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Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension
Author(s) -
Wang Zhihui,
Bao Xiufang,
Song Limeng,
Tian Yuying,
Sun Ping
Publication year - 2021
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29552
Subject(s) - endocrinology , oxidative stress , medicine , nitric oxide synthase , protein kinase a , superoxide dismutase , kinase , mapk/erk pathway , malondialdehyde , nitric oxide , signal transduction , biology , biochemistry
We aim to investigate the role of miR‐106‐mediated mitogen‐activated protein kinase (MAPK) signaling pathway in oxidative stress (OS) injury and inflammatory infiltration in the liver of the mouse with gestational hypertension (GH). Ninety specific pathogen‐free mice (Kunming species) during middle to late gestation were selected for the study. Fifteen mice were used as control, while the rest were used for establishing the GH model. The mice were assigned to six groups: normal group (normal gestation), model group (GH model), negative control group (GH model, intravenously injected with negative control vector), miR‐106a‐mimic group (GH model, intravenously injected with vector overexpressing miR‐106a, which mimics the overexpression of endogenous mature miR‐106a), SB203580 group (GH model, intravenously injected with MAPK pathway inhibitor SB203580), and miR‐106a‐mimic+SB203580 group (GH model, intravenously injected with SB203580 and vector overexpressing miR‐106a). Fourteen days after electrical stimulation, all the groups except for the normal group had elevated blood pressure vs those on day 0 and 7. Compared with the normal group, the other groups had lower levels of miR‐106a expression, nitric oxide, nitric oxide synthase, catalase, superoxide dismutase, S cell ratio, and interleukin‐4 (IL‐4) and IL‐10 in the serum and liver as opposed to increased levels of blood pressure, p38MAPK mRNA expression, p‐p38MAPK positive expression rate, protein expressions of p‐p38MAPK, p‐ERK, and p‐JNK, H 2 O 2 and malondialdehyde in liver, G0/G1 cell ratio, apoptosis rate, and IL‐6, interferon‐γ (IFN‐γ), and IFN‐α in the serum and liver (all P < .05). The miR‐106 overexpression or inhibiting MAPK signaling pathway can attenuate OS injury and inflammatory response in the liver of the mouse with GH, and the effect can be even better if both miR‐106a overexpression and inhibiting MAPK pathway are applied. In conclusion, miR‐106a overexpression can inhibit OS injury and inflammatory infiltration in the liver of the mouse with GH by mediating MAPK signaling pathway.