Accession Number : ADA298627

Title :   Skeletal Muscle Ischemia and Heat Shock Proteins.

Descriptive Note : Annual rept. 1 Jul 94-30 Jun 95,

Corporate Author : CALIFORNIA UNIV SAN DIEGO LA JOLLA

Personal Author(s) : Dillmann, Wolfgang H.

PDF Url : ADA298627

Report Date : 04 AUG 1995

Pagination or Media Count : 28

Abstract : This research effort is directed at subobjective 2 as defined in the recent shock trauma mediators review memo from the U.S. Army Institute of Surgical Research. Specifically, we aimed at the prevention of secondary damage after hemorrhage by temporizing fundamental physiological or biochemical processes leading to cell death and organ failure. For this purpose, increased expression of the inducible heat shock 70 (hsp70I) will be employed. Hsp7OI works as a chaperone attaching to short hydrophobic peptide sequences as they are exposed in ischemic cells in which proteins undergo denaturation. By the association of hsp70 with such protein sequences further protein aggregation and cell damage is prevented. This leads to a faster recovery of cell function after the ischemic or hemorrhage episodes. Our results which are further summarized in the body indicate that overexpression of hsp70 in the heart of transgenic mice leads to marked protection against cardiac ischemic injury (1). In preliminary studies in collaboration with Dr. P. Lyden, UCSD and Dr. B. Nishimura, UCLA, we have found that the hsp70 transgene is also expressed in CNS-neurons and exerts a protective effect against ischemic damage in the brain as judged by behavioral scores in these transgenic mice.

Descriptors :   *MUSCULOSKELETAL SYSTEM, *HEAT, *SHOCK(PATHOLOGY), *ISCHEMIA, RECOVERY, ARMY RESEARCH, DAMAGE, BRAIN, PEPTIDES, BIOCHEMISTRY, PROTEINS, SEQUENCES, SHOCK, PROTECTION, CLONES, PHYSIOLOGY, BEHAVIOR, DEATH, CELLS(BIOLOGY), CULTURES(BIOLOGY), SCORING, TRAUMA, HYDROPHOBIC PROPERTIES, ORGANS(ANATOMY), HEMORRHAGE, MUSCULOSKELETAL DISEASES.

Subject Categories : Medicine and Medical Research
      Anatomy and Physiology

Distribution Statement : APPROVED FOR PUBLIC RELEASE