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Differential regulation of serum microRNA expression by HNF1? and HNF1? transcription factors.

ABSTRACT: We aimed to identify microRNAs (miRNAs) under transcriptional control of the HNF1? transcription factor, and investigate whether its effect manifests in serum.The Polish cohort (N?=?60) consisted of 11 patients with HNF1B-MODY, 17 with HNF1A-MODY, 13 with?GCK-MODY, an HbA1c-matched type 1 diabetic group (n?=?9) and ten healthy controls. Replication was performed in 61 clinically-matched British patients mirroring the groups in the Polish cohort. The Polish cohort underwent miRNA serum level profiling with quantitative real-time PCR (qPCR) arrays to identify differentially expressed miRNAs. Validation was performed using qPCR. To determine whether serum content reflects alterations at a cellular level, we quantified miRNA levels in a human hepatocyte cell line (HepG2) with small interfering RNA knockdowns of HNF1? or HNF1?.Significant differences (adjusted p?

SUBMITTER: Fendler W

PROVIDER: S-EPMC4901123 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Differential regulation of serum microRNA expression by HNF1β and HNF1α transcription factors.

Fendler Wojciech W Madzio Joanna J Kozinski Kamil K Patel Kashyap K Janikiewicz Justyna J Szopa Magdalena M Tracz Adam A Borowiec Maciej M Jarosz-Chobot Przemyslawa P Mysliwiec Malgorzata M Szadkowska Agnieszka A Hattersley Andrew T AT Ellard Sian S Malecki Maciej T MT Dobrzyn Agnieszka A Mlynarski Wojciech W

Diabetologia 20160408 7

<h4>Aims/hypothesis</h4>We aimed to identify microRNAs (miRNAs) under transcriptional control of the HNF1β transcription factor, and investigate whether its effect manifests in serum.<h4>Methods</h4>The Polish cohort (N = 60) consisted of 11 patients with HNF1B-MODY, 17 with HNF1A-MODY, 13 with GCK-MODY, an HbA1c-matched type 1 diabetic group (n = 9) and ten healthy controls. Replication was performed in 61 clinically-matched British patients mirroring the groups in the Polish cohort. The Polish ...[more]

PMID: 27059371

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Project description:Methamphetamine (METH) is an addictive and neurotoxic psychostimulant widely abused in the USA and throughout the world. When administered in large doses, METH can cause depletion of striatal dopamine terminals, with preservation of midbrain dopaminergic neurons. Because alterations in the expression of transcription factors that regulate the development of dopaminergic neurons might be involved in protecting these neurons after toxic insults, we tested the possibility that their expression might be affected by toxic doses of METH in the adult brain. Male Sprague-Dawley rats pretreated with saline or increasing doses of METH were challenged with toxic doses of the drug and euthanized two weeks later. Animals that received toxic METH challenges showed decreases in dopamine levels and reductions in tyrosine hydroxylase protein concentration in the striatum. METH pretreatment protected against loss of striatal dopamine and tyrosine hydroxylase. In contrast, METH challenges caused decreases in dopamine transporters in both saline- and METH-pretreated animals. Interestingly, METH challenges elicited increases in dopamine transporter mRNA levels in the midbrain in the presence but not in the absence of METH pretreatment. Moreover, toxic METH doses caused decreases in the expression of the dopamine developmental factors, Shh, Lmx1b, and Nurr1, but not in the levels of Otx2 and Pitx3, in saline-pretreated rats. METH pretreatment followed by METH challenges also decreased Nurr1 but increased Otx2 and Pitx3 expression in the midbrain. These findings suggest that, in adult animals, toxic doses of METH can differentially influence the expression of transcription factors involved in the developmental regulation of dopamine neurons. The combined increases in Otx2 and Pitx3 expression after METH preconditioning might represent, in part, some of the mechanisms that served to protect against METH-induced striatal dopamine depletion observed after METH preconditioning.

Dataset Information

Differential regulation of serum microRNA expression by HNF1? and HNF1? transcription factors.

Publications

Differential regulation of serum microRNA expression by HNF1β and HNF1α transcription factors.

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