Related Experiment Video
Updated: Jul 7, 2026

04:33
Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
Published on: March 12, 2019
Glucocorticoid deficiency increases phospholipase A2 activity in rats
B S Vishwanath1, F J Frey, M J Bradbury
1Department of Medicine, University of Bern, Switzerland.
The Journal of Clinical Investigation
|October 1, 1993
Summary
Low glucocorticoids increase phospholipase A2 (PLA2) and decrease its inhibitor, lipocortin-I, potentially driving inflammation. This study investigated PLA2 regulation in adrenalectomized rats, revealing key molecular changes linked to inflammatory states.
Area of Science:
- Endocrinology
- Molecular Biology
- Immunology
Background:
- Glucocorticoids inhibit phospholipase A2 (PLA2), a key enzyme in inflammatory mediator release.
- Low endogenous glucocorticoid levels are associated with inflammatory and immunological diseases.
Purpose of the Study:
- To investigate the regulation of PLA2 mRNA, protein, and enzyme activity in adrenalectomized (ADX) rats with low glucocorticoid levels.
- To explore the role of PLA2 and its inhibitor, lipocortin-I, in hypoglucocorticoid states.
Main Methods:
- Adrenalectomized (ADX) rats were used to create a hypoglucocorticoid state.
- Quantitative PCR (PCR) measured PLA2 group I and II mRNA levels.
- Western blotting assessed PLA2 protein expression and lipocortin-I concentrations.
- PLA2 enzyme activity was measured in various tissues.
Main Results:
- ADX rats showed significant upregulation of group II PLA2 mRNA (126%) and protein (70-100%) in multiple tissues.
- Exogenous corticosterone administration reversed these increases.
- PLA2 enzyme activity increased disproportionately to mRNA and protein levels.
- Lipocortin-I concentrations decreased in ADX rats, correlating inversely with PLA2 activity.
Conclusions:
- Hypoglucocorticoid states lead to PLA2 upregulation and lipocortin-I downregulation.
- These molecular changes in PLA2 and lipocortin-I likely contribute to the enhanced inflammatory response observed in low glucocorticoid conditions.
More Related Videos
Related Concept Videos
GPCRs Regulate Adenylyl Cylase Activity
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Two...
cAMP-dependent Protein Kinase Pathways
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Cushing Syndrome I: Introduction
Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
Cushing Syndrome II: Pathophysiology
Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...

