild-type C57BJL (WT) and P2x7r knockout (P2X7R KO) mice underwent intraperitoneal injection (IP) with mouse recombinant IL-1 β or PBS for four consecutive days. Placenta was harvested from dams at embryonic (E) day 18. The Agarose gel at the bottom panel demonstrates multiplex PCR-based genotyping of genomic DNA samples for the detection of P2x7r (+/+) and P2x7r (−/−) genotypes. (B) At E18, fetal viability was determined as the percentage of fetuses that were viable. WT groups: PBS, n = 40 from 5 dam; IL-1 β , n = 78 from 11 dam; P2x7r −/− groups: PBS, n = 43 from 6 dam; IL-1 β , n = 43 from 7 dam. (C,D) Gel images of SAA2 expression in the placenta and statistical analysis normalized to the levels of actin as a loading control. WT groups: PBS, n = 5; IL-1 β , n = 7; P2X7R −/− groups: PBS, n = 4; IL-1 β , n = 6. One sample from the control P2X7R −/− group was excluded from analysis because the band was not fully resolved, as indicated by the vertical arrow. (E) Placental IL-1β expression following maternal inflammation as determined by ELISA. WT groups: PBS, n = 4; IL-1 β , n = 3; P2x7r −/− groups: PBS, n = 4; IL-1 β , n = 3. (F) Immunoprecipitation followed by Western blot analysis of RAW264.7 cells exposed to inflammatory conditions. IP: immunoprecipitation. Values are expressed as the mean ± SEM, Chi-square test (B) and Student’s t-test (D,E) , * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Cells were cultured with the addition of mouse SAA2 protein (CUSABIO Technology, Houston, TX) at 100–1,000 ng/mL or LPS (1 μg/mL) based on published in vitro studies ( ; ; ) and pilot experiments showing macrophage activation within this range.

    Techniques: Knock-Out, Injection, Recombinant, Agarose Gel Electrophoresis, Multiplex Assay, Expressing, Control, Enzyme-linked Immunosorbent Assay, Immunoprecipitation, Western Blot

    Expression patterns of SAA1 and SAA2 in the human term placenta. (A) Representative images of SAA1 and SAA2 expression in the stem villi. (B) Representative images of SAA1and SAA2 expression in the terminal villi. (C,F) Representative images of SAA1 and macrophage marker, IBA-1expression in the stem villi. (D,G) Representative images of SAA1 and endothelial marker, vimentin expression in the terminal villi. (E,H) Representative images of SAA1 and trophoblast marker, cytokeratin expression in the terminal villi. n = 5 placentas, 6 images per placenta examined, Scale bars: 10 μm for insect images; 50 μm for all other images.

    Journal: Frontiers in Pharmacology

    Article Title: Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation

    doi: 10.3389/fphar.2026.1749966

    Figure Lengend Snippet: Expression patterns of SAA1 and SAA2 in the human term placenta. (A) Representative images of SAA1 and SAA2 expression in the stem villi. (B) Representative images of SAA1and SAA2 expression in the terminal villi. (C,F) Representative images of SAA1 and macrophage marker, IBA-1expression in the stem villi. (D,G) Representative images of SAA1 and endothelial marker, vimentin expression in the terminal villi. (E,H) Representative images of SAA1 and trophoblast marker, cytokeratin expression in the terminal villi. n = 5 placentas, 6 images per placenta examined, Scale bars: 10 μm for insect images; 50 μm for all other images.

    Article Snippet: Cells were cultured with the addition of mouse SAA2 protein (CUSABIO Technology, Houston, TX) at 100–1,000 ng/mL or LPS (1 μg/mL) based on published in vitro studies ( ; ; ) and pilot experiments showing macrophage activation within this range.

    Techniques: Expressing, Marker

    a MA-plot comparing mammary glands from NP (MG NP ) and N (MG N ) mice. Red and blue dots indicate significantly upregulated and downregulated genes, respectively (adjusted p-value < 0.05); gray dots represent non-significant changes. b Box plots show eight upregulated and seven downregulated secretory genes with adjusted p-values < 0.05. Gene expression levels in MG NP are shown in red, and those in MG N are shown in cyan. c MTT assay results showing the effects of secretory peptides on HER2/neu+ mammary tumor cell proliferation. Cells were treated with either vehicle control, SAA1, SAA2, or THBS4 peptides, and cell viability was assessed at 1, 2, or 3 days post-treatment. All comparisons to the vehicle control yielded p < 0.05, except for the optical density measured 3 days after SAA2 treatment. d Representative images from Boyden chamber assays showing the migration of HER2/neu+ mammary tumor cells in response to secretory peptides, SAA1, SAA2, or THBS4. Ctrl, vehicle control. e Transcriptional expression of SAA1 and SAA2 in breast cancer samples from the TCGA and METABRIC databases, stratified by TP53 status (WT, wild-type vs. Mut, mutant).

    Journal: NPJ Breast Cancer

    Article Title: Stromal fibroblastic mutant Trp53 promotes mammary tumor development via enhanced secretion of paracrine factors

    doi: 10.1038/s41523-025-00876-y

    Figure Lengend Snippet: a MA-plot comparing mammary glands from NP (MG NP ) and N (MG N ) mice. Red and blue dots indicate significantly upregulated and downregulated genes, respectively (adjusted p-value < 0.05); gray dots represent non-significant changes. b Box plots show eight upregulated and seven downregulated secretory genes with adjusted p-values < 0.05. Gene expression levels in MG NP are shown in red, and those in MG N are shown in cyan. c MTT assay results showing the effects of secretory peptides on HER2/neu+ mammary tumor cell proliferation. Cells were treated with either vehicle control, SAA1, SAA2, or THBS4 peptides, and cell viability was assessed at 1, 2, or 3 days post-treatment. All comparisons to the vehicle control yielded p < 0.05, except for the optical density measured 3 days after SAA2 treatment. d Representative images from Boyden chamber assays showing the migration of HER2/neu+ mammary tumor cells in response to secretory peptides, SAA1, SAA2, or THBS4. Ctrl, vehicle control. e Transcriptional expression of SAA1 and SAA2 in breast cancer samples from the TCGA and METABRIC databases, stratified by TP53 status (WT, wild-type vs. Mut, mutant).

    Article Snippet: The SAA1 (Aviva Systems Biology, OPCA03381), SAA2 (Aviva Systems Biology, OPCA00215), or THBS4 (Aviva Systems Biology, OPCA07418) peptides were added to the culture medium individually with a final concentration of 100 nM.

    Techniques: Gene Expression, MTT Assay, Control, Migration, Expressing, Mutagenesis