0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
ARTICLE |

Heat Shock Induces IκB-α and Prevents Stress-Induced Endothelial Cell Apoptosis

Susan L. DeMeester, MD; Timothy G. Buchman, PhD, MD; Yuyu Qiu; Ammini K. Jacob, MBBS, PhD; Keith Dunnigan, MS; Richard S. Hotchkiss, MD; Irene Karl, PhD; J. Perren Cobb, MD
Arch Surg. 1997;132(12):1283-1288. doi:10.1001/archsurg.1997.01430360029005.
Text Size: A A A
Published online

Objective:  To determine whether prior heat shock would attenuate endothelial cell apoptosis and whether any effect of preemptive heat shock is mediated through a nuclear factor kappa B and inhibitor kappa B α mechanism.

Design:  A randomized, controlled in vitro study.

Setting:  A laboratory in a large, academic medical center.

Interventions:  Cultured primary porcine endothelial cells were treated with increasing doses of sodium arsenite (40-160 μmol/L), after which the interval until subsequent apoptotic (lipopolysaccharide-arsenite) challenge was varied (4-16 hours). The degree of cell death and apoptosis were determined using neutral red uptake and staining with annexin V and propidium iodide, respectively. Inducible heat shock protein 70 and inhibitor kappa B α levels in treated cells were determined by Western blot analysis. Lipopolysaccharide-induced nuclear factor kappa B activity was assessed using an electrophoretic mobility shift assay.

Results:  Prior arsenite treatment decreased cell death by apoptosis in a time- and dose-dependent manner. Specifically, a higher sodium arsenite concentration and shorter intervals afforded better protection (P=.01, 160 μmol/L at 4 hours). Protection against apoptosis correlated with increased heat shock protein 70 and inhibitor kappa B α levels and decreased nuclear factor kappa B binding activity.

Conclusions:  Arsenite, an inducer of the heat shock response, decreased stress-induced endothelial cell apoptosis. The mechanism of this protection may include decreased nuclear factor kappa B activity or increased inducible heat shock protein 70 levels. Heat shock protein 70 may serve as a molecular marker to determine not only the phenotypic state of the cell but also the durability of protection afforded by heat shock. These data support the hypothesis that stress-induced changes in transcription factor activity and protein expression can regulate the induction of apoptosis.Arch Surg. 1997;132:1283-1288

Topics

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

Figures

Tables

References

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

Related Content

Customize your page view by dragging & repositioning the boxes below.

Jobs
brightcove.createExperiences();