Journal: American Journal of Respiratory and Critical Care Medicine

Article Title: The Inflammatory Preatherosclerotic Remodeling Induced by Intermittent Hypoxia Is Attenuated by RANTES/CCL5 Inhibition

doi: 10.1164/rccm.201012-2033oc

Figure Lengend Snippet: Figure 1. Intermittent hypoxia (IH) induces splenocyte activation. Splenocyte proliferation in response to concanavalin-A after 5 (A) and 14 (B) days of IH or air (N); *P less than 0.05 versus N (n ¼ 6–12 per group). Splenocyte mRNA expression of regulated upon activation, normal T-cell expressed and secreted (RANTES)/ chemokine ligand 5 (CCL5) (C), MIP-1a/CCL3 (D), MIP-1b/CCL4 (E), and MCP-1/CCL2 (F). Measurements were normalized to the eukary- otic 18S ribosomal-RNA (G) and expressed as fold induction of their baseline values; *P less than 0.05 versus N (n ¼ 6 per group). Spleno- cyte migration toward RANTES/CCL5 after 14 days of IH or air (H). Splenocytes were tested without stimulation or after 50 ng.ml-1 IFN-g stimulation; P less than 0.05 versus unstimu- lated* or stimulatedy splenocytes from N-mice (n ¼ 4). RANTES ¼ regulated upon activation, normal T cell expressed and secreted; MIP ¼ mac- rophage inflammatory protein; MCP ¼ monocyte chemotactic protein, CCL ¼ CC chemokine ligand.

Article Snippet: To confirm the role of RANTES/ CCL5 in IH-induced vascular remodeling, additional mice were treated as previously described (25), using a rat anti-mouse RANTES/CCL5 monoclonal antibody (R&D systems; intraperitoneal injection, 250 mg, three times per wk) or its rat IgG isotype control (ATCC, Molsheim, France) throughout the 14-day exposure to IH or air.

Techniques: Activation Assay, Expressing, Migration

Journal: American Journal of Respiratory and Critical Care Medicine

Article Title: The Inflammatory Preatherosclerotic Remodeling Induced by Intermittent Hypoxia Is Attenuated by RANTES/CCL5 Inhibition

doi: 10.1164/rccm.201012-2033oc

Figure Lengend Snippet: Figure 5. Regulated upon activation, normal T-cell expressed and secreted (RANTES)/chemokine ligand 5 (CCL5) neutralization attenuates in- termittent hypoxia (IH)-induced aorta remodeling. Mice were exposed to IH or air (N) for 14 days, and treated either with the anti-RANTES/CCL5 monoclonal antibody or with the control IgG throughout the exposure. (A) Intima–media thickness (n ¼ 7–8 each). (B) Cytosolic a-smooth muscle actin (a-SMA) expression with representative immunoblotting and quantitative analysis (n ¼ 5–7 each). (C) Nuclear factor-kB (NF-kB)–p50 expression with representative immunoblotting and quantitative analysis (n ¼ 4–7 each). (D) Quantification of T-cell infiltration in the aortic wall (n ¼ 7–8 each). (E) Representative RANTES/CCL5 immunostaining (10 3 20 magnification). (F) IFN-g mRNA expression normalized to ubiquitin (n ¼ 4–9 each). *P less than 0.05 versus N-IgG; yP less than 0.05 versus anti-RANTES–treated IH mice. (G) Regulation pathway of NF-kB activation and subsequent leukocyte recruitment and activation (adapted by permission from Reference [44]). GAPDH ¼ glyceraldehyde phosphate dehydrogenase.

Article Snippet: To confirm the role of RANTES/ CCL5 in IH-induced vascular remodeling, additional mice were treated as previously described (25), using a rat anti-mouse RANTES/CCL5 monoclonal antibody (R&D systems; intraperitoneal injection, 250 mg, three times per wk) or its rat IgG isotype control (ATCC, Molsheim, France) throughout the 14-day exposure to IH or air.

Techniques: Activation Assay, Neutralization, Control, Expressing, Western Blot, Immunostaining, Ubiquitin Proteomics

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: Effects of BME pre-treatment on antioxidant status in L132 cells against SNP-induced cytotoxicity

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: A Dose-dependent effects of SNP on LDH release. B Protective effect of BME and L-NAME on SNP-induced LDH release in L132 cells. The data presented are mean ± SEM of three independent experiments. *p < 0.05 versus control group and # p < 0.05 versus SNP treated group. C Effects of BME on SNP-induced morphological alterations in L132 cells by phase-contrast microscopy. a Control cells with no treatment, b BME (100 μg/ml), c SNP (500 μM) d cells pre-treated with BME (100 μg/ml) for 1 h and then treated with SNP (500 μM) and e cells pre-treated with L-NAME (200 μM) for 1 h and then treated with SNP (500 μM)

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control, Microscopy

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: Protective effects of BME against SNP induced NO production in L132 cells. The data presented are mean ± SEM of three independent experiments. *p < 0.05 versus control group and # p < 0.05 versus SNP treated group

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: A Estimation of ROS production by 2′,7′ DCFH-DA using a spectrofluorimeter. B The ROS production in L132 cells was monitored by fluorescence microscopy (Olympus) a Control cells with no treatment, b BME (100 μg/ml), c SNP (500 μM) d cells pre-treated with BME (100 μg/ml) for 1 h and then treated with SNP (500 μM) and e cells pre-treated with L-NAME (200 μM) for 1 h and then treated with SNP (500 μM)

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Fluorescence, Microscopy, Control

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: Protective effect of BME against SNP induced lipid peroxidation in L132 cells. The data presented are mean ± SEM of three independent experiments. *p < 0.05 versus control group and # p < 0.05 versus SNP treated group

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: A Effect of BME on DNA damage induced by SNP in L132 cells. a Control cells with no treatment, b BME (100 μg/ml), c SNP (500 μM) d cells pre-treated with BME (100 μg/ml) for 1 h and then treated with SNP (500 μM) and e cells pre-treated with L-NAME (200 μM) for 1 h and then treated with SNP (500 μM). B Tail movement of COMET (%) C Effect of BME on SNP-induced decrease of mitochondrial membrane potential determined by spectrofluorimetric method. The data presented are mean ± SEM of three independent experiments. *p < 0.05 versus control group and # p < 0.05 versus SNP treated group

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control, Membrane

Journal: Cytotechnology

Article Title: Anti-apoptotic mechanism of Bacoside rich extract against reactive nitrogen species induced activation of iNOS/Bax/caspase 3 mediated apoptosis in L132 cell line

doi: 10.1007/s10616-013-9634-7

Figure Lengend Snippet: A Dose-dependent effects of SNP on L132 cell viability. B Dose-dependent protective effect of BME on SNP-induced cytotoxicity in L132 cells. C Dose-dependent protective effect of L-NAME on SNP-induced cytotoxicity in L132 cells. The data presented are mean ± SEM of three independent experiments. *p < 0.05 versus control group and # p < 0.05 versus SNP treated group

Article Snippet: Cell culture and treatments The L132 cells used in current study were supplied by the National Centre for Cell Science, Pune, India.

Techniques: Control