PMID- 30842884
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2049-9434 (Print)
IS  - 2049-9442 (Electronic)
IS  - 2049-9434 (Linking)
VI  - 0
IP  - 0
DP  - 2019 Feb
TI  - Alteration in cardiac PI3K/Akt/mTOR and ERK signaling pathways with the use of 
      growth hormone and swimming, and the roles of miR21 and miR133.
PG  - 1-10
LID - 10.3892/br.2018.1179 [doi]
AB  - Athletes misuse recombinant human growth hormone (r-hGH) to enhance their 
      performance. Although r-hGH is known to increase cardiac hypertrophy, the 
      underlying molecular mechanism remains unclear. The aim of the present study was 
      to investigate the role of r-hGH in cardiac intracellular signaling pathways and 
      of miR-21 and miR-133 expression in rat hearts during exercise. A total of 36 
      adult male Sprague-Dawley rats were divided into sedentary control (SC, n=9), 
      swimming exercise (SE, n=8), r-hGH (GH, n=10) and swimming exercise plus r-hGH 
      (SE-GH, n=9) groups. The exercise groups completed a 1-h swimming exercise 5 
      times a week for 8 weeks. Subcutaneous r-hGH was administered as 0.3 mg/kg/day. 
      Phosphoinositide-3-kinase (PI3K), serine/threonine protein kinase 1 (AKT1), 
      extracellular signal-regulated kinase (ERK), microRNA (miR)-21 and miR-133 
      expression was evaluated in ventricular muscle by real-time quantitative 
      polymerase chain reaction. Protein expression of PI3K, AKT1, ERK and mechanistic 
      target of rapamycin (mTOR) was also assessed by immunohistochemistry. Statistical 
      differences were analyzed by two-way ANOVA. PI3K and AKT1 expression and the gene 
      and protein levels was notably increased in the SE-GH group compared with in SC 
      ventricular tissues (P<0.05). mTOR protein expression was higher in the GH, SE 
      and SE-GH groups compared with in the SC group (P<0.05, <0.05 and <0.001, 
      respectively). ERK gene/protein expression was similar across all groups. miR-21 
      and miR-133 levels in ventricular muscle were higher in the SE and GH groups than 
      those in the SC group. In summary, growth hormone application coupled with 
      swimming exercise appeared to affect the PI3K/AKT/mTOR signaling pathway in the 
      left ventricular tissue of rats; however, ERK signaling pathway appeared inactive 
      in physiological left ventricular hypertrophy caused by swimming and GH 
      administration over 8 weeks. Furthermore, GH treatment resulted in increased 
      miR-21 and miR-133 expression. Future study by our group will aim to assess the 
      effects of higher dose GH treatment.
FAU - Palabiyik, Orkide
AU  - Palabiyik O
AD  - Department of Medical Services and Techniques, Trakya University Health Services 
      Vocational College, Edirne 22030, Turkey.
FAU - Tastekin, Ebru
AU  - Tastekin E
AD  - Department of Pathology, Trakya University Faculty of Medicine, Edirne 22030, 
      Turkey.
FAU - Doganlar, Zeynep Banu
AU  - Doganlar ZB
AD  - Department of Medical Biology, Trakya University Faculty of Medicine, Edirne 
      22030, Turkey.
FAU - Tayfur, Pinar
AU  - Tayfur P
AD  - Department of Physiology, Trakya University Faculty of Medicine, Edirne 22030, 
      Turkey.
FAU - Dogan, Ayten
AU  - Dogan A
AD  - Department of Medical Biology, Trakya University Faculty of Medicine, Edirne 
      22030, Turkey.
FAU - Vardar, Selma Arzu
AU  - Vardar SA
AD  - Department of Physiology, Trakya University Faculty of Medicine, Edirne 22030, 
      Turkey.
LA  - eng
PT  - Journal Article
DEP - 20181213
PL  - England
TA  - Biomed Rep
JT  - Biomedical reports
JID - 101613227
PMC - PMC6391709
OTO - NOTNLM
OT  - cardiac hypertrophy
OT  - growth hormone
OT  - heart
OT  - microRNA
OT  - swimming
EDAT- 2019/03/08 06:00
MHDA- 2019/03/08 06:01
PMCR- 2018/12/13
CRDT- 2019/03/08 06:00
PHST- 2018/09/10 00:00 [received]
PHST- 2018/12/05 00:00 [accepted]
PHST- 2019/03/08 06:00 [entrez]
PHST- 2019/03/08 06:00 [pubmed]
PHST- 2019/03/08 06:01 [medline]
PHST- 2018/12/13 00:00 [pmc-release]
AID - BR-0-0-1179 [pii]
AID - 10.3892/br.2018.1179 [doi]
PST - ppublish
SO  - Biomed Rep. 2019 Feb;0(0):1-10. doi: 10.3892/br.2018.1179. Epub 2018 Dec 13.