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Author Kumaran, C. ♦ Shivakumar, K.
Source Sree Chitra Tirunal Institute for Medical Sciences & Technology
Content type Text
Publisher American Journal of Physiology-heart and Circulatory Physiology
File Format PDF
Language English
Subject Domain (in DDC) Natural sciences & mathematics ♦ Life sciences; biology ♦ Physiology & related subjects ♦ Biochemistry ♦ Technology ♦ Medicine & health
Subject Domain (in MeSH) Amino Acids, Peptides, and Proteins ♦ Biological Factors ♦ Chemical Actions and Uses ♦ Chemicals and Drugs ♦ Chemical Phenomena ♦ Biological Sciences
Subject Keyword Biochemistry
Abstract Substance P is released from nerve endings in the heart under pathological conditions like ischemia, but its action on cardiac cells has not been investigated. This study tested the hypothesis that substance P is mitogenic to adult cardiac fibroblasts and delineated the underlying mechanism(s). Substance P, acting via neurokinin-1 (NK-1) receptors, stimulated cellular hyperplasia over a range of 1-10 mumol/l. It elicited no change in net collagen production, total protein synthesis, or cell protein content but increased Ca-45 uptake and superoxide generation. EGTA, N-acetyl-cysteine, and superoxide dismutase attenuated the hyperplastic response to substance P. A combination of substance P and EGTA enhanced superoxide generation without an increase in DNA synthesis, showing that an increase in superoxide production does not result in hyperplasia when extracellular Ca2+ is chelated. Together, the data suggest that substance P may activate, via NK-1 receptors, a hyperplastic but not hypertrophic response in adult cardiac fibroblasts and that alterations in redox state and Ca2+ homeostasis may act in concert to mediate its mitogenic action.
Education Level UG and PG
Learning Resource Type Article
Educational Framework Medical Council of India (MCI)
Journal American Journal of Physiology-Heart and Circulatory Physiology
Volume Number 282
Issue Number 5