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Overexpression of Rap1B alleviate central precocious puberty and neurodevelopmental damage
1Department of Pediatrics, Huangshan Huaze integrated traditional Chinese and Western Medicine Hospital, 54 Qianyuan South Road, Tunxi District, Huangshan 245041, Anhui, China.
Insights
Overexpressing Rap1B alleviates central precocious puberty (CPP) by reducing harmful hormones and inflammation. This finding offers a potential new treatment strategy for CPP in children and adolescents.
Area of Science:
- Endocrinology
- Neuroscience
- Molecular Biology
Background:
- Central precocious puberty (CPP) negatively impacts children's physical and psychological health.
- The role of Rap1B in mitigating CPP development is currently unknown.
Purpose of the Study:
- To investigate the potential of Rap1B in alleviating central precocious puberty (CPP).
- To explore the molecular mechanisms underlying Rap1B's effects on CPP and neurodevelopmental damage.
Main Methods:
- Bioinformatics analysis of Rap1B expression.
- Establishment of a high-fat diet (HFD)-induced CPP rat model with AAV-Rap1B injection.
- Histological examination (HE staining), cell smear analysis, Western blot, RT-qPCR, IHC, and ELISA to assess CPP markers and related gene/protein expression.
- In vitro studies using a Rap1B cell line to evaluate the impact of fatty acids on cell proliferation, apoptosis, and inflammation.
Main Results:
- Overexpression of Rap1B alleviated HFD-induced CPP in rats, reducing serum hormone levels (LH, FSH, E2, T, AMH) and hypothalamic expression of GnRH, Kiss1, and Kiss1R.
- Rap1B overexpression mitigated hypothalamic injury and reversed fatty acid-induced damage in GT1-7 cells.
- Reduced levels of inflammatory factors (IL-6, IL-1β, TNF-α) were observed in GT1-7 cells overexpressing Rap1B.
Conclusions:
- Overexpression of Rap1B effectively alleviates central precocious puberty (CPP) and associated neurodevelopmental damage.
- Rap1B presents a promising new therapeutic target for the treatment of CPP.
Introduction:
The central precocious puberty (CPP) in children and adolescents can adversely impact their overall well-being, affecting both their physical and psychological health. Whether Rap1B can mitigate the development of CPP remains unknown.
Methods:
The expression of Rap1B was investigated through a comprehensive bioinformatics analysis. Precocious puberty model in rats was established through high-fat feeding (HFD), and further injected AAV-Rap1B. Then, HE staining, vaginal exfoliated cell smear and other methods were used to explore the incidence of precocious puberty in rats in each group. In addition, Western blot, RT-qPCR, and IHC was used to detect the expression of GnRH, GnRHR, Kiss1, Kiss1R, NeuN, BDNF, TH, AVP. The contents of LH, FSH, E2, T, and AMH in serum of rats were detected by ELISA. The Rap1B cell line was constructed at the cellular level to explore the effects of FFA(OA + PA) induction on cell proliferation, apoptosis and inflammation.
Results:
The expression of Rap1B was significantly up-regulated in overexpressing MKRN3 cells, where overexpressing MKRN3 can alleviate the occurrence of CPP. Overexpression of Rap1B alleviates HFD-induced CPP models, including reduce the content of LH, FSH, E2, T, and AMH in serum, and inhibit the expression of GnRH, Kiss1 and Kiss1R in hypothalamus, and alleviates hypothalamus injury. Furthermore, overexpression of Rap1B in the GT1-7 cell. Overexpression of Rap1B can significantly reverse FFA damage to GT1-7 cells and reduce FFA-induced increase of inflammatory factors (IL-6, IL-1β and TNF-α) in GT1-7 cells.
Conclusion:
This study indicated that overexpression of Rap1B alleviate CPP and neurodevelopmental damage. Our study offers a new approach for the treatment of CPP.
