Growth regulation by T cell calcium stores

• Main Author: Weil, Keri Rene
• Format: Others
• Published: Scholarly Commons 2002
• Subjects: Cellular biology; Biological sciences; Biology; Life Sciences
• Online Access: https://scholarlycommons.pacific.edu/uop_etds/2741; https://scholarlycommons.pacific.edu/cgi/viewcontent.cgi?article=3740&context=uop_etds

The role of calcium in cell signaling has gained widespread attention due to its role in a number of pathological and physiological processes. Capacitative calcium entry, in which depletion of calcium from the endoplasmic reticulum (ER) stores induces the influx of extracellular calcium, is essential for proper activation of mammalian T lymphocytes. Although alterations in intracellular calcium homeostasis has been implicated in both proliferation and apoptosis of various cell types, large gaps still exist in the understanding of how these mechanisms are regulated. In order to gain further insight into calcium's role in T cell growth regulation these studies look at the effects of various pharmacological and physiological regulators of T cell calcium stores. The growth effects they have on Jurkat lymphocytes were determined with cell proliferation assays and calcium sensitive fluorescent assays were used to investigate the changes in intracellular calcium levels. Both phytohemagglutinin (PHA) and thapsigargin (TG) significantly suppressed cell growth and showed evidence of morphological and biochemical characteristics of apoptosis. It was found that the PHA treated cells had depleted ER calcium stores and appeared to have shifted calcium into the mitochondria. The shifting of calcium stores from the ER to the mitochondria may play a central role in the commitment to apoptosis.