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Mechanisms involved in calcium-mobilizing agonist responses
Advances in Cyclic Nucleotide and Protein Phosphorylation Research
|January 1, 1986
Summary
Hormones like epinephrine increase intracellular calcium (Ca2+) and diacylglycerol, triggering cellular responses. Myo-inositol 1,4,5-P3 and diacylglycerol act as key second messengers, activating protein kinase C and calmodulin pathways.
Area of Science:
- Cellular Biology
- Biochemistry
- Molecular Pharmacology
Background:
- Many hormones and neurotransmitters mediate effects via intracellular calcium (Ca2+) and 1,2-diacylglycerol signaling.
- Key agonists include epinephrine, norepinephrine, acetylcholine, vasopressin, cholecystokinin, and angiotensin II.
Purpose of the Study:
- To elucidate the general mechanisms by which Ca2+-mobilizing agonists induce physiological responses.
- To identify the roles of second messengers like myo-inositol 1,4,5-P3 and diacylglycerol in cellular signaling.
Main Methods:
- Investigated the mobilization of Ca2+ from intracellular stores and across the plasma membrane.
- Examined the turnover of cellular phosphoinositides, particularly phosphatidylinositol 4,5-P2 breakdown.
- Studied the activation of protein kinase C and the Ca2+-calmodulin complex.
Main Results:
- Phosphatidylinositol 4,5-P2 breakdown generates myo-inositol 1,4,5-P3, which releases Ca2+ from the endoplasmic reticulum.
- Diacylglycerol activates protein kinase C, a Ca2+-phospholipid-dependent kinase.
- The Ca2+-calmodulin complex interacts with various enzymes, including multifunctional calmodulin-dependent protein kinase, altering protein activities.
Conclusions:
- Myo-inositol 1,4,5-P3 is a critical second messenger for Ca2+-dependent hormones.
- Diacylglycerol and Ca2+-calmodulin pathways are central to agonist-induced cellular responses.
- Further research is ongoing to define protein kinase C substrates and additional Ca2+-calmodulin targets.