title: Inhibition of heat-induced apoptosis in rat small intestine and IEC-6 cells through the AKT signaling pathway.
abstract: BACKGROUND
  As the world warms up, heat stress is becoming a major cause of economic loss in the livestock industry. Long-time exposure of animals to hyperthermia causes extensive cell apoptosis, which is harmful to them. AKT and AKT-related serine-threonine kinases are known to be involved in signaling cascades that regulate cell survival, but the mechanism remains elusive. In the present study, we demonstrate that phosphoinositide 3-kinase (PI3K) /AKT signal pathway provides protection against apoptosis induced by heat stress to ascertain the key point for treatment.
  
  
  RESULTS
  Under heat stress, rats showed increased shedding of intestinal epithelial cells. These rats also had elevated levels of serum cortisol and improved expression of heat shock proteins (Hsp27, Hsp70 and Hsp90) in response to heat stress. Apoptosis analysis by TUNEL assay revealed a higher number of villi epithelial cells that were undergoing apoptosis in heat-treated rats than in the normal control. This is supported by gene expression analysis, which showed an increased ratio of Bax/Bcl-2 (p < 0.05), an important indicator of apoptosis. During heat-induced apoptosis, more AKTs were activated, showing increased phosphorylation. An increase of BAD phosphorylation, which is an inhibitory modification, ensued. In rat IEC-6 cell line, a significant higher level of AKT phosphorylation was observed at 2 h after heat exposure. This coincided with a marked reduction of apoptosis.
  
  
  CONCLUSIONS
  Together, these results suggest that heat stress caused damages to rat jejunum and induced apoptosis to a greater degree. HSPs and pro-survival factors were involved in response to heat stress. Among them, AKT played a key role in inhibiting heat-induced apoptosis.
authors.affiliation: College of Veterinary Medicine, South China Agricultural University, Tianhe, Guangzhou, Guangdong 510642, R, P China. xujianqincau@126.com.
authors.forename: Zhimin
authors.initials: Z
authors.lastname: Gao
authors.forename: Fenghua
authors.initials: F
authors.lastname: Liu
authors.forename: Peng
authors.initials: P
authors.lastname: Yin
authors.forename: Changrong
authors.initials: C
authors.lastname: Wan
authors.forename: Shasha
authors.initials: S
authors.lastname: He
authors.forename: Xiaoxi
authors.initials: X
authors.lastname: Liu
authors.forename: Hong
authors.initials: H
authors.lastname: Zhao
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.forename: Jianqin
authors.initials: J
authors.lastname: Xu
authors.forename: Shining
authors.initials: S
authors.lastname: Guo
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002460:Cell Line; D006358:Hot Temperature / Q000009:adverse effects; D007421:Intestine, Small / Q000378:metabolism / Q000502:physiology*; D008297:Male; D051058:Oncogene Protein v-akt / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D051058:Oncogene Protein v-akt