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  • 93
    Santa Cruz Biotechnology polyclonal cx3cr1 ab
    Postnatal microglia-depleted neuronal cultures express <t>CX3CR1</t> and overexpress CX3CR1 under OGD. ( A) Mature hippocampal cultures prepared from postnatal C57BL/6 mice and treated with 2.5 μM cytosine arabinoside (AraC) were stained with anti-CX3CR1 (red) and anti-MAP2 (green). CX3CR1 significantly co-localizes with MAP2 + cell bodies in normal hippocampal culture (middle panel). Compared to normal culture conditions, OGD-treated neurons overexpressed CX3CR1 (upper panel). Normal cultures without CX3CR1 staining served as experimental controls (lower panel). Scale bars = 100 µm, n = 4/group. ( B ) CX3CR1 expression was evaluated by calculating the mean density with the VisionWorks ® LS Image Acquisition and Analysis Software (UVP, LLC, CA, USA).
    Polyclonal Cx3cr1 Ab, supplied by Santa Cruz Biotechnology, 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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    92
    Miltenyi Biotec anti cx3cr1 antibody
    Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and <t>Cx3cr1.</t>
    Anti Cx3cr1 Antibody, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Torrey Pines Biolabs rabbit anti cx3cr1 antibody
    Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and <t>Cx3cr1.</t>
    Rabbit Anti Cx3cr1 Antibody, supplied by Torrey Pines Biolabs, 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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    Bioss anti cx3cr1
    Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and <t>Cx3cr1.</t>
    Anti Cx3cr1, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bioss cx3cr1
    Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and <t>Cx3cr1.</t>
    Cx3cr1, supplied by Bioss, 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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    Image Search Results


    Postnatal microglia-depleted neuronal cultures express CX3CR1 and overexpress CX3CR1 under OGD. ( A) Mature hippocampal cultures prepared from postnatal C57BL/6 mice and treated with 2.5 μM cytosine arabinoside (AraC) were stained with anti-CX3CR1 (red) and anti-MAP2 (green). CX3CR1 significantly co-localizes with MAP2 + cell bodies in normal hippocampal culture (middle panel). Compared to normal culture conditions, OGD-treated neurons overexpressed CX3CR1 (upper panel). Normal cultures without CX3CR1 staining served as experimental controls (lower panel). Scale bars = 100 µm, n = 4/group. ( B ) CX3CR1 expression was evaluated by calculating the mean density with the VisionWorks ® LS Image Acquisition and Analysis Software (UVP, LLC, CA, USA).

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: Postnatal microglia-depleted neuronal cultures express CX3CR1 and overexpress CX3CR1 under OGD. ( A) Mature hippocampal cultures prepared from postnatal C57BL/6 mice and treated with 2.5 μM cytosine arabinoside (AraC) were stained with anti-CX3CR1 (red) and anti-MAP2 (green). CX3CR1 significantly co-localizes with MAP2 + cell bodies in normal hippocampal culture (middle panel). Compared to normal culture conditions, OGD-treated neurons overexpressed CX3CR1 (upper panel). Normal cultures without CX3CR1 staining served as experimental controls (lower panel). Scale bars = 100 µm, n = 4/group. ( B ) CX3CR1 expression was evaluated by calculating the mean density with the VisionWorks ® LS Image Acquisition and Analysis Software (UVP, LLC, CA, USA).

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Staining, Expressing, Software

    CX3CR1 was upregulated in neurons of the infarct brain in pMCAO mice. ( A ) Representative CX3CR1 stains in the peri-infarction (1), hippocampus (2), and striatum (3) of the ipsilateral hemisphere (bottom panel), the counterparts in the contralateral hemisphere (middle panel), and the intact control hemisphere (upper panel) in C57BL/6 mice 24 hours after pMCAO. ( B ) Double staining with CX3CR1 and NeuN demonstrated that CX3CR1 was mainly expressed in ischemic neurons in the infarct. ( C ) Semi-quantification analysis showed that the number of CX3CR1/NeuN positive cells significantly increased 24 hours after pMCAO (**p < 0.01). Cells were counted in 5 randomly chosen 200× magnification fields on five sections in four replicate mice per group in three separate experiments. ( D ) CX3CR1 protein expression in brain ischemia. Western blot analysis was performed using brain homogenate obtained from the ipsilateral, contralateral, and intact control hemispheres 24 hours after pMCAO. The results were quantified and normalized to β-Actin. Scale bars = 100 µm, n = 4/group.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: CX3CR1 was upregulated in neurons of the infarct brain in pMCAO mice. ( A ) Representative CX3CR1 stains in the peri-infarction (1), hippocampus (2), and striatum (3) of the ipsilateral hemisphere (bottom panel), the counterparts in the contralateral hemisphere (middle panel), and the intact control hemisphere (upper panel) in C57BL/6 mice 24 hours after pMCAO. ( B ) Double staining with CX3CR1 and NeuN demonstrated that CX3CR1 was mainly expressed in ischemic neurons in the infarct. ( C ) Semi-quantification analysis showed that the number of CX3CR1/NeuN positive cells significantly increased 24 hours after pMCAO (**p < 0.01). Cells were counted in 5 randomly chosen 200× magnification fields on five sections in four replicate mice per group in three separate experiments. ( D ) CX3CR1 protein expression in brain ischemia. Western blot analysis was performed using brain homogenate obtained from the ipsilateral, contralateral, and intact control hemispheres 24 hours after pMCAO. The results were quantified and normalized to β-Actin. Scale bars = 100 µm, n = 4/group.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Double Staining, Expressing, Western Blot

    Coupling of CX3CR1 to apoptotic neuronal cell death in pMCAO mice. ( A ) Triple staining with cleaved Caspase-3 (apoptotic marker), CX3CR1, and NeuN (neuron marker) was performed and demonstrated that CX3CR1 was coupled to apoptotic neurons in ischemic damage 24 hours following pMCAO. Scale bars = 100 µm, n = 4/group. ( B ) Semi-quantification analysis showed that the number of Caspase-3/CX3CR1/NeuN positive cells was significantly increased in the ipsilateral hemisphere (**p < 0.01 vs. contralateral and intact control), whereas no difference was observed in these sites between the contralateral and control hemispheres. Cells were counted in 5 randomly chosen 200× magnification fields on five sections in four replicate mice per group in three separate experiments.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: Coupling of CX3CR1 to apoptotic neuronal cell death in pMCAO mice. ( A ) Triple staining with cleaved Caspase-3 (apoptotic marker), CX3CR1, and NeuN (neuron marker) was performed and demonstrated that CX3CR1 was coupled to apoptotic neurons in ischemic damage 24 hours following pMCAO. Scale bars = 100 µm, n = 4/group. ( B ) Semi-quantification analysis showed that the number of Caspase-3/CX3CR1/NeuN positive cells was significantly increased in the ipsilateral hemisphere (**p < 0.01 vs. contralateral and intact control), whereas no difference was observed in these sites between the contralateral and control hemispheres. Cells were counted in 5 randomly chosen 200× magnification fields on five sections in four replicate mice per group in three separate experiments.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Staining, Marker

    CX3CR1 deficiency attenuated infarct volume and neurological deficit after pMCAO. ( A ) Cerebral blood flow (CBF) analysis showed that the blood flow of the right middle cerebral artery territory decreased dramatically after occlusion (normal 168.3 ± 8.5 ml/100 g/min vs. pMCAO 37.3 ± 10.3 ml/100 g/min). There was no difference between the CX3CR1 +/+ and CX3CR1 −/− groups. ( B ) Apparent diffusion coefficient (ADC) and T2-weighted MRI imaging, respectively, showed the damaged volume at 30 min and the infarction volume 24 hours after pMCAO between the CX3CR1 +/+ and CX3CR1 −/− groups. ( C ) TTC staining demonstrated the same infarction volume as seen in the T2 images. ( D ) Quantification analysis showed the damaged volume was similar between the two groups 30 min post-pMCAO, whereas the infarction volume 24 hours post-pMCAO was significantly smaller in CX3CR1 −/− mice (*p < 0.05 vs. CX3CR1 +/+ ). ( E ) Among damaged brains with similar ADC, 96.7% of the CX3CR1 +/+ group versus 71.9% of the CX3CR1 −/− group proceeded to ischemia in 24 hours, as shown in the T2-weighted MRI. ( F ) CX3CR1 deficiency relieved the neurological deficits in mice 24 hours after ischemia (*p < 0.05). Representative images were shown; n = 9–13 per group.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: CX3CR1 deficiency attenuated infarct volume and neurological deficit after pMCAO. ( A ) Cerebral blood flow (CBF) analysis showed that the blood flow of the right middle cerebral artery territory decreased dramatically after occlusion (normal 168.3 ± 8.5 ml/100 g/min vs. pMCAO 37.3 ± 10.3 ml/100 g/min). There was no difference between the CX3CR1 +/+ and CX3CR1 −/− groups. ( B ) Apparent diffusion coefficient (ADC) and T2-weighted MRI imaging, respectively, showed the damaged volume at 30 min and the infarction volume 24 hours after pMCAO between the CX3CR1 +/+ and CX3CR1 −/− groups. ( C ) TTC staining demonstrated the same infarction volume as seen in the T2 images. ( D ) Quantification analysis showed the damaged volume was similar between the two groups 30 min post-pMCAO, whereas the infarction volume 24 hours post-pMCAO was significantly smaller in CX3CR1 −/− mice (*p < 0.05 vs. CX3CR1 +/+ ). ( E ) Among damaged brains with similar ADC, 96.7% of the CX3CR1 +/+ group versus 71.9% of the CX3CR1 −/− group proceeded to ischemia in 24 hours, as shown in the T2-weighted MRI. ( F ) CX3CR1 deficiency relieved the neurological deficits in mice 24 hours after ischemia (*p < 0.05). Representative images were shown; n = 9–13 per group.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Diffusion-based Assay, Imaging, Staining

    CX3CR1 deficiency decreased Caspase-3 positive neuronal cells after pMCAO. ( A ) Immunohistochemical staining of Caspase-3 antibody in the ipsilateral (1) peri-infarct region, (2) hippocampus, and (3) striatum 24 hours after pMCAO. ( B ) Semi-quantification analysis of the number of Caspase-3 positive cells demonstrated that CX3CR1 deficiency decreased the number of apoptotic cells in the peri-infarction region, hippocampus, and striatum (*p < 0.05, **p < 0.01 vs. CX3CR1 +/+ group). ( C ) Double staining with Caspase-3 and NeuN showed that CX3CR1 −/− mice had fewer apoptotic neurons in the infarct than CX3CR1 +/+ mice after pMCAO. ( D ) Semi-quantification analysis of Caspase-3/NeuN-positive cells demonstrated that CX3CR1 deficiency decreased the number of the apoptotic neurons in the infarct region (**p < 0.01 vs. CX3CR1 +/+ group). Representative images were shown; scale bars = 50 µm, n = 4/group. Cells were counted in 5 randomly chosen 200× magnification fields on five sections from mice in three independent experiments.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: CX3CR1 deficiency decreased Caspase-3 positive neuronal cells after pMCAO. ( A ) Immunohistochemical staining of Caspase-3 antibody in the ipsilateral (1) peri-infarct region, (2) hippocampus, and (3) striatum 24 hours after pMCAO. ( B ) Semi-quantification analysis of the number of Caspase-3 positive cells demonstrated that CX3CR1 deficiency decreased the number of apoptotic cells in the peri-infarction region, hippocampus, and striatum (*p < 0.05, **p < 0.01 vs. CX3CR1 +/+ group). ( C ) Double staining with Caspase-3 and NeuN showed that CX3CR1 −/− mice had fewer apoptotic neurons in the infarct than CX3CR1 +/+ mice after pMCAO. ( D ) Semi-quantification analysis of Caspase-3/NeuN-positive cells demonstrated that CX3CR1 deficiency decreased the number of the apoptotic neurons in the infarct region (**p < 0.01 vs. CX3CR1 +/+ group). Representative images were shown; scale bars = 50 µm, n = 4/group. Cells were counted in 5 randomly chosen 200× magnification fields on five sections from mice in three independent experiments.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Immunohistochemical staining, Staining, Double Staining

    CX3CR1 deficiency protected neurons against glutamate-induced apoptosis in vitro . ( A ) Morphological changes of neurons after exposure to glutamate for 30 min. (1 and 2) Cultured healthy CX3CR1 +/+ and CX3CR1 −/− neurons extended several dendritic trunks, and the dendrites had numerous protrusions. (3) Glutamate treatment caused the rupture of the dendrites and shrinking of the cell body in CX3CR1 +/+ neurons, whereas (4) CX3CR1 deficiency protected the neurons against this damage, resulting in the induced formation of bead-like structures and a decrease of fine protrusions only. (5) Neutralizing the CX3CR1 with anti-CX3CR1 antibody could attenuate the damage of glutamate, (6) while the same animal source of anti-IgG antibody could not attenuate the damage. ( B ) Cell death was assessed by measuring LDH release from neurons in all groups. Glutamate treatment could increase the LDH release, whereas CX3CR1 deficiency can attenuate the increase of LDH. Moreover, neutralizing the CX3CR1 could also attenuate this increase of LDH. ( C ) An MTT assay was performed to evaluate neuronal survival after glutamate treatment. CX3CR1 deficiency and neutralization could reduce glutamate-induced neuronal death (*p < 0.05, **p < 0.01). Representative images were shown; scale bars = 50 µm, n = 10/group.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: CX3CR1 deficiency protected neurons against glutamate-induced apoptosis in vitro . ( A ) Morphological changes of neurons after exposure to glutamate for 30 min. (1 and 2) Cultured healthy CX3CR1 +/+ and CX3CR1 −/− neurons extended several dendritic trunks, and the dendrites had numerous protrusions. (3) Glutamate treatment caused the rupture of the dendrites and shrinking of the cell body in CX3CR1 +/+ neurons, whereas (4) CX3CR1 deficiency protected the neurons against this damage, resulting in the induced formation of bead-like structures and a decrease of fine protrusions only. (5) Neutralizing the CX3CR1 with anti-CX3CR1 antibody could attenuate the damage of glutamate, (6) while the same animal source of anti-IgG antibody could not attenuate the damage. ( B ) Cell death was assessed by measuring LDH release from neurons in all groups. Glutamate treatment could increase the LDH release, whereas CX3CR1 deficiency can attenuate the increase of LDH. Moreover, neutralizing the CX3CR1 could also attenuate this increase of LDH. ( C ) An MTT assay was performed to evaluate neuronal survival after glutamate treatment. CX3CR1 deficiency and neutralization could reduce glutamate-induced neuronal death (*p < 0.05, **p < 0.01). Representative images were shown; scale bars = 50 µm, n = 10/group.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: In Vitro, Cell Culture, MTT Assay, Neutralization

    CX3CR1 deficiency reduces calcium influx in glutamate-treated neurons. ( A ) Representative traces of calcium influx were shown. The influx occurred soon after glutamate treatment and reached the peak rapidly, whereas CX3CR1 deficiency and neutralization dramatically decreased the influx. ( B ) The volume of calcium influx was calculated by the fold increase in calcium. Calcium was increased by approximately six-fold in CX3CR1 +/+ neurons, but only by approximately two-fold in the CX3CR1 −/− group. Neutralizing the CX3CR1 could attenuate the calcium increase. ( C ) The time to reach half of the peak calcium concentration was recorded, which represented the rate of calcium influx. CX3CR1 deficiency and neutralization decreased the rate of calcium influx significantly (**p < 0.01). n = 20–30/group.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: CX3CR1 deficiency reduces calcium influx in glutamate-treated neurons. ( A ) Representative traces of calcium influx were shown. The influx occurred soon after glutamate treatment and reached the peak rapidly, whereas CX3CR1 deficiency and neutralization dramatically decreased the influx. ( B ) The volume of calcium influx was calculated by the fold increase in calcium. Calcium was increased by approximately six-fold in CX3CR1 +/+ neurons, but only by approximately two-fold in the CX3CR1 −/− group. Neutralizing the CX3CR1 could attenuate the calcium increase. ( C ) The time to reach half of the peak calcium concentration was recorded, which represented the rate of calcium influx. CX3CR1 deficiency and neutralization decreased the rate of calcium influx significantly (**p < 0.01). n = 20–30/group.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Neutralization, Concentration Assay

    Diagram of the neurodegenerative mechanism of neuronal CX3CR1 in ischemic stroke in mice. Neuronal CX3CR1 mediates the neuronal apoptosis in ischemic stroke through its activation of caspases and glutamate-induced calcium influx. Consequently, CX3CR1 deficiency improved the outcome of mice in a model of ischemic stroke.

    Journal: Scientific Reports

    Article Title: Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1

    doi: 10.1038/s41598-017-18774-0

    Figure Lengend Snippet: Diagram of the neurodegenerative mechanism of neuronal CX3CR1 in ischemic stroke in mice. Neuronal CX3CR1 mediates the neuronal apoptosis in ischemic stroke through its activation of caspases and glutamate-induced calcium influx. Consequently, CX3CR1 deficiency improved the outcome of mice in a model of ischemic stroke.

    Article Snippet: When necessary, cells were pre-treated with polyclonal CX3CR1 Ab (10 μg/ml, 30 min; sc-30030, Santa Cruz, Dallas, TX, USA) or rabbit IgG (10 μg/ml, 30 min; BA-1000, Vector laboratories, Burlingame, CA, USA) in culture medium; drugs were present during and after the glutamate challenge.

    Techniques: Activation Assay

    Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and Cx3cr1.

    Journal: Clinical & experimental gastroenterology & hepatology

    Article Title: Differential Sensitivity of Kupffer Cells and Hepatic Monocyte-Derived Macrophages to Bacterial Lipopolysaccharide

    doi: 10.31531/edwiser.jcegh.1000106

    Figure Lengend Snippet: Livers from bone marrow transplanted mice were perfused and digested with collagenase. Nonparenchymal cells were separated from hepatocytes by centrifugation. Kupffer cells were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.2 and F4/80. MDMs were purified from the nonparenchymal cell fraction via immunomagnetic bead separation using antibodies against CD45.1 and Cx3cr1.

    Article Snippet: The pellet was resuspended in MACS Buffer containing anti-CX3CR1 antibody (Miltenyi Biotec) (12 μl CX3CR1 antibody in 60 μl MACS buffer per 10 8 cells).

    Techniques: Centrifugation, Purification