Calcium Metabolism, Serum Thyroid-Stimulating Hormone, Prolactin, and Growth Hormone in Spontaneously Hypercholesterolemic Rats

Shiota, Kunio; Takahashi, Michio; Masaki, Tsuneo; Sudo, Katsuichi

doi:10.3181/00379727-190-42853

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…Each miRNA is predicted to target and down-regulate many transcripts directly or indirectly (12). miRNA deregulation has been implicated in cancers (13–15) such as glioma (16–18); and similar to coding genes, CpG island methylation-associated silencing of miRNAs with tumor suppressor features have been discovered in human cancer (19–22). …”

Section: Introductionmentioning

confidence: 99%

Tumor-Suppressive miR148a Is Silenced by CpG Island Hypermethylation in IDH1-Mutant Gliomas

Chowdhury

Liu

et al. 2014

Clinical Cancer Research

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Purpose IDH1/2 mutant gliomas harbor a distinct CpG island methylation profile (G-CIMP) that may promote the initiation and progression of secondary pathway gliomas by silencing tumor suppressive genes. The potential role of tumor suppressive miRNAs in this process is not understood. Experimental Design To identify potential tumor suppressive microRNAs hypermethylated in glioma, the methylation profiles of IDH1/2WT gliomas (n=11) and IDH1MUT glioma (n=20) were compared by using massively parallel reduced representation bisulfite sequencing (RRBS). The methylation status of selected miRNA was validated by using targeted bisulfite sequencing (BiSEQ) in a large cohort of glioma tissue samples including 219 IDH1WT and 72 IDH1/2MUT samples. The expression of selected miRNAs was determined by using TaqMan qPCR. Functional analyses of miRNA-148a were conducted and target genes were identified. Results We identify miR-148a as a novel, G-CIMP associated miRNA whose methylation is tightly correlated with IDH1 mutation and associated with improved survival in malignant glioma patients. We confirm that down-regulation of miR-148a can occur via DNA methylation. We demonstrate that IDH1 mutation provides a mechanism of miR-148a methylation and downregulation, and that restoration of miR-148a reduced tumorigenic properties of glioma cells, possibly by targeting DNMT1. Conclusions We identify miR-148a as a novel G-CIMP associated miRNA, and provide results suggesting that miR-148a restoration may have therapeutic implications.

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Section: Introductionmentioning

confidence: 99%

Tumor-Suppressive miR148a Is Silenced by CpG Island Hypermethylation in IDH1-Mutant Gliomas

Chowdhury

Liu

et al. 2014

Clinical Cancer Research

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Placental Lactogen Secretion during Prolonged-Pregnancy in the Rat: The Ovary Plays a Pivotal Role in the Control of Placental Function.

1991

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The serum of rats at mid-pregnancy contains at least 2 distinct placental lactogen (PL)-like substances tentatively termed placental lactogen-alpha (PL-alpha) and placental lactogen-beta (PL-beta) (Endocrinol Japon 38: 533-540, 1991). We have investigated the secretory patterns of three placental lactogens (PL-alpha, PL-beta and placental lactogen-II) during normal pregnancy and in two prolonged-pregnancy models. Pregnancy was prolonged by the introduction of new corpora lutea by inducing ovulation on day 15 of pregnancy by successive treatments with PMSG (30 IU/rat, sc on day 12) and hCG (10 IU/rat, iv on day 14), and in the second model by progesterone implants on day 15 of pregnancy. During normal pregnancy, each of the 3 PLs exhibited only one secretory peak in the serum; PL-alpha and PL-beta on day 12 and placental lactogen II (PL-II) on day 20. Interestingly, in the rats with new sets of corpora lutea, serum PL-alpha and PL-beta levels began to increase again on day 18 and showed peaks on day 20 for PL-alpha and on day 22 for PL-beta. In this model, the initiation of PL-II secretion was not affected, but high levels were maintained until day 26, when parturition occurred. In rats receiving either PMSG or hCG, the secretory patterns of the PLs were similar to as those during normal pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Biochemical Analysis of the Bone of SHC Rats with Spontaneous Hypercholesterolemia and Renal Dysfunction.

et al. 1992

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Spontaneously hypercholesterolemic (SHC) rats exhibit severe abnormalities in renal function and bone metabolism at old ages, in addition to hypercholesterolemia. SHC rats were also found to show endocrine abnormalities such as hyperthyroidism from young ages. In this study, biochemical and microdensitometric analyses were carried out using femurs to characterize further the abnormality in bone metabolism: whether biochemical markers of the bone may be affected by these abnormalities. At 6 weeks of age, the ashed weight and calcium content of the dried femurs were slightly lower in SHC rats than in age-matched Sprague-Dawley (SD) rats. None of the markers of microdensitometric analysis was changed. At 24 weeks of age, the ashed weight of dried femurs and the density of the marrow region of femurs were lower in the SHC rats. The results indicate that SHC rats exhibit severe abnormality in bone metabolism leading to biochemical changes in the bone at old ages whereas changes in bone markers were minimal at young ages before the onset of severe renal dysfunction.

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Calcium Metabolism, Serum Thyroid-Stimulating Hormone, Prolactin, and Growth Hormone in Spontaneously Hypercholesterolemic Rats

Cited by 3 publications

References 29 publications

Tumor-Suppressive miR148a Is Silenced by CpG Island Hypermethylation in IDH1-Mutant Gliomas

Tumor-Suppressive miR148a Is Silenced by CpG Island Hypermethylation in IDH1-Mutant Gliomas

Placental Lactogen Secretion during Prolonged-Pregnancy in the Rat: The Ovary Plays a Pivotal Role in the Control of Placental Function.

Biochemical Analysis of the Bone of SHC Rats with Spontaneous Hypercholesterolemia and Renal Dysfunction.

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