Skip to main content
ARS Home » Midwest Area » West Lafayette, Indiana » Livestock Behavior Research » Research » Publications at this Location » Publication #171938


item Rogers, Colin
item Collins, Jeremy
item Lay, Jr, Donald - Don
item Cheng, Heng Wei
item Sartin, James
item Schwartz, Dean

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2007
Publication Date: 3/31/2005
Citation: Rogers, C.B., Collins, J.S., Lay Jr, D.C., Cheng, H., Sartin, J.L., Schwartz, D.D. 2005. Reduced expression of proteasome 26s in hypothalamus of heat stressed pigs and hypothalamic cells. Experimental Biology.

Interpretive Summary:

Technical Abstract: The loss of proteasome function has been suggested to underlie the delayed neuronal death induced by transient forebrain ischemia as well as to Alzheimer's disease pathogenesis. In the hypothalamus of 12-hr heat-stressed pigs the expression of proteasome 26S was reduced as determined by differential display PCR and confirmed by real-time RT-PCR. Next, we determined whether the expression of proteasome 26S was also altered in a hypothalamic cell line in response to heat stress. Cells grown in serum-free media were heat-stress at 43 degrees for 15 min and then returned to 37 degrees C for up to 5 hr. Total RNA was isolated and real-time RT-PCR was used to evaluate the expression of genes of interest. Glyceraldehyde-3-phosphate dehydrogenase mRNA expression was used as an internal control and did not show a change in expression in the 5-hr recovery period. Expression of heat shock protein (HSP70) was increased 6.2 ± 2, 14.3 ± 5 and 14.7 ± 7 fold at 1, 2, and 3 hours, respectively, and returned to baseline by 5 hours. Over the same time period, there was a persistent decrease in the expression of proteasome 26S subunit in cells beginning 2 hr after heat stress. The altered expression of proteasome 26S in both the hypothalamus of heat stress pigs and in hypothalamic cells suggests that impairment of the proteolytic pathway may be involved in the neuronal response to heat stress.