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1.
Figure 2

Figure 2. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Immunocytochemistry of WT (A and C) and VDR-KO (B and D) isolated mouse cardiomyocytes after incubation with a mouse monoclonal antibody against VDR (sc-13133; A and B) or a mouse monoclonal antibody against DHPR (E and F). VDR staining is seen in a striated pattern in WT cells (A) and is absent in KO cells (B). DHPR staining corresponding to the localization of t-tubules is seen in both VDR-WT (C) and VDR-KO (D) cells.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.
2.
Figure 6

Figure 6. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Effect of 1,25(OH)2D3 (1 nm) on VDR density and location in adult rat cardiomyocytes. Cells were antibody (sc-1009) labeled for VDR by immunofluorescence at time 0, 30, and 60 min after treatment with 1 nm 1,25(OH)2D3. Histograms showing VDR (fluorescein isothiocyanate; green) distribution and intensity relative to nuclear staining (4′,6′-diamino-2-phenylindole; blue) are shown below each immunofluorescence image.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.
3.
Figure 4

Figure 4. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Baseline contractile differences between ventricular myocytes isolated from 6-month-old VDR-WT and VDR-KO mice (littermates). Ten twitches per myocyte were collected for each sample (n = 20). Resting sarcomere length and peak shortening were unaffected; however, TTP and TTR25%-75% were reduced in VDR-KO cardiomyocytes. Rates of both contraction (−dl/dt) and relaxation (+dl/dt) were significantly increased in the KO (−dl/dt = 41.77 ± 1.649, +dl/dt = 33.97 ± 1.250) cells, compared with the WT (−dl/dt = 25.48 ± 1.258, +dl/dt = 25.48 ± 1.258) cells, indicating hypercontractility in the KO cells. *, P < 0.05.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.
4.
Figure 5

Figure 5. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Effect of 1,25(OH)2D3 on VDR-WT and VDR-KO mouse ventricular myocytes. The VDR-WT and VDR-KO mice are 6-month-old littermates. Ten twitches per myocyte were collected for each sample (n = 20). After treatment with 1 nm 1,25(OH)2D3, WT cells exhibited reduced TTP and TTR75% and unchanged rate of contraction (−dl/dtmax: 33.56 ± 1.375 control, 34.34 ± 0.9398 treated; P = 0.64), whereas the rate of relaxation was significantly increased (+dl/dtmax: 25.48 ± 1.258 control, 31.60 ± 1.592 treated; P < 0.005). There are no effects after 1,25(OH)2D3 treatment in VDR-KO cells. Crosshatch bars, baseline; black bars, treated. *, P < 0.05.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.
5.
Figure 3

Figure 3. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Western blot of fractionated homogenized rat hearts (A) and 3[H]1,25(OH)2D3 binding analysis of the t-tubule (40K) fraction (B and C). Fractions analyzed by Western blot (A) include whole homogenate (WH), 0–7,700 g (7K), 7,700–40,000 g (40K), 40,000–110,000 g (110K), and cytosol (CYT). VDR is present in the 40K fraction, which is also enriched for the LTCC, DHPR, SERCA2, and caveolin-3 (CAV-3; A). This fraction shows very little of the mitochondrial marker COX IV or the nuclear marker Sp1 (A). Total, nonspecific, and specific binding of 3[H]1,25(OH)2D3 to the 40K membrane fraction in counts per minute (CPM) is shown in B. Saturation and Scatchard analysis of 3[H]1,25(OH)2D3 binding to the 40K fraction shows saturable and specific binding (C). Bmax, Maximal binding capacity; Kd, dissociation constant.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.
6.
Figure 1

Figure 1. From: Functional Vitamin D Receptor (VDR) in the T-Tubules of Cardiac Myocytes: VDR Knockout Cardiomyocyte Contractility.

Immunofluorescent confocal microscopy of adult rat cardiac myocytes. The transverse staining pattern of VDR (sc-13133; mouse monoclonal) is evident at ×40 (A; image enlarged in C). Antimouse secondary antibody alone is shown in B. Double labeling using a different antibody against VDR (sc-1009; rabbit polyclonal, D) and an antibody against DHPR (MA3–921; mouse monoclonal; E) show similar staining patterns, whereas a merge (F) shows colocalization. Double labeling against VDR (sc-1009; rabbit polyclonal; G) and SERCA-2 (sc-8094; goat polyclonal; H) show a similar staining pattern, whereas a merge (I) shows some association. Double labeling using an antibody against T-cap (sc-20171; rabbit polyclonal; red) and VDR (sc-1009, rabbit polyclonal, green) show dissimilar staining patterns and incomplete overlap in a merged image (J). A third primary VDR antibody, a rabbit polyclonal directed against the C terminus of VDR (sc-1008), is shown in K. A cardiomyocyte incubated with both sc-1008 and a blocking peptide for VDR (sc1008p) is shown in L, demonstrating the specificity of this antibody for VDR.

Daniel X. Tishkoff, et al. Endocrinology. 2008 February;149(2):558-564.

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