mu-Crystallin is an
NADPH-dependent cytosolic T3-binding
protein. A knockout study in mice showed that
mu-crystallin has a physiological function as a reservoir of T3 in the cytoplasm in vivo. Patients with
nonsyndromic deafness were reported to have point mutations in the
mu-crystallin gene. The expression of
mu-crystallin is regulated by multiple factors. The present study was performed to determine whether thyroid function is related to the expression of
mu-crystallin mRNA in peripheral mononuclear cells. We examined 23 normal healthy male and female subjects and 15 patients with
Graves' disease.
mu-Crystallin protein expression was determined immunohistochemically in peripheral mononuclear cells. The expression of
mu-crystallin mRNA was assessed by reverse transcription of total
RNA from peripheral mononuclear cells followed by quantitative PCR.
mu-Crystallin protein was detected in peripheral mononuclear cells. The
mRNA expression was negatively correlated with age in normal female subjects. The values in female subjects were significantly higher than those in males. The values were positively correlated with serum TSH concentration. The values of the thyrotoxic patients with
Graves' disease were lower than those in healthy subjects. A transient increase in
mu-crystallin expression was observed within 14-42 days after the initial treatment with antithyroid medication.
Thyroid hormone inversely relates to the expression of
mu-crystallin mRNA in euthyroid mononuclear cells. Abrupt suppression of thyroid function leads to overexpression of
mu-crystallin mRNA in thyrotoxic mononuclear cells.
Thyroid hormone-regulated
mu-crystallin expression may control
thyroid hormone action via the intracytoplasmic T (3) capacity.