ArticleThe Biochemical journal1996
Induction of cell surface blebbing by increased cellular Pi concentration.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Tumour cell blebbing and extracellular vesicle shedding: key role of matrikines and ribosomal protein SA.British journal of cancer · 2019Article
- Involvement of Membrane Blebbing in Immunological Disorders and Cancer.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2016Review
- Phosphate is a specific signal for ATDC5 chondrocyte maturation and apoptosis-associated mineralization: possible implication of apoptosis in the regulation of endochondral ossification.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2003Article
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Authors and funding
1 author.
Funding
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Abstract
Cell surface blebbing is an early, reversible characteristic of anoxia described in several different cell types. Blebbing may lead to the formation of large terminal blebs, and ultimately cell death upon rupture of the membrane. In the present work, evidence is presented indicating that Pi may be the immediate mediator of cell surface blebbing: (1) cell surface blebbing can be induced in normoxic Ehrlich ascites tumour cells by a high extracellular concentration of Pp leading to an increase in the cellular Pi concentration; (2) anoxia induces sustained elevation of the cellular Pi concentration and (3) cell surface blebbing during anoxia is reversed upon reoxygenation, and the disappearance of blebbing depends on the decrease in cellular Pi concentration. The rate of disappearance of blebs may be enhanced by the simultaneous addition of adenine and inosine to the growth medium. This leads to a decrease in cellular Pi concentration and to an almost complete restoration of the cellular ATP concentration. It is suggested that Pi is an important mediator of anoxia induced cell damage.
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