tenacibaculum  (ATCC)

Journal: JACC: Basic to Translational Science

Article Title: Yes-Associated Protein (YAP) Facilitates Pressure Overload–Induced Dysfunction in the Diabetic Heart

doi: 10.1016/j.jacbts.2019.05.006

Figure Lengend Snippet: Up-Regulation of YAP Contributes to the Development of Cardiac Dysfunction in Response to Pressure Overload in the Presence of HFD (A) Schematic representation of the experimental protocol. In B–D , mice were fed with either ND or HFD for 8 weeks. Four weeks after the start of ND or HFD, mice were subjected to either sham operation or transverse aortic constriction (TAC) for 4 weeks (4w). (B) Time course of percent fractional shortening (%FS) and left ventricular end-diastolic dimension (LVEDD) evaluated with echocardiography (n = 6, each). (C) Left ventricular end-diastolic pressure (LVEDP) and pressure gradient, evaluated by hemodynamic measurements (n = 6, each). (D) Kaplan-Meier survival curves after TAC. (E) Representative gel pictures of YAP, TEAD1, OSM, MYH7, ACTA2, RUNX1, and α-tubulin in the heart (n = 6, each). All results are mean ± SEM. *p < 0.05 by analysis of variance. Abbreviations as in Figure 1 .

Article Snippet: The following primary antibodies were used: YAP (Cell Signaling, #14074, Cell Sugnaling Technology, Danvers, Massachusetts), phospho-YAP (Ser127) (Cell Signaling, #4911), LATS2 (Bethyl Laboratories, #A300-479A, Bethyl Laboratories, Montgomery, Texas), phospho-LATS2 (Thr1041) (Cell Signaling, #8654), atrial natriuretic peptide (Abcam, #ab180649, Abcam, Cambridge, United Kingdom), TEAD1 (Sigma-Aldrich, #AV39521), MYH7 (Sigma-Aldrich, # M8421), ACTA2 (Sigma-Aldrich, #A5228), OSM (Santa Cruz, #sc374039, Santa Cruz Biotechnology, Dallas, Texas), OSMR (Santa Cruz, #sc30011), cardiac troponin T antibody (Abcam, #ab33589), sarcomeric actinin (Abcam, #ab68167), CD45 (Abcam, #ab10558), CD68 (Abcam, #ab31630), Ly6G (Abcam, #ab25377), and α-tubulin (Sigma-Aldrich, #T6199).

Techniques:

Journal: JACC: Basic to Translational Science

Article Title: Yes-Associated Protein (YAP) Facilitates Pressure Overload–Induced Dysfunction in the Diabetic Heart

doi: 10.1016/j.jacbts.2019.05.006

Figure Lengend Snippet: Verteporfin Improves Pressure Overload–Induced Cardiac Hypertrophy in the Presence of HFD (A) Schematic representation of the experimental protocol. Mice were fed with either ND or HFD for 8 weeks. Four weeks after the start of ND or HFD, mice were subjected to either sham operation or TAC in the presence or absence of verteporfin for 4 weeks. (B) Kaplan-Meier survival curves for HFD-fed mice after TAC in the presence or absence of verteporfin. (C) %FS and LVEDD evaluated with echocardiography 4 weeks after TAC, with or without verteporfin treatment (n = 6, each). (D) Left ventricular weight to tibial length (LV W/ TL) ratio (n = 6, each). (E) Lung weight to tibial length (Lung W/ TL) ratio (n = 6, each). (F) Representative gel pictures of YAP, TEAD1, OSM, MYH7, ACTA2, RUNX1, and α-tubulin in the heart (n = 6, each). All results are mean ± SEM. *p < 0.05, **p < 0.01 by analysis of variance. i.p. = intraperitoneal; N.S. = not significant; Op = operation; post op = postoperative; other abbreviations as in Figures 1 and .

Article Snippet: The following primary antibodies were used: YAP (Cell Signaling, #14074, Cell Sugnaling Technology, Danvers, Massachusetts), phospho-YAP (Ser127) (Cell Signaling, #4911), LATS2 (Bethyl Laboratories, #A300-479A, Bethyl Laboratories, Montgomery, Texas), phospho-LATS2 (Thr1041) (Cell Signaling, #8654), atrial natriuretic peptide (Abcam, #ab180649, Abcam, Cambridge, United Kingdom), TEAD1 (Sigma-Aldrich, #AV39521), MYH7 (Sigma-Aldrich, # M8421), ACTA2 (Sigma-Aldrich, #A5228), OSM (Santa Cruz, #sc374039, Santa Cruz Biotechnology, Dallas, Texas), OSMR (Santa Cruz, #sc30011), cardiac troponin T antibody (Abcam, #ab33589), sarcomeric actinin (Abcam, #ab68167), CD45 (Abcam, #ab10558), CD68 (Abcam, #ab31630), Ly6G (Abcam, #ab25377), and α-tubulin (Sigma-Aldrich, #T6199).

Techniques:

Journal: JACC: Basic to Translational Science

Article Title: Yes-Associated Protein (YAP) Facilitates Pressure Overload–Induced Dysfunction in the Diabetic Heart

doi: 10.1016/j.jacbts.2019.05.006

Figure Lengend Snippet: TEAD1 Deletion Attenuates Pressure Overload–Induced Cardiac Disfunction in the Presence of HFD Control (Ctr) mice and TEAD1 heterozygous knockout (TEAD1 +/− ) mice were fed with either ND or HFD for 8 weeks. Four weeks after the start of ND or HFD, mice were subjected to either sham operation or TAC. (A) %FS and LVEDD evaluated with echocardiography 4 weeks after TAC (n = 6, each). (B) LVEDP and pressure gradient, evaluated by hemodynamic measurements (n = 6, each). (C) LV W/ TL ratio (n = 6, each). (D) Lung W/ TL ratio (n = 6, each). (E) Representative gel pictures of YAP, TEAD1, OSM, ACTA2, RUNX1, and α-tubulin. All results are expressed as mean ± SEM. *p < 0.05, **p < 0.01 by analysis of variance. Abbreviations as in Figures 1 , , and .

Article Snippet: The following primary antibodies were used: YAP (Cell Signaling, #14074, Cell Sugnaling Technology, Danvers, Massachusetts), phospho-YAP (Ser127) (Cell Signaling, #4911), LATS2 (Bethyl Laboratories, #A300-479A, Bethyl Laboratories, Montgomery, Texas), phospho-LATS2 (Thr1041) (Cell Signaling, #8654), atrial natriuretic peptide (Abcam, #ab180649, Abcam, Cambridge, United Kingdom), TEAD1 (Sigma-Aldrich, #AV39521), MYH7 (Sigma-Aldrich, # M8421), ACTA2 (Sigma-Aldrich, #A5228), OSM (Santa Cruz, #sc374039, Santa Cruz Biotechnology, Dallas, Texas), OSMR (Santa Cruz, #sc30011), cardiac troponin T antibody (Abcam, #ab33589), sarcomeric actinin (Abcam, #ab68167), CD45 (Abcam, #ab10558), CD68 (Abcam, #ab31630), Ly6G (Abcam, #ab25377), and α-tubulin (Sigma-Aldrich, #T6199).

Techniques: Control, Knock-Out