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Cerebral expression and serum detectability of secretagogin, a recently cloned EF-hand Ca(2+)-binding protein
W Gartner1, W Lang, F Leutmetzer
1Department of Medicine III, Division of Clinical Endocrinology and Metabolism, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
Insights
Secretagogin, a novel EF-hand calcium-binding protein, is specifically expressed in brain neurons. Elevated serum secretagogin levels indicate hypoxic neuronal damage, suggesting its potential as a clinical marker for neurological injury.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Secretagogin is a novel EF-hand calcium-binding protein identified in neuroendocrine cells.
- Its expression pattern and potential role in neuronal function and damage were previously uncharacterized.
Purpose of the Study:
- To investigate the cerebral expression pattern of secretagogin.
- To evaluate secretagogin as a potential serum biomarker for hypoxic neuronal damage.
Main Methods:
- Immunohistochemistry and blotting techniques (Northern-blot, Western-blot) were used to determine secretagogin's expression in the brain.
- A newly developed sandwich capture ELISA was employed to quantify secretagogin levels in patient serum.
Main Results:
- Secretagogin exhibits a neuron-specific expression pattern in the brain, notably in cerebellar, pituitary, neocortical, hypothalamic, and hippocampal neurons.
- Serum secretagogin levels were significantly elevated in patients with hypoxic neuronal damage, peaking 2-3 days post-infarction.
- Control sera and patients with minor neurological deficits showed undetectable secretagogin levels.
Conclusions:
- Secretagogin is widely expressed in specific neuronal populations within the central nervous system.
- Serum secretagogin levels correlate with the presence and severity of hypoxic neuronal damage, positioning it as a promising biomarker for neurological injury.
Abstract:
Recently we identified a novel EF-hand Ca-binding protein termed secretagogin, which is expressed in neuroendocrine cells. Immunohistochemical investigations, using a murine monoclonal and an affinity purified rabbit polyclonal anti-secretagogin antibody as well as Northern-blot and Western-blot analysis revealed a neuron-specific cerebral expression pattern. Secretagogin was detected in high quantity in basket and stellate cells of the cerebellar cortex, in secretory neurons of the anterior part of the pituitary gland and in singular neurons of the frontal and parietal neocortex. Remarkable staining intensity was observed in hypothalamic and in hippocampal neurons. Using a newly developed sandwich capture ELISA we show presence of secretagogin in serum of patients suffering from hypoxic neuronal damage. In sera obtained from 32 patients with different forms of neurological symptoms due to focal cerebral ischemia, secretagogin levels ranged from 3 to 236 pg/ml, with highest levels observed on days 2 and 3 after infarction. Three patients exhibiting minor, reversible neurological deficits had nondetectable serum secretagogin levels at time points of testing. In 50 control sera, secretagogin was below the detection limit of our ELISA. Parallel analysis of secretagogin and the established neurobiochemical marker S-100B in 14 representative patients revealed comparable results. However, S-100B levels were higher and exhibited different kinetics than secretagogin. Our data present the cerebral expression pattern of secretagogin and give evidence that this protein might represent a clinically relevant serum marker indicative for neuronal damage.
