PubMed · 11630288
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
W Machleidt, M Putscher. 1994. [Not Available].. https://pubmed.ncbi.nlm.nih.gov/11630288/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The title question of this short paper has been addressed to me countless times by persons from all walks of life. The paper is a concise answer to the question; it might go halfway towards satisfying the questioners, but not more than halfway. This paper identifies the uniqueness of mangrove ecosystems in that they are created and sustained by a small number of rooted vascular plants in the intertidal area of the tropics. In addition to being a marginal ecosystem, a mangrove is unique in that, as an ecosystem it has various interactions with other ecosystems, both adjoining and remote in space and time. Another unique feature of mangroves is that, unlike most marginal ecosystems, they are highly productive and dynamic. Healthy mangrove ecosystems also have the peculiar ability to immobilize heavy metals.
The effects of proteasome inhibition (PI) on heat-shock protein (HSP) expression in cardiomyocytes were investigated. Neonatal rat cardiomyocytes were incubated with MG132 (0.1-10 microM) for 1 h. Induction of various HSPs was determined by real-time PCR and Western blotting. PI induced a 2- to 3-fold increase in HSP27, HSP60, and HSP90, and a 18-fold increase in HSP70 mRNA expression, whereas HSP40 levels were unaffected. Western blotting revealed increased protein expression for HSP70 after PI. Similar results were obtained with MG262. HSP induction correlated with enhanced survival of neonatal cardiomyocytes after sublethal heat stress in XTT testing. In papillary muscles, pretreatment with MG132 (10 microM, 90 min) was associated with enhanced recovery of the contractile parameters after a 40-min hypoxia. In these proof-of-principle experiments, we show that PI induces differential heat-shock response in cardiomyocytes, accompanied by enhanced cell survival and functional recovery after various forms of stress.
Explore the source record for details and available documents.