Identification and characterization of a novel transcript of the murine growth hormone receptor gene exhibiting development- and tissue-specific expression

Menon, Ram K.; Shaufl, Angel L.; Yu, Jae Hong; Stephan, Dietrich A.; Friday, Robert P.

doi:10.1016/s0303-7207(00)00375-0

Cited by 40 publications

(29 citation statements)

References 28 publications

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“…Real-time PCR quantification was then performed using TaqMann 18S controls. Relative quantification of PCR products were then based on value differences between the target and 18S control using the comparative C T method (24). Cycle parameters were 55°C ϫ 5 min, 95°C ϫ 10 min, and then 40 cycles of 95°C ϫ 15 s 58°C ϫ 60 s. For every sample, each PCR reaction was performed on three separate occasions; in each set of reactions, every sample was present in triplicate.…”

Section: Methodsmentioning

confidence: 99%

Intestinal Microcirculatory Dysfunction During the Development of Experimental Necrotizing Enterocolitis

et al. 2007

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ABSTRACT:The aim of this study was to evaluate changes in intestinal microcirculation during necrotizing enterocolitis (NEC) and to examine the effect of endothelin (ET)-1 on the intestinal microcirculation. Prematurely born rats were either hand-fed formula (NEC) or dam fed (DF) and were exposed to asphyxia and cold stress twice daily to induce disease. At 0, 2, 3, and 4 d after the birth, the microcirculation in the ileum was examined using in vivo microscopic methods. The nutritive microvascular perfusion in the NEC group was progressively compromised from d 3 to d 4 (35% and 50% decrease, respectively) when compared with DF rats. Concomitantly, intestinal blood flow assessed by laser Doppler flowmetry was significantly reduced at d 2, 3, and 4 (by 31%, 36%, and 73%, respectively). Levels of ET-1 mRNA in the ileum were increased 3.7-fold. Microvascular responses to topically applied ET-1 were significantly increased in the NEC group, which was associated with decreased expression of ET B receptor. These results suggest that microcirculatory dysfunction in the distal ileum of neonatal rats with NEC contributes to disease progression and that enhanced microvascular responsiveness to ET-1 may participate in these microcirculatory disturbances. (Pediatr Res 61: 180-184, 2007)

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Section: Methodsmentioning

confidence: 99%

Intestinal Microcirculatory Dysfunction During the Development of Experimental Necrotizing Enterocolitis

et al. 2007

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“…Before the use of GAPDH as a control, serial dilutions of cDNA are quantified to prove the validity of using GAPDH as an internal control. Relative quantification of PCR products are then based upon value differences between the target and GAPDH control using the comparative C T method (28)…”

Section: Animalsmentioning

confidence: 99%

IUGR Alters Postnatal Rat Skeletal Muscle Peroxisome Proliferator-Activated Receptor-γ Coactivator-1 Gene Expression in a Fiber Specific Manner

et al. 2003

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Uteroplacental insufficiency and subsequent intrauterine growth retardation (IUGR) increase the risk of insulin resistance in humans and rats. Aberrant skeletal muscle lipid metabolism contributes to the pathogenesis of insulin resistance. Peroxisome proliferator-activated receptor-␥ co-activator-1 (PGC-1) is a transcriptional co-activator that affects gene expression of key lipid metabolizing enzymes such as carnitine palmitoyltransferase I (mCPTI). Because gene expression of lipid metabolizing enzymes is altered in IUGR postnatal skeletal muscle, and we hypothesized that PGC-1 expression would be similarly affected. To prove this hypothesis, bilateral uterine artery ligation and sham surgery were used to produce IUGR and control rats respectively. Western Blotting demonstrated that PGC-1 hind limb skeletal muscle protein levels were increased in perinatal and postnatal IUGR rats. Conventional RT-PCR demonstrated that PGC-1 mRNA levels were similarly increased in perinatal hind limb skeletal muscle and juvenile extensor digitorum longus (EDL), but were decreased in juvenile soleus. Because a gender specific trend was noted in PGC-1 mRNA levels, real time RT-PCR was used for further differentiation. Real time RT-PCR revealed that changes in postnatal skeletal muscle PGC-1 expression were more marked in male IUGR rats versus female IUGR rats. Down stream targets of PGC-1 followed a similar pattern of expression. We conclude that PGC-1 expression is altered in rat IUGR skeletal muscle and speculate that it contributes to the pathogenesis of insulin resistance in the IUGR rat. Barker's Fetal Origins of Adult Disease Hypothesis proposes that fetal adaptation to a deprived intrauterine milieu leads to permanent changes in cellular biology and systemic physiology (1). Intrauterine growth retardation (IUGR) predisposes affected newborns toward the development of insulin resistance and dyslipidemia (2). Although both insulin deficiency and resistance contribute to the IUGR diabetic phenotype, asymmetrical IUGR individuals are often characterized by insulin resistance. Uteroplacental insufficiency, a morbidity associated with many common complications of pregnancy induces asymmetrical IUGR (3, 4). In the rat, uteroplacental insufficiency results in juvenile IUGR animals whose glucose homeostasis is abnormal only when physiologically challenged on a pharmacological level (5). By adulthood, these IUGR rats develop overt diabetes that is characterized by insulin resistance and hypertriglyceridemia (5,19,20).An important component contributing to the pathogenesis of skeletal muscle insulin resistance is altered fatty acid homeostasis (6, 7

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“…Changes in gene expression include altering transcription levels and/or diversifying the transcriptome through alternative use of 5′ start-sites, alternative exon splicing, and differential use of polyadenylation sites. The use of alternative 5′ start-sites can influence the cell type that expresses a gene, transcription levels, mRNA stability, and/or encoded protein structure (1)(2)(3). Several methods for high-throughput sequencing of cDNA have been recently developed to interrogate the transcriptome (denoted RNA-Seq) (4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

5′RNA-Seq identifies Fhl1 as a genetic modifier in cardiomyopathy

et al. 2014

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The transcriptome is subject to multiple changes during pathogenesis, including the use of alternate 5′ startsites that can affect transcription levels and output. Current RNA sequencing techniques can assess mRNA levels, but do not robustly detect changes in 5′ start-site use. Here, we developed a transcriptome sequencing strategy that detects genome-wide changes in start-site usage (5′RNA-Seq) and applied this methodology to identify regulatory events that occur in hypertrophic cardiomyopathy (HCM). Compared with transcripts from WT mice, 92 genes had altered start-site usage in a mouse model of HCM, including four-and-a-half LIM domains protein 1 (Fhl1). HCM-induced altered transcriptional regulation of Fhl1 resulted in robust myocyte expression of a distinct protein isoform, a response that was conserved in humans with genetic or acquired cardiomyopathies. Genetic ablation of Fhl1 in HCM mice was deleterious, which suggests that Fhl1 transcriptional changes provide salutary effects on stressed myocytes in this disease. Because Fhl1 is a chromosome X-encoded gene, stress-induced changes in its transcription may contribute to gender differences in the clinical severity of HCM. Our findings indicate that 5′RNA-Seq has the potential to identify genomewide changes in 5′ start-site usage that are associated with pathogenic phenotypes.

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Identification and characterization of a novel transcript of the murine growth hormone receptor gene exhibiting development- and tissue-specific expression

Cited by 40 publications

References 28 publications

Intestinal Microcirculatory Dysfunction During the Development of Experimental Necrotizing Enterocolitis

Intestinal Microcirculatory Dysfunction During the Development of Experimental Necrotizing Enterocolitis

IUGR Alters Postnatal Rat Skeletal Muscle Peroxisome Proliferator-Activated Receptor-γ Coactivator-1 Gene Expression in a Fiber Specific Manner

5′RNA-Seq identifies Fhl1 as a genetic modifier in cardiomyopathy

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