4.7 Article

Essential roles of Cdc42 and MAPK in cadmium-induced apoptosis in Litopenaeus vannamei

期刊

AQUATIC TOXICOLOGY
卷 163, 期 -, 页码 89-96

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.aquatox.2015.03.023

关键词

Litopenaeus vannamei; Cdc42; MAPKs; dsRNA interfering technique; Apoptosis; THC; ROS production

资金

  1. National Nature Science Foundation of China [31372205]
  2. Guangdong Provincial Oceanic Fisheries Science and Technology Project [A201208B03, A201105G03]
  3. Guangdong province science and technology research spark project [2013 B020503060]

向作者/读者索取更多资源

Cadmium, one of the most toxic heavy metals in aquatic environments, has severe effects on marine invertebrates and fishes. The MAPK signaling pathway plays a vital role in stress responses of animals. The mitogen-activated protein kinase (MAPK) signaling pathway plays a vital role in animals' stress responses, including mediation of apoptosis induced by the Rho GTPase Cdc42. However, there is limited knowledge about its function in shrimps, although disorders exacerbated by environmental stresses (including heavy metal pollution) have caused serious mortality in commercially cultured shrimps. Thus, we probed roles of Cdc42 in Litopenaeus vannamei shrimps (LvCdc42) during cadmium exposure by inhibiting its expression using dsRNA-mediated RNA interference. The treatment successfully reduced expression levels of MAPKs (including p38, JNK, and ERK). Cadmium exposure induced significant increases in expression levels of LvCdc42 and MAPKs, accompanied by reductions in total hemocyte counts (THC) and increases in apoptotic hemocyte ratios and ROS production. However, all of these responses were much weaker in LvCdc42-suppressed shrimps, in which mortality rates were higher than in controls. Our results suggest that the MAPK pathway plays a vital role in shrimps' responses to Cd2+. They also indicate that LvCdc42 in shrimps participates in its regulation, and thus plays key roles in ROS production, regulation of apoptosis and associated stress responses. (C) 2015 Elsevier B.V. All rights reserved.

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