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Figure 7. NOS1 inhibition abolishes the differ- ence in PLB Ser16 phosphorylation and LV myo- cytes relaxation and [Ca2]i decay between ge- notypes. NOS1 inhibition with SMTC reduced PLB Ser16 phosphorylation in mGCH1-Tg LV myocytes without affecting total PLB and abolished the ge- notypes’ difference in PLB Ser16 phosphorylated fraction (n4 hearts per genotype; *P0.01, A) and in the rate of myocyte relaxation and [Ca2]i decay (dL/dt, n13–33 cells, tau1, 10–25 cells, *P0.5, **P0.01, from 2–3 hearts per genotype, B). XOR inhibition with Oxypurinol (100 mol/L) did not affect LV myocytes shortening or relaxation (n52 cells from 4 hearts per genotype, ***P0.01 versus WT, C). NOS indicates nitric oxide syn- thases; PLB, <t>phospholamban;</t> SMTC, S-methyl-L- thiocitrulline acetate salt; LV, left ventricle; mGCH1, myocardial guanosine triphosphate cyclo- hydrolase; Tg, transgenic; XOR, xanthine oxidoreductase.
Phospholamban, 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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Figure 7. NOS1 inhibition abolishes the differ- ence in PLB Ser16 phosphorylation and LV myo- cytes relaxation and [Ca2]i decay between ge- notypes. NOS1 inhibition with SMTC reduced PLB Ser16 phosphorylation in mGCH1-Tg LV myocytes without affecting total PLB and abolished the ge- notypes’ difference in PLB Ser16 phosphorylated fraction (n4 hearts per genotype; *P0.01, A) and in the rate of myocyte relaxation and [Ca2]i decay (dL/dt, n13–33 cells, tau1, 10–25 cells, *P0.5, **P0.01, from 2–3 hearts per genotype, B). XOR inhibition with Oxypurinol (100 mol/L) did not affect LV myocytes shortening or relaxation (n52 cells from 4 hearts per genotype, ***P0.01 versus WT, C). NOS indicates nitric oxide syn- thases; PLB, phospholamban; SMTC, S-methyl-L- thiocitrulline acetate salt; LV, left ventricle; mGCH1, myocardial guanosine triphosphate cyclo- hydrolase; Tg, transgenic; XOR, xanthine oxidoreductase.

Journal: Circulation Research

Article Title: Cardiomyocyte GTP Cyclohydrolase 1 and Tetrahydrobiopterin Increase NOS1 Activity and Accelerate Myocardial Relaxation

doi: 10.1161/circresaha.112.274464

Figure Lengend Snippet: Figure 7. NOS1 inhibition abolishes the differ- ence in PLB Ser16 phosphorylation and LV myo- cytes relaxation and [Ca2]i decay between ge- notypes. NOS1 inhibition with SMTC reduced PLB Ser16 phosphorylation in mGCH1-Tg LV myocytes without affecting total PLB and abolished the ge- notypes’ difference in PLB Ser16 phosphorylated fraction (n4 hearts per genotype; *P0.01, A) and in the rate of myocyte relaxation and [Ca2]i decay (dL/dt, n13–33 cells, tau1, 10–25 cells, *P0.5, **P0.01, from 2–3 hearts per genotype, B). XOR inhibition with Oxypurinol (100 mol/L) did not affect LV myocytes shortening or relaxation (n52 cells from 4 hearts per genotype, ***P0.01 versus WT, C). NOS indicates nitric oxide syn- thases; PLB, phospholamban; SMTC, S-methyl-L- thiocitrulline acetate salt; LV, left ventricle; mGCH1, myocardial guanosine triphosphate cyclo- hydrolase; Tg, transgenic; XOR, xanthine oxidoreductase.

Article Snippet: Immunoblotting in LV homogenates was performed using primary antibodies against NOS1 (Santa Cruz Biotechnology), NOS3 (Santa Cruz Biotechnology), NOS2 (Abcam), SERCA2A (Santa Cruz Biotechnology), total phospholamban (PLB, Badrilla), phospho Thr17-PLB (Badrilla), phospho Ser16-PLB (Badrilla), NCX1 (Santa Cruz), GAPDH (Santa Cruz Biotechnology), human GCH1 (Sigma), HA-tag (Roche), and murine GCH1 (Sigma).

Techniques: Inhibition, Phospho-proteomics, Transgenic Assay