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Involvement of Prokineticin 2 and Prokineticin Receptor 1 in Lipopolysaccharide-Induced Testitis in Rats

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Abstract

Prokineticin 2, a newly discovered proinflammatory peptide, has been amply evidenced to be involved in the occurrence and progress of local and systematical inflammation. Although the presence of Prokineticn 2 in mammal testis has been documented clearly, research targeting the involvement of prokineticin 2 in testicular pathology, especially testitis, is rather scarce. Employing a lipopolysaccharide-induced testitis rat model, we for the first time demonstrated the expression and upregulation of prokineticin 2 in orchitis at several levels. Our effort also addressed the differential expression patterns of prokineticin 2 and interleukin-1β, a key inflammation indicator, during testitis suggesting Prokineticn 2 serves more than a proinflammatory factor in the context of testitis. Given one of the cognate receptors of prokineticin 2, prokineticin receptor 1 (PKR1) was also significantly upregulated in orchitis as discussed in the current study, it is very likely that PK2/PKR1 signaling contribute to the development of inflammation-related testicular diseases.

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ACKNOWLEDGMENTS

This work was supported by the Fundamental Research Funds for the Central Universities of China (Grant No. 2013TS107).

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Correspondence to Huiping Zhang.

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All the animal experiments and procedures in this study were approved by the Institutional Animal Care and Use Committee of Tongji Medical College, Huazhong University of Science and Technology. All procedures involving animals were performed in accordance with the ethical standards of the institution or practice at which the studies were conducted.

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All the authors hereby declare that they do not have any relevant financial conflict of interest.

Additional information

Biao Chen and Lili Yu contributed equally to this work.

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Chen, B., Yu, L., Wang, J. et al. Involvement of Prokineticin 2 and Prokineticin Receptor 1 in Lipopolysaccharide-Induced Testitis in Rats. Inflammation 39, 534–542 (2016). https://doi.org/10.1007/s10753-015-0277-z

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