PMID- 33215409
OWN - NLM
STAT- MEDLINE
DCOM- 20210624
LR  - 20210624
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 21
DP  - 2020 Nov
TI  - MiR-210 inhibits apoptosis of cranial nerves in preeclampsia rats through 
      suppressing the TGF-beta signaling pathway.
PG  - 10960-10965
LID - 23579 [pii]
LID - 10.26355/eurrev_202011_23579 [doi]
AB  - OBJECTIVE: To explore the protective effect of micro ribonucleic acid (miR)-210 
      on cranial nerves in rats with preeclampsia (PE) by regulating the transforming 
      growth factor-beta (TGF-beta) signaling pathway. MATERIALS AND METHODS: A total of 36 
      pregnant Sprague-Dawley rats were randomly divided into normal group (n=12), 
      model group (n=12), and miR-210 mimics group (n=12). The rats were fed normally 
      in the normal group. In the latter two groups, the PE model was established, 
      followed by injection of normal saline or miR-210 mimics via the caudal vein, 
      respectively. The above intervention lasted until 20 d of gestational age in 
      pregnant rats. Then, the systolic blood pressure of the caudal vein was measured. 
      The relative levels of Caspase3, phosphorylated TGF-beta (p-TGF-beta), and miR-210 were 
      detected via immunohistochemistry, Western blotting, and quantitative Polymerase 
      Chain Reaction (qPCR). Cell apoptosis was determined by terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: The systolic 
      blood pressure of the caudal vein significantly increased in the other two groups 
      compared with that in the normal group (p<0.05), while it significantly decreased 
      in the miR-210 mimics group compared with that in the model group (p<0.05). The 
      results of immunohistochemistry showed that the positive expression of Caspase3 
      significantly rose in the other two groups compared with that in the normal group 
      (p<0.05), while it remarkably declined in miR-210 mimics group compared with that 
      in the model group (p<0.05). The results of Western blotting revealed that the 
      protein expression of p-TGF-beta was evidently higher in the other two groups than 
      that in the normal group (p<0.05), while it was evidently lower in the miR-210 
      mimics group than that in the model group (p<0.05). Moreover, it was found via 
      qPCR that the other two groups had remarkably lower relative expression of 
      miR-210 than normal group (p<0.05), while miR-210 mimics group had remarkably 
      higher relative expression of miR-210 than the model group (p<0.05). According to 
      the results of TUNEL assay, the apoptosis rate markedly increased in the other 
      two groups compared with that in the normal group (p<0.05), while it markedly 
      decreased in the miR-210 mimics group compared with that in the model group 
      (p<0.05). CONCLUSIONS: MiR-210 inhibits apoptosis via suppressing the TGF-beta 
      signaling pathway, thereby exerting a protective effect on cranial nerves in PE 
      rats.
FAU - Han, H-Y
AU  - Han HY
AD  - Department of Obstetrics, Dongying People's Hospital of Shandong, Dongying, 
      China. rongandhui@hotmail.com.
FAU - Liu, K
AU  - Liu K
FAU - Wang, J-R
AU  - Wang JR
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (MIRN210 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (Protective Agents)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cranial Nerves/*metabolism/pathology
MH  - Female
MH  - MicroRNAs/*metabolism
MH  - Pre-Eclampsia/*metabolism/pathology
MH  - Pregnancy
MH  - Protective Agents/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - Transforming Growth Factor beta/*metabolism
EDAT- 2020/11/21 06:00
MHDA- 2021/06/25 06:00
CRDT- 2020/11/20 05:52
PHST- 2020/11/20 05:52 [entrez]
PHST- 2020/11/21 06:00 [pubmed]
PHST- 2021/06/25 06:00 [medline]
AID - 23579 [pii]
AID - 10.26355/eurrev_202011_23579 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):10960-10965. doi: 
      10.26355/eurrev_202011_23579.