Journal: PLoS Pathogens

Article Title: Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis

doi: 10.1371/journal.ppat.1009526

Figure Lengend Snippet: A Viruses pseudotyped with early (E) or late (L) X4 Envs from 5 patients of the ACS were used to infect CD4TL w/or w/o CXCL12 at increasing concentrations. Mean (± range) (open symbols) and individual (colored symbols) IC 50 s of CXCL12 are shown. The same color code as shown here is used throughout the article. Blue dotted lines represent the range of CXCL12/CXCR4 affinities. The X4 HIV-1 strain NL4-3 was used as control. B Mean and individual IC 50 s for neutralization by CCL4 of viruses pseudotyped with early (E) or late (L) R5 Envs from 5 patients of the ACS. Red dotted lines represent the range of CCL4/CCR5 affinities. The JR-FL and Bx08 strains are controls. C CXCL12-mediated inhibition of recombinant viruses pseudotyped with Envs from plasma of patients diagnosed at a chronic (green symbols) or late stage (yellow and red symbols) of infection. Group-2 and group-1 comprise Envs that are, or are not, more resistant to CXCL12 than NL4-3 or chronic Envs, respectively. Each data point represents the mean IC 50 of CXCL12 for neutralization of a given virus. D CXCL12-mediated neutralization of recombinant viruses expressing Envs isolated from plasma of patients at the time of PHI. Each data point is the mean IC 50 of CXCL12 (± SEM) for the indicated virus, calculated from independent experiments on CD4TL (left) and/or R5X4JT cells (right). Statistics are relative to NL4-3.

Article Snippet: MVC and AMD3100 were obtained from Sigma-Aldrich (cat# PZ0002 and A5602, respectively) and CXCL12 from Miltenyi Biotec (cat# 130-093-998).

Techniques: Control, Neutralization, Inhibition, Recombinant, Clinical Proteomics, Infection, Virus, Expressing, Isolation

Journal: PLoS Pathogens

Article Title: Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis

doi: 10.1371/journal.ppat.1009526

Figure Lengend Snippet: A Specific binding (SB) of gp120/sCD4 complexes to PBMC membranes. A representative experiment with gp120s #1 (SENS) and #6 (RES) (P#39) is shown. Gp120 #16 (SENS) and #28 (RES) (P#208) gave similar results. The extrapolated B max (i.e. maximum level of binding) were 2.9 and 1.6 pmole/mg for SENS and RES gp120s, respectively. B and C Displacement of gp120 binding by CXCL12. Forty and 80 nM of SENS or RES gp120/sCD4, respectively, were used, leading to similar levels of SB in the absence of CXCL12 (inset). D Effects of anti-CXCR4 mAbs on infection of CD4TL with SENS and RES viruses, expressed as percent infection relative to untreated control (100%). Means ± SEM of 5 independent experiments are shown, carried out with 20 ng of p24 of the viruses pseudotyped with Envs # 1 (SENS), # 6 (RES), # 16 (SENS), # 28 (RES) or NL4-3 Env. E Effects of anti-CXCR4 mAbs on virus population F8. Ten μM MVC was added to the assay medium. F Displacement of binding of anti-CXCR4 mAbs to CD4TL by CXCL12. Results (means ± SEM) are expressed relative to binding in the absence of CXCL12 (100%). The competition curves gave Ki values for CXCL12 ranging between 2.6 and 8.7 nM. G Displacement of binding of mAbs 4G10 and 12G5 to U87-CXCR4 cells by CXCL12. H Specific binding of 4G10 to U87-CXCR4 cells in the presence or absence of 1 μM CXCL12. Non-specific binding on parental U87 cells is also shown (grey symbols). Results are expressed as percent of maximal binding of 4G10 in the absence of CXCL12. 4G10 had similar affinity constants in the presence or absence of CXCL12 (Kd = 0.16 vs 0.25 μg/ml). Statistics are relative to binding w/o CXCL12.

Article Snippet: MVC and AMD3100 were obtained from Sigma-Aldrich (cat# PZ0002 and A5602, respectively) and CXCL12 from Miltenyi Biotec (cat# 130-093-998).

Techniques: Binding Assay, Infection, Control, Virus

Journal: PLoS Pathogens

Article Title: Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis

doi: 10.1371/journal.ppat.1009526

Figure Lengend Snippet: A Tropism of SENS and RES viruses for Tn, Tcm, Tem and Temra CD4TL. For each cell subset, the panel represents its proportion (PR) within CD4TL that have fused with viruses, compared to its proportion among all cells (infected and uninfected cells). BLaM-vpr-containing viruses pseudotyped with the SENS or RES Envs of P#39, #208, #1120, #8332 and #704 were used. NL4.3 (X4) and JRFL (R5) Envs served as controls. Results are means ± SEM of three independent experiments. B Fusion of SENS and RES viruses with CD4TL subsets in the absence or presence of 30 or 300 nM CXCL12. Percent fusion for each virus is expressed relative to fusion in the absence of CXCL12 (100%). C Infectivity of SENS and RES viruses in sorted CD4TL subsets. Percent infection of each T cell subset is expressed relative to infection of all CD4TL subsets (100%). Means ± SEM of three experiments are shown. D Infection experiments were repeated in the presence or absence of 300 nM CXCL12. Results are expressed relative to infectivity in the absence of CXCL12 (100%).

Article Snippet: MVC and AMD3100 were obtained from Sigma-Aldrich (cat# PZ0002 and A5602, respectively) and CXCL12 from Miltenyi Biotec (cat# 130-093-998).

Techniques: Infection, Virus

Journal: PLoS Pathogens

Article Title: Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis

doi: 10.1371/journal.ppat.1009526

Figure Lengend Snippet: A Percent depletion of bystander Tem cells among the fraction of SSC-high CD4TL in the presence of R5X4JT cells infected with SENS or RES viruses, compared to conditions with uninfected cells, w/ or w/o 10 μM AMD3100 or 300 nM CXCL12. B Percentage of Live/Dead and Annexin V positive cells within the fraction of SSC-high CD4TL after incubation with R5X4JT cells, in the presence or absence of AMD3100 or CXCL12. Results are means ± SEM of two independent experiments.

Article Snippet: MVC and AMD3100 were obtained from Sigma-Aldrich (cat# PZ0002 and A5602, respectively) and CXCL12 from Miltenyi Biotec (cat# 130-093-998).

Techniques: Infection, Incubation

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α decreased the number of mitochondria in chondrocytes. A . GO enrichment analysis based on RNA sequencing showing cellular metabolic changes in chondrocytes induced by SDF-1α at 200 ng/ml for 24 h. B . Representative CLSM images showing mitochondrial changes in chondrocytes after treatment with SDF-1α at 200 ng/ml for 48 h. Cells were counterstained with nuclei (DAPI, blue) and actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). C . Linear fluorescence quantification showing the distribution of mitochondria in chondrocytes (B). D . Total fluorescence quantification (per cell), validating the mitochondrial area in chondrocytes (B). Data were derived from six replicates based on three independent experiments ( n = 3). E . Representative western blot images showing changes in Cs protein levels in chondrocytes treated with SDF-1α at different concentrations for 48 h. Images were obtained from three independent experiments ( n = 3). F . Quantification of Cs protein in chondrocytes (E). Data were obtained from three independent experiments ( n = 3). G . Representative TEM images showing the changes in mitochondrial number in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Boxed areas (right panels) display enlarged fields to allow clearer visualization of individual mitochondria (indicated by arrows). Images were obtained from four independent experiments ( n = 4). H . Quantification of the mitochondrial number (per cell) in chondrocytes (G). Data are based on five cells per group from three independent experiments (n = 3). Data in C , D , F , and H are presented as the mean ± SD. Significance analyses in D and H were based on Two-tailed Student’s t-tests. Data in F were analyzed using a one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: RNA Sequencing, Fluorescence, Derivative Assay, Western Blot, Two Tailed Test

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α causes an imbalance in mitochondrial dynamics. A . Representative TEM images showing changes in mitochondrial morphology in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Images were obtained from three independent experiments ( n = 3). B . Quantification of mitochondrial morphology in chondrocytes (A). The data are presented based on three independent experiments ( n = 3). C . Representative CLSM images showing the mitochondrial changes in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Cyan boxes indicate morphological changes in mitochondrial networks by ImageJ. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). D . Quantification of mitochondrial branch junctions and mean branch length (per cell) in chondrocytes (C). Data are presented as seven cells per group from three independent experiments ( n = 3). E . Representative western blot images showing changes in Mfn1, Mfn2, Opa1, Drp1, and Fis1 in chondrocytes treated with SDF-1α at different concentrations for 48 h. Images were obtained from three independent experiments ( n = 3). F . Quantification of Mfn1, Mfn2, Opa1, Drp1 and Fis1 in chondrocytes (E). Data were obtained from three independent experiments ( n = 3). G . ATP assay showing ATP content in chondrocytes treated with SDF-1α for 48 h, presented as nmol/mg protein after normalization to total protein measured by BCA. Data were obtained from three independent experiments ( n = 3). H . Representative CLSM images showing Drp1 changes in chondrocytes after treatment with SDF-1α at 200 ng/ml for 48 h. Cells were counterstained with nuclei (DAPI, blue) and actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). I . Linear fluorescence quantification showing the distribution of Drp1 in the chondrocytes (H). Data in B , D , F , G , and I are presented as the mean ± SD. Significance analyses in B and D were based on Two-tailed Student’s t-tests. Data in F and G were analyzed using a one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Western Blot, ATP Assay, Fluorescence, Two Tailed Test

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α promotes mitophagy in chondrocytes. A . Representative CLSM images showing changes in mitochondria (red) and LC3B (green) expression in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Cells were counterstained with nuclei (DAPI, blue). Images were obtained from three independent experiments ( n = 3). B . Linear fluorescence quantification showing the distribution of mitochondria and LC3B in chondrocytes (A). Purple arrows indicate colocalization peaks of the mitochondria and LC3B. C . Statistical analysis illustrating changes in colocalized proportions of LC3B and mitochondria in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Data are based on three independent experiments ( n = 3). D . mRFP-GFP-LC3 adenovirus double-label assay showing changes in autophagic flux in chondrocytes induced by SDF-1α at 200 ng/ml for 48 h. Free red dots represent autolysosomes (indicated by red arrows). Yellow dots represent autophagosomes (indicated by yellow arrows). Images were selected from three independent experiments ( n = 3). E . Quantification of autolysosomes and autophagosomes (per cell) in chondrocytes (D). Data are based on six cells per group from three independent experiments ( n = 3). F . Representative western blot images showing changes in Bnip3, LC3B, p62, Parkin, and PINK1 in chondrocytes treated with SDF-1α at different concentrations for 48 h. Images were obtained from three independent experiments ( n = 3). G. Quantification of Bnip3, LC3B, p62, Parkin, and PINK1 in chondrocytes (F). Data were obtained from three independent experiments ( n = 3). H . Representative western blot images showing changes in PGC1α in chondrocytes treated with SDF-1α at different concentrations for 48 h. Images were obtained from three independent experiments ( n = 3). I . Quantification of PGC1α in chondrocytes (H). Data were obtained from three independent experiments ( n = 3). Data in C , E , G , and I are presented as the mean ± SD. Significance analysis in E was based on Two-tailed Student’s t-test. Data in G and I were based on one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Expressing, Fluorescence, Western Blot, Two Tailed Test

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α promotes activation of AMPKα signaling in chondrocytes. A . Schematic diagram illustrating AMPKα signaling-mediated mitochondrial function. B . Protein–protein interaction network demonstrating the impact of AMPKα signaling on mitochondrial dynamics and mitophagy. C . Representative western blot images showing changes in AMPKα and p-AMPKα in chondrocytes treated with SDF-1α at different concentrations for 6 h. Images were obtained from three independent experiments ( n = 3). D . Quantification of p-AMPKα in chondrocytes (C). Data were obtained from three independent experiments ( n = 3). E . Representative CLSM images showing changes in the nuclear translocation of p-AMPKα in chondrocytes induced by SDF-1α at 200 ng/ml for 6 h. Cells were counterstained with nuclei (DAPI, blue) and actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). F . Total fluorescence quantification (per cell) confirming the expression of p-AMPKα in chondrocytes (E). Data were obtained from 19 replicates of three independent experiments ( n = 3). G . Linear fluorescence quantification illustrating the distribution of p-AMPKα in the chondrocytes (E). H . Representative CLSM images showing mitochondrial alterations in chondrocytes pretreated with CC (10 μM, 1 h) and subsequently stimulated with SDF-1α (200 ng/ml, 48 h). Cyan boxes indicate morphological changes in the mitochondrial networks. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). I . Quantification of mitochondrial branch junctions and mean branch length (per cell) in chondrocytes (H). The data were based on eight replicates from three independent experiments. Data in D , F , G , and I are presented as the mean ± SD. Significance analysis in F was based on Two-tailed Student’s t-test. Data in D and I were based on one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Activation Assay, Western Blot, Translocation Assay, Fluorescence, Expressing, Two Tailed Test

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α regulates mitochondrial dynamics via CXCR4. A . Schematic depicting the entry of SDF-1α into chondrocytes mainly via CXCR4. B . Representative western blot images showing changes in Cs protein in chondrocytes by knockdown of CXCR4 in the presence of SDF-1α at 200 ng/ml for 48 h. Images were obtained from three independent experiments ( n = 3). C . Representative CLSM images showing mitochondrial changes in chondrocytes after CXCR4 knockdown in the presence of SDF-1α at 200 ng/ml for 48 h. Cyan boxes indicate morphological changes in the mitochondrial networks. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). D . Quantification of mitochondrial branch junctions and mean branch length (per cell) in chondrocytes (C). The data were based on eight replicates from three independent experiments. E . Representative western blotting images showing changes in Mfn1, Mfn2, Opa1, Drp1, and Fis1 in chondrocytes after CXCR4 knockdown in the presence of SDF-1α at 200 ng/ml for 48 h. Images were obtained from three independent experiments ( n = 3). F . Quantification of Mfn1, Mfn2, Opa1, Drp1, and Fis1 proteins in chondrocytes (E). Data were obtained from three independent experiments ( n = 3). G . Representative CLSM images showing Drp1 changes in chondrocytes following knockdown of CXCR4 in the presence of SDF-1α at 200 ng/ml for 48 h. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). H . Total fluorescence quantification (per cell) confirming the expression of Drp1 in chondrocytes (G). Data were obtained from 18 replicates derived from three independent experiments ( n = 3). I . Linear fluorescence quantification illustrating the distribution of Drp1 in chondrocytes (G). J . Representative CLSM images showing p-AMPKα changes in chondrocytes following knockdown of CXCR4 in the presence of SDF-1α at 200 ng/ml for 6 h. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). K . Total fluorescence quantification (per cell) confirming the expression of p-AMPKα in chondrocytes (J). Data were obtained from 16 replicates of three independent experiments ( n = 3). L . Linear fluorescence quantification showing the distribution of p-AMPKα in chondrocytes (J). Data in D , F , H , I , K , and L are presented as the mean ± SD. Significance analyses in D , F , H , and K were based on one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Western Blot, Knockdown, Fluorescence, Expressing, Derivative Assay

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α promotes MAPK/ERK signaling in chondrocytes. A . KEGG pathway analysis based on RNA sequencing showing upregulated pathways in chondrocytes induced by SDF-1α at 200 ng/ml for 24 h. B . Representative western blot images showing changes in ERK, p-ERK, JNK, p-JNK, p38, and p-p38 in chondrocytes treated with SDF-1α at different concentrations for 1 h. Images were obtained from three independent experiments ( n = 3). C . Quantification of p-ERK, p-JNK and p-p38 in chondrocytes (B). Data were obtained from three independent experiments ( n = 3). D . Representative western blotting images showing changes in ERK, p-ERK, AMPKα, and p-AMPKα in chondrocytes after CXCR4 knockdown in the presence of SDF-1α at 200 ng/ml for 6 h. Images were obtained from three independent experiments ( n = 3). E . Quantification of p-ERK and p-AMPKα in chondrocytes (D). Data were obtained from three independent experiments ( n = 3). F . Representative western blot images showing changes in ERK, p-ERK, AMPKα, and p-AMPKα in chondrocytes induced by SDF-1α at 200 ng/ml for 6 h in the presence or absence of PD98059 (10 μM). Images were obtained from three independent experiments ( n = 3). G . Quantification of p-ERK and p-AMPKα in chondrocytes (F). Data were obtained from three independent experiments ( n = 3). H . Representative CLSM images showing p-AMPKα changes in chondrocytes pretreated with PD98059 (10 μM, 2 h) and subsequently stimulated with SDF-1α (200 ng/ml, 6 h). Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). I . Total fluorescence quantification (per cell) confirming the expression of p-AMPKα in chondrocytes (H). Data were obtained from 14 replicates derived from three independent experiments ( n = 3). J . Linear fluorescence quantification illustrating the distribution of p-AMPKα in chondrocytes (H). Data in C , E , G , I , and J are presented as the mean ± SD. Significance analyses in C , E , G , and I were based on one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: RNA Sequencing, Western Blot, Knockdown, Fluorescence, Expressing, Derivative Assay

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: SDF-1α regulates mitochondrial dynamics via MAPK/ERK signaling. A . Representative western blot images showing changes in Cs in chondrocytes pretreated with PD98059 (10 μM, 2 h) and subsequently stimulated with SDF-1α (200 ng/ml, 48 h). Images were obtained from three independent experiments ( n = 3). B . Quantification of Cs in chondrocytes in (A). Data were obtained from three independent experiments ( n = 3). C . Representative CLSM images showing mitochondrial changes in chondrocytes pretreated with PD98059 (10 μM, 2 h) and subsequently stimulated with SDF-1α (200 ng/ml, 48 h). Cyan boxes indicate morphological changes in the mitochondrial networks. Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). D . Quantification of mitochondrial branch junctions and mean branch length (per cell) in chondrocytes (C). The data are based on eight cells per group from three independent experiments. E . Representative western blot images showing changes in Mfn1, Mfn2, Opa1, Drp1, and Fis1 in chondrocytes pretreated with PD98059 (10 μM, 2 h) and subsequently stimulated with SDF-1α (200 ng/ml, 48 h). Images were selected from three independent experiments ( n = 3). F . Quantification of Mfn1, Mfn2, Opa1, Drp1, and Fis1 in chondrocytes (E). Data were obtained from three independent experiments ( n = 3). G . Representative CLSM images showing Drp1 changes in chondrocytes pretreated with PD98059 (10 μM, 2 h) and subsequently stimulated with SDF-1α (200 ng/ml, 48 h). Cells were counterstained with nuclei (DAPI, blue) and the actin cytoskeleton (F-actin, green). Images were obtained from three independent experiments ( n = 3). H . Total fluorescence quantification (per cell) confirming the expression of Drp1 in chondrocytes (G). Data were obtained from 12 replicates of three independent experiments ( n = 3). I . Linear fluorescence quantification illustrating the distribution of Drp1 in chondrocytes (G). Data in B , D , F , H , and I are presented as the mean ± SD. Significance analyses in B , D , F , and H were based on one-way ANOVA. Statistical significance ( p ) value < 0.05.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Western Blot, Fluorescence, Expressing

Journal: Cell Communication and Signaling : CCS

Article Title: The SDF-1α/CXCR4 axis regulates chondrocyte mitochondrial dynamics via the ERK/AMPKα pathway

doi: 10.1186/s12964-026-02827-x

Figure Lengend Snippet: Schematic diagram showing the regulatory mechanism of mitochondrial dynamics in chondrocytes induced by SDF-1α. This work demonstrates that SDF-1α signals through CXCR4 to activate p-ERK signaling, thereby promoting the phosphorylation and nuclear translocation of p-AMPKα. This signaling cascade promotes mitochondrial fission and mitophagy and reduces mitochondrial fusion in chondrocytes. Collectively, these findings establish that SDF-1α/CXCR4 regulates mitochondrial dynamics in chondrocytes via the ERK/AMPKα axis.

Article Snippet: For inhibition experiments, cells were preincubated with 10 μM PD98059 (HY-12028, MedChemExpress) for 2 h or 10 μM CC (HY-13418 A, MedChemExpress) for 1 h before SDF-1α exposure [ ].

Techniques: Phospho-proteomics, Translocation Assay

Journal: Frontiers in Psychiatry

Article Title: Plasma Chemokines in Patients with Alcohol Use Disorders: Association of CCL11 (Eotaxin-1) with Psychiatric Comorbidity

doi: 10.3389/fpsyt.2016.00214

Figure Lengend Snippet: Plasma chemokine concentrations in abstinent alcohol use disorders (AUD) patients and control subjects . (A) CXCL8 [interleukin-8 (IL-8)]; (B) CXCL12 [stromal cell-derived factor-1 (SDF-1)]; (C) CX 3 CL1 (fractalkine); (D) CCL2 [monocyte chemoattractant protein-1 (MCP-1)]; (E) CCL3 [macrophage inflammatory protein-1 alpha (MIP-1α)]; and (F) CCL11 (eotaxin-1) concentrations according to “history of AUD.” Bars are estimated marginal means and 95% confidence intervals (95% CI) (picograms per milliliter). Data were analyzed by two-way analysis of covariance (ANCOVA) and * p < 0.05 and *** p < 0.001 denote a significant main effect of “history of AUD.” (G) CCL3 (MIP-1α) and (H) CCL11 (eotaxin-1) concentrations according to “history of AUD” and “sex.” Bars are marginal means and 95% CI (picograms per milliliter). Data were analyzed by two-way ANCOVA and * p < 0.05 denotes a significant main effect of “sex.” +++ p < 0.001 denotes significant differences compared to male AUD patients because there was an interaction of factors.

Article Snippet: CXCL12 (SDF-1), CX 3 CL1 (fractalkine), and CCL11 (eotaxin-1) were measured in rat plasma with commercial enzyme-linked immunosorbent assay (ELISA) kits in 96-well plate format following the manufacturer’s instructions: ELISA Kit for SDF-1 (product #: SEA122Ra; Cloud-Clone Corp., Wuhan, Hubei, PR China), Rat Fractalkine ELISA Kit (CX 3 CL1) (product #: ab100760; Abcam, Cambridge, UK), and Rat Eotaxin 1 (Eotaxin 1/CCL11/ECF) ELISA Kit (product #: CSB-E07319r; Cusabio, College Park, MD, USA).

Techniques: Derivative Assay

Journal: Frontiers in Psychiatry

Article Title: Plasma Chemokines in Patients with Alcohol Use Disorders: Association of CCL11 (Eotaxin-1) with Psychiatric Comorbidity

doi: 10.3389/fpsyt.2016.00214

Figure Lengend Snippet: Plasma concentrations of CXCL12 [stromal cell-derived factor-1 (SDF-1)], CX 3 CL1 (fractalkine), and CCL11 (eotaxin-1) in male Wistar rats exposed to ethanol and acute stress . (A) CXCL12 (SDF-1) and (B) CX 3 CL1 (fractalkine) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle. (C) CCL11 (eotaxin-1) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle with/without acute stress before ethanol exposure. Bars are means and SEM (nanograms per milliliter). CXCL12 and CX 3 CL1 concentrations were analyzed by Student’s t -test and && p < 0.01 denotes significant differences compared to the vehicle group. CCL11 concentrations were analyzed by two-way analysis of variance (ANOVA) and ** p < 0.01 and *** p < 0.001 denote significant main effect of “stress” and “ethanol exposure,” respectively. (D) CXCL12 (SDF-1); (E) CX 3 CL1 (fractalkine); and (F) CCL11 (eotaxin-1) concentrations were determined in rats exposed to acute ethanol (3 g/kg, i.g.) at 0, 30, 60, 120, and 240 min after ethanol exposure. Circles are means and SEM (nanograms per milliliter). CXCL12, CX 3 CL1, and CCL11 concentrations were analyzed by one-way ANOVA and * p < 0.05, ** p < 0.01, and *** p < 0.001 denote significant main effect of “time.” + p < 0.05 and ++ p < 0.01 denote significant differences compared to t = 0 min. White circles are means and SEM (nanograms per milliliter) at t = 240 min with no ethanol exposure and concentrations were analyzed by Student’s t -test. & p < 0.05 denotes significant differences compared to t = 0 or 240 min with no ethanol.

Article Snippet: CXCL12 (SDF-1), CX 3 CL1 (fractalkine), and CCL11 (eotaxin-1) were measured in rat plasma with commercial enzyme-linked immunosorbent assay (ELISA) kits in 96-well plate format following the manufacturer’s instructions: ELISA Kit for SDF-1 (product #: SEA122Ra; Cloud-Clone Corp., Wuhan, Hubei, PR China), Rat Fractalkine ELISA Kit (CX 3 CL1) (product #: ab100760; Abcam, Cambridge, UK), and Rat Eotaxin 1 (Eotaxin 1/CCL11/ECF) ELISA Kit (product #: CSB-E07319r; Cusabio, College Park, MD, USA).

Techniques: Derivative Assay