PMID- 31472066
OWN - NLM
STAT- MEDLINE
DCOM- 20200303
LR  - 20200303
IS  - 2191-0251 (Electronic)
IS  - 0334-018X (Linking)
VI  - 32
IP  - 10
DP  - 2019 Oct 25
TI  - Micro-RNA 196a2 expression and miR-196a2 (rs11614913) polymorphism in T1DM: a 
      pilot study.
PG  - 1171-1179
LID - 10.1515/jpem-2019-0226 [doi]
AB  - Background Recent emerging evidence supports the role of miR-196a2 in various 
      human diseases. However, its role in type 1 diabetes mellitus (T1DM) is still 
      underestimated. We aimed, for the first time, to investigate the expression of 
      miR-196a2 in T1DM and the association of miR-196a2 (rs11614913) polymorphism with 
      susceptibility of T1DM in a sample of patients from Cairo, Egypt. Methods The 
      study included 150 patients and 150 healthy subjects. Evaluation of rs11614913 
      genotypes and miR-196a2 expression was done using the allelic discrimination and 
      quantitative reverse transcriptase polymerase chain reaction (PCR) method, 
      respectively. Results The Hardy-Weinberg equilibrium of single nucleotide 
      polymorphism(SNP) was detected among controls (p = 0.2). Our results revealed 
      that the TT genotype was more frequent in patients (22.6%) than controls (10%) 
      while the CC genotype was more frequent in controls (47.3%) than patients (39.3%) 
      (p = 0.01). The frequency of the T allele was significantly higher in patients 
      than in controls (41.7 vs. 31.3%), while the C allele was more frequent in 
      controls (p = 0.008). After adjustment for traditional risk factors, the 
      association of the TT genotype with T1DM remained significant (TT vs. CC, odds 
      ration [OR] = 3.2, 95% confidence interval [CI]: 1.4-7.4, p = 0.005). Power 
      analysis of the data yielded a statistical power of 80% for the miR-196a2 
      rs11614913 with T1DM. Relative expression of miR-196a2 showed significant 
      decrease in patients compared to controls (median = 0.09, 0.5, interquartile 
      range [IQR] = 0.03-1.6, 0.1-2.1). However, miR-196a2 expression showed no 
      significant difference between different rs11614913 genotypes (p = 0.5). 
      Conclusions Our findings demonstrated that miR-196a rs11614913 is associated with 
      T1DM and decreased expression of miR-196a2 may play a role in pathogenesis of 
      T1DM.
FAU - Ibrahim, Alshaymaa A
AU  - Ibrahim AA
AD  - Clinical and Chemical Pathology Department, National Research Centre, El Buhouth 
      St, Dokki, Cairo 12311, Egypt, Phone: 00201006193988, Fax: +20233370931.
FAU - Ramadan, Abeer
AU  - Ramadan A
AD  - Molecular Genetics and Enzymology Department, Human Genetic and Genome Research 
      Division, National Research Centre, Cairo, Egypt.
FAU - Wahby, Aliaa Ahmed
AU  - Wahby AA
AD  - Clinical and Chemical Pathology Department, National Research Centre, Cairo, 
      Egypt.
FAU - Hassan, Mirhane
AU  - Hassan M
AD  - Clinical and Chemical Pathology Department, National Research Centre, Cairo, 
      Egypt.
FAU - Soliman, Hend M
AU  - Soliman HM
AD  - Pediatric Department, Cairo University, Cairo, Egypt.
FAU - Abdel Hamid, Tamer A
AU  - Abdel Hamid TA
AD  - Pediatric Department, Cairo University, Cairo, Egypt.
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - J Pediatr Endocrinol Metab
JT  - Journal of pediatric endocrinology & metabolism : JPEM
JID - 9508900
RN  - 0 (Biomarkers)
RN  - 0 (MIRN196 microRNA, human)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Biomarkers/*analysis
MH  - Case-Control Studies
MH  - Child
MH  - Child, Preschool
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 1/epidemiology/*genetics/pathology
MH  - Egypt/epidemiology
MH  - Female
MH  - Follow-Up Studies
MH  - Genetic Predisposition to Disease
MH  - Genotype
MH  - Humans
MH  - Infant
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Pilot Projects
MH  - *Polymorphism, Single Nucleotide
MH  - Prognosis
MH  - Risk Factors
MH  - Young Adult
OTO - NOTNLM
OT  - T1DM
OT  - expression
OT  - miR-196a2
OT  - polymorphism
OT  - rs11614913
EDAT- 2019/09/01 06:00
MHDA- 2020/03/04 06:00
CRDT- 2019/09/01 06:00
PHST- 2019/05/20 00:00 [received]
PHST- 2019/08/02 00:00 [accepted]
PHST- 2019/09/01 06:00 [pubmed]
PHST- 2020/03/04 06:00 [medline]
PHST- 2019/09/01 06:00 [entrez]
AID - /j/jpem.ahead-of-print/jpem-2019-0226/jpem-2019-0226.xml [pii]
AID - 10.1515/jpem-2019-0226 [doi]
PST - ppublish
SO  - J Pediatr Endocrinol Metab. 2019 Oct 25;32(10):1171-1179. doi: 
      10.1515/jpem-2019-0226.