Sentences with phrase «cre +»

Cxcr6GFP / + (RRID: MGI: 3616633), Ccr6GFP / + (RRID: MGI: 3852186), Ccr6 + / --(RRID: MGI: 4359785), Pycard + / — , CAG - KiKGR +, S1pr1f / f, CreERt2 +, Lyve1 - Cre + Sphk1f / f Sphk2 — / — mice (RRID: MGI: 4421697), and Icam1 + / — mice were previously described and were from JAX or from an internal colony.

(C) Isolated [3H] TRLs from control ASO - and ApoC - III ASO — treated Ldlr — / — Ndst1fl / fl Alb - Cre + mice were injected i.v. into ApoC - III ASO — treated Ndst1fl / fl Alb - Cre + mice (n = 3).

In contrast, Tsc1GFAPCKO mice (Cre +; Tsc1 flox / flox) showed genotype - dependent changes in some transcripts analyzed.

ApoC - III ASO treatment reduced TG levels in chylomicrons, VLDL, and remnant particles in all of the mutants as measured by size - exclusion fast protein liquid chromatography (FPLC)(Figure 2, A — E), but had no effect in Ldlr — / — Lrp1fl / fl Alb - Cre + mice (Figure 2F).

Binding and uptake of radiolabeled ApoC - III — depleted TRLs was significantly increased in hepatocytes isolated from Ndst1fl / fl Alb - Cre + mice (i.e., in mice expressing both LDLR and LRP1) when compared with ApoC - III — bearing TRLs (Figure 10).

Ndst1fl / fl Alb - Cre + mice were generated and genotyped as described previously (22, 42).

(C) Hepatic VLDL production was determined in overnight - fasted Ldlr — / — Lrp1fl / fl Alb - Cre + mice after injection with tyloxapol to inhibit lipolysis.

Treatment with ApoC - III ASO reduced postprandial plasma TGs in all of the mutants except in Ldlr — / — Lrp1fl / fl Alb - Cre + mice (Figure 4, A and B).

Ldlr — / — Ndst1fl / flAlb - Cre + mice were treated for 4 weeks with a control ASO or ApoC - III ASO.

However, the ASO had no effect on plasma TG levels in mice lacking both Lrp1 and Ldlr (Ldlr — / — Lrp1fl / fl Alb - Cre +)(Figure 1, D and E).

(A and B) Plasma TGs were measured before and after heparin injection in WT, Ldlr — / — Ndst1fl / fl Alb - Cre +, and Ldlr — / — Lrp1fl / fl Alb - Cre + mice treated for 4 weeks with control or ApoC - III ASO (A) after an overnight fast or (B) 3 hours after a fat challenge.

To examine whether hepatic clearance via these receptors contributed to an ApoC - III ASO — mediated reduction of plasma TGs, we administered the ApoC - III ASO for 4 weeks to mice lacking LDLR (Ldlr — / ---RRB-, HSPGs (Ndst1fl / fl Alb - Cre +), or hepatic LRP1 (Lrp1fl / fl Alb - Cre +), and to mice lacking various pairs of these receptors (depicted in Figure 1B).

These results support the notion that the increased clearance of ApoC - III — depleted [3H] TRLs in Ndst1fl / fl Alb - Cre + mice, and not in Ldlr — / — Lrp1fl / fl Alb - Cre + mice, is a consequence of increased uptake by LDLR / LRP1 on hepatocytes.

ApoC - III — depleted TRLs were cleared much faster than were ApoC - III — rich TRLs in Ndst1fl / fl Alb - Cre + mice (t1 / 2 = 2.8 min vs. 8.2 min, respectively)(Figure 9C).

In contrast, no difference in the catabolic rate between ApoC - III — depleted and ApoC - III — bearing TRLs was observed when the particles were injected into Ldlr — / — Lrp1fl / fl Alb - Cre + mice (t1 / 2 = 16.2 min vs. 16.8 min, respectively)(Figure 9E).

The high - fat diet raised plasma TG levels in Ldlr — / — , Ldlr — / — Ndst1fl / fl Alb - Cre +, and Ldlr — / — Lrp1fl / fl Alb - Cre + mice, reaching values of 515 to 1,045 mg / dl (Figure 5A).

In contrast, primary mouse hepatocytes from Ldlr — / — Lrp1fl / fl Alb - Cre + mice did not show a significant difference in binding or uptake between ApoC - III — depleted and ApoC - III — bearing TRLs (Figure 10).

(E)[3H] TRLs isolated from control ASO - treated (white circles) and ApoC - III ASO — treated (black circles) Ldlr — / — Ndst1fl / fl Alb - Cre + mice were injected i.v. into ApoC - III ASO — treated Ldlr — / — Lrp1fl / fl Alb - Cre — mice (n = 3).

The accelerated catabolic rate of ApoC - III — depleted TRLs in Ndst1fl / fl Alb - Cre + mice was associated with increased [3H] TRL uptake in the liver (Figure 9D), whereas liver accumulation did not differ when ApoC - III — bearing [3H] TRLs were injected into Ldlr — / — Lrp1fl / fl Alb - Cre + mice (Figure 9F).

Binding and uptake of isolated [3H] TRLs (50 μg / ml) from control ASO - and ApoC - III ASO — treated Ldlr — / — Ndst1fl / fl Alb - Cre + mice in primary hepatocytes isolated from Ndst1fl / fl Alb - Cre + and Ldlr — / — Lrp1fl / fl Alb - Cre — mice after a 4 - hour incubation at 37 °C (n = 3 / condition).

Donor [3H] retinol - labeled TRLs were collected from ApoC - III ASO — treated and control ASO - treated Ldlr — / — Ndstfl / fl Alb - Cre + mice 3 hours after a fat load to generate ApoC - III — depleted TRLs and ApoC - III — bearing TRLs, respectively (Figure 9A).

In a second approach, [3H] retinol - radiolabeled ApoC - III — depleted and ApoC - III — bearing TRLs (Figure 9A and Supplemental Figure 6) were evaluated for their uptake by primary hepatocytes isolated from Ndst1fl / fl Alb - Cre + and Ldlr — / — Lrp1fl / fl Alb - Cre + mice.

In some cases affected transcripts in Cre +; Tsc1 flox / flox mice showed significant variation among individuals that can not simply be explained by differential effectiveness of CRE - mediated knockout since, except one animal, all Cre +; Tsc1 flox / flox mice showed similarly reduced expression levels of Tsc1 mRNA.

Overall binding of both [3H] TRL preparations was significantly reduced in hepatocytes isolated from Ldlr — / — Lrp1fl / fl Alb - Cre + mice compared with hepatocytes isolated from Ndst1fl / fl Alb - Cre + mice (Figure 10).

Not exact matches

Impaired Ca2 + Signaling in β - Cells Lacking Leptin Receptors by Cre - loxP Recombination.

Activation of endogenous Wnt signalling in Prom1 (+ / C - L) mice containing a Cre - dependent mutant allele of beta - catenin (Ctnnb1 (lox (ex3)-RRB--RRB- resulted in a gross disruption of crypt architecture and a disproportionate expansion of Prom1 (+) cells at the crypt base.

(vet was happy he has «filled back out») however his appetite seems insatiable now,,, blood work was normal ranges except BUN was high (42 + mg / dL) and CRE (1.6).

The vet scan VS2 last taken showed ALB 3.3 g / dL, ALP 94 U / L, ALT 32 U / L, AMY 227 U / L, TBIL 0.3 mg / dL, * BUN 30 + mg / dL, CA 11.5 mg / dL, * PHOS 8.5 +, CRE 1.0 mg / DL, * GLU 119 + mg / DL, NA + 140 mmol / L, K + 4.7 mmol / L, TP 6.9 g / dL, GLOB 3.6 g / dL.

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