Abstract
Obesity has become a global health problem. Research suggests that leptin, a hormone that responds to fat deposition, may be involved in mammalian reproduction; however, its precise role in embryo implantation is poorly understood. Here, primary porcine endometrium epithelium cells (PEECs) were cultured in vitro and used to evaluate the regulatory role of different leptin levels on β3-integrin, MMP9, HB-EGF, and IL-1β, which are, respectively, involved in four critical steps of embryo implantation. Results showed that only 0.01 nM leptin significantly improved β3-integrin mRNA expression (p < 0.05). MMP9 and HB-EGF mRNA expressions were upregulated by 0.10–10.00 nM leptin (p < 0.05). The IL-1β expression level was only increased by 10.00 nM leptin (p < 0.05). β3-integrin, MMP9, HB-EGF, and IL-1β mRNA and protein have a similar fluctuant response to increased leptin. Leptin’s influence on β3-integrin, MMP9, HB-EGF, and IL-1β disappeared when the JAK2, PI(3)K, or MAPK signaling pathways were blocked, respectively. In conclusion, leptin affected porcine implantation by regulating the expression of β3-integrin, MMP9, HB-EGF, and IL-1β in a dose-dependent manner. The signaling pathways of JAK2, PI(3)K, and MAPK may participate in this regulatory process. These findings will contribute to further understanding the mechanisms of reproductive disorders in obesity.
Highlights
Obesity is a global health problem and its negative effects on reproduction have recently been highlighted
The regulation of leptin on β3-integrin, MMP9, Heparin binding EGF-like growth factor (HB-EGF), and IL-1β was initially determined based on the transcriptional expression using RT-PCR (Figure 1A–D)
porcine endometrium epithelial cells (PEECs) treated with 0.10–10.00 nM leptin had higher MMP9 and HB-EGF mRNA levels than the control group and 0.01 nM leptin group (p < 0.05)
Summary
Obesity is a global health problem and its negative effects on reproduction have recently been highlighted. Leptin, which has a similar action in obesity to that of insulin in diabetes, is a hormone that responds to fat deposition. It participates in the regulation of sugar, fat, and energy metabolism; reduces nutrient intake; increases energy release; and inhibits the synthesis of fat, thereby increasing weight loss. The first is ob gene mutation, which causes insufficient leptin, and the second is resistance to leptin that forces the ob gene to be overexpressed. The ob gene mutation causing leptin deficiency is rare in the vast majority of obese people, but ob gene overexpression inducing supra physiologi levels of leptin is common [1]. Both leptin and its long-form receptor were shown to be overexpressed at implantation sites compared with inter-implantation sites in porcine endometrium, which suggests that leptin may
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