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Title Signaling Role of Prokineticin 2 on the Estrous Cycle of Female Mice Permalink
| Content Provider | Semantic Scholar |
|---|---|
| Author | Xiao, Ling Zhang, Chengkang Li, Xiao-Han Gong, Shiaoching Hu, Ren-Ming Balasubramanian, Ravikumar Crowley, W. William F. Hastings, Michael H. Zhou, Qun-Yong |
| Copyright Year | 2014 |
| Abstract | The possible signaling role of prokineticin 2 (PK2) and its receptor, prokineticin receptor 2 (PKR2), on female reproduction was investigated. First, the expression of PKR2 and its co-localization with estrogen receptor (ERa) in the hypothalamus was examined. Sexually dimorphic expression of PKR2 in the preoptic area of the hypothalamus was observed. Compared to the male mice, there was more widespread PKR2 expression in the preoptic area of the hypothalamus in the female mice. The likely co-expression of PKR2 and ERa in the preoptic area of the hypothalamus was observed. The estrous cycles in female PK2-null, and PKR2-null heterozygous mice, as well as in PK2-null and PKR2-null compound heterozygous mice were examined. Loss of one copy of PK2 or PKR2 gene caused elongated and irregular estrous cycle in the female mice. The alterations in the estrous cycle were more pronounced in PK2-null and PKR2-null compound heterozygous mice. Consistent with these observations, administration of a small molecule PK2 receptor antagonist led to temporary blocking of estrous cycle at the proestrous phase in female mice. The administration of PKR2 antagonist was found to blunt the circulating LH levels. Taken together, these studies indicate PK2 signaling is required for the maintenance of normal female estrous cycles. Citation: Xiao L, Zhang C, Li X, Gong S, Hu R, et al. (2014) Signaling Role of Prokineticin 2 on the Estrous Cycle of Female Mice. PLoS ONE 9(3): e90860. doi:10.1371/journal.pone.0090860 Editor: Shin Yamazaki, University of Texas Southwestern Medical Center, United States of America Received August 18, 2013; Accepted February 6, 2014; Published March 14, 2014 Copyright: 2014 Xiao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by NIH grant HD15788. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. * E-mail: qzhou@uci.edu. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://cloudfront.escholarship.org/dist/prd/content/qt4ct115wk/qt4ct115wk.pdf?t=n8xen7 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
