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This version published online on February 1, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-1600
A more recent version of this article appeared on May 1, 2005
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Submitted on August 11, 2004
Accepted on January 24, 2005

Immunoglobulin G subclasses and prolactin (PRL) isoforms in macroprolactinemia due to anti-PRL autoantibodies

NAOKI HATTORI*, KATSUJI IKEKUBO, YASUHISA NAKAYA MA, KAORI KITAGAWA, and CHIYOKO INAGAKI

Department of Pharmacology (N.H., Y.N., K.K., C.I.), Kansai Medical University, Osaka and Department of Nuclear Medicine (K.I.), Kobe City Hospital, Kobe, Japan

* To whom correspondence should be addressed. E-mail: hattorin{at}takii.kmu.ac.jp.

Although macroprolactinemia due to anti-prolactin (PRL) autoantibodies is not uncommon among hyperprolactinemic patients, the pathogenesis of such macroprolactinemia is still unknown. We examined IgG (IgG) subclasses of anti-PRL autoantibodies by enzyme immunoassay, and PRL phosphorylation and isoforms by Western blotting, mass spectrometry and two dimensional electrophoresis in 6 patients with anti-PRL autoantibodies and 29 controls. PRL specific IgG subclasses in patients with anti-PRL autoantibodies were heterogeneous but 5 of 6 patients showed IgG4 predominance, which is known to be produced by chronic antigen stimulation. Western blot and mass spectrometric analyses revealed that human pituitary PRL was phosphorylated at serine 194 and serine 163, while serine 163 in serum PRL was dephosphorylated. On two dimensional electophoresis serum PRL mainly consisted of isoform with pI 6.58 in control hyperprolactinemic patients, while acidic isoforms (pIs 6.43 and 6.29) were also observed in patients with anti-PRL autoantibodies. Our data first demonstrate that human pituitary PRL is serine phosphorylated and partially dephosphorylated in serum, and suggest that the acidic isoforms may give rise to chronic antigen stimulation in patients with anti-PRL autoantibodies.
Key words: prolactin • autoantibody • phosphorylation • macroprolactinemia




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N. Hattori, Y. Nakayama, K. Kitagawa, T. Li, and C. Inagaki
Development of Anti-PRL (Prolactin) Autoantibodies by Homologous PRL in Rats: A Model for Macroprolactinemia
Endocrinology, May 1, 2007; 148(5): 2465 - 2470.
[Abstract] [Full Text] [PDF]


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