2. Academic Validation
  3. Involvement of CaMKII in regulating the release of diplotene-arrested mouse oocytes by pAkt1 (Ser473)

Involvement of CaMKII in regulating the release of diplotene-arrested mouse oocytes by pAkt1 (Ser473)

  • Cell Cycle. 2019 Nov;18(21):2986-2997. doi: 10.1080/15384101.2019.1666596.
Lingling Liu 1 2 3,  Hanwen Li 4,  Ben Labbe 5,  Yang Wang 2,  Shitao Mao 6,  Yu Cao 2,  Mingjing Zhao 6,  Shuo Liu 6,  Hang Yu 7,  Xin Deng 1 2 6
Affiliations

Affiliations

  • 1 Central Laboratory of the Fourth Affiliated Hospital, CMU , Shenyang , PR China.
  • 2 Department of Physiology, China Medical University (CMU) , Shenyang , PR China.
  • 3 Mouse Genome Editing Core, Dept of Laboratory Animal Science, Shanghai Public Health Clincial Center, Fudan University , Shanghai , PR China.
  • 4 Department of Anorectum, the Fourth Affiliated Hospital, China Medical University (CMU) , Shenyang , PR China.
  • 5 Department of Microbiology and Immunology, Indiana University School of Medicine , Indianapolis, IN , USA.
  • 6 Department of Pneumology, the Fourth Affiliated Hospital, CMU , Shenyang , PR China.
  • 7 Department of Biophysics, China Medical University (CMU) , Shenyang , China.
PMID: 31530151 DOI: 10.1080/15384101.2019.1666596
Abstract

Calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMKII) had been reported to play a role in the process of fertilization. However, the role of CaMKII in the release of diplotene-arrested oocytes is poorly understood. In this study, we explored the potential effect of CaMKII on Akt1 and the relationship among CaMKII, Akt1 and phosphatidylinositol (3,4,5)-trisphosphate (PIP3) during the meiotic resumption of mouse oocytes. We found that inhibition of CaMKII aggravated diplotene arrest. We detected the expression and distribution of pCaMKII (Thr286), pAkt1 (Ser473), Cdc25B and pCdc2 (Tyr15) when oocytes were treated with KN-93, SH-6, LY294002 or PIP3, respectively. Our data showed that down-regulated CaMKII by KN-93 decreased the levels of pAkt1 (Ser473) and rearranged the distribution of pAkt1 (Ser473). Meanwhile, down-regulated pAkt1 (Ser473) by SH-6 also decreased the levels of pCaMKII (Thr286), Cdc25B and pCdc2 (Tyr15) significantly and rearranged the distributions of pCaMKII (Thr286). Furthermore, our data showed that exogenous PIP3 up-regulated GVBD rates significantly and increased the levels of pCaMKII (Thr286) and pAkt1 (Ser473). On the contrary, down-regulation of PIP3 by LY294002 decreased GVBD rates and the levels of pCaMKII (Thr286) and pAkt1 (Ser473), respectively. Our results showed that Akt1 and CaMKII regulated each other, and PIP3 may be involved in these regulations during the release of mouse oocytes from diplotene arrest.

Keywords

Calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMKII); diplotene arrest; mouse oocyte; protein kinase B alpha (PKBα/Akt1).

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Products
  • Cat. No.
    Product Name
    Description
    Target
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  • HY-15465
    99.19%, CaMK II Inhibitor‎