Autoantibodies against a novel 51 kDa islet antigen and glutamate decarboxylase isoforms in autoimmune polyendocrine syndrome type I

Velloso, Lı́cio A.; Winqvist, Ola; Gustafsson, J; K�mpe, O.; Karlsson, F. Anders

doi:10.1007/s001250050073

Cited by 8 publications

(7 citation statements)

References 22 publications

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“…This 51-kDa Ab was subsequently identified as l-amino-acid decarboxylase (55). Depletion of the GAD protein from the islet lysate did not affect the amount of 51-kDa Ab, demonstrating that the latter is unrelated to GAD (54).…”

Section: Minor Clinical Manifestationsmentioning

confidence: 96%

Autoimmune Polyglandular Syndrome Type 1

Betterle

Greggio

Volpato³

1998

The Journal of Clinical Endocrinology & Metabolism

342

231

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Section: Minor Clinical Manifestationsmentioning

confidence: 96%

Autoimmune Polyglandular Syndrome Type 1

Betterle

Greggio

Volpato³

1998

The Journal of Clinical Endocrinology & Metabolism

342

231

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“…Aliquots of the resulting supernatants containing 5.0 mg of total protein were used for immunoprecipitation with antibodies against IR, IRS-1, and IRS-2 at 4°C overnight, followed by SDS/PAGE, transfer to nitrocellulose membranes, and blotting with anti-phosphotyrosine, anti-IR, anti-IRS-1, anti-IRS-2, or anti-p85/PI3-kinase. In direct immunoblot experiments, 0.2 mg protein extract obtained from each tissue was separated by SDS-PAGE, transferred to nitrocellulose membranes, and blotted with anti-IR, -IRS-1, -IRS-2, -Akt, -ERK, -GLUT-4, -phospho-Akt, or -phospho-ERK antibodies as described [31].…”

Section: Tissue Extraction Immunoblotting and Immunoprecipitationmentioning

confidence: 99%

β3-Adrenergic-dependent and -independent mechanisms participate in cold-induced modulation of insulin signal transduction in brown adipose tissue of rats

Gasparetti

Alvarez-Rojas

Araújo

et al. 2004

Pflugers Arch - Eur J Physiol

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During cold exposure, homeothermic animals mobilize glucose with higher efficiency than at thermoneutrality. An interaction between the insulin signal transduction machinery and high sympathetic tonus is thought to play an important role in this phenomenon. In the present study, rats were exposed to cold during 8 days and treated, or not, with a beta3-adrenergic agonist, BRL37344 sodium 4-2-2-(3-chlorophenyl)-2-hydroxyethyl amino propyl phenoxy-acetic acid sodium (BRL37344), or antagonist, SR59230A 3-(2-ethylphenoxy)-[(1S)-1,2,3,4-tetrahydronaphth-1-ylamino]-(2S)-2-propanol oxalate (SR59230A), to evaluate the cross-talk between insulin and beta3-adrenergic intracellular signaling in brown adipose tissue. The drugs did not modify food ingestion, body temperature, and body weight in control and cold-exposed rats. Treatment of control rats with BRL37344 led to higher insulin-induced tyrosine phosphorylation of the insulin receptors, insulin receptor substrate (IRS)-1 and ERK, higher insulin-induced IRS-1/PI3-kinase association, and higher [Ser(473)] phosphorylation of Akt. Cold exposure alone promoted higher insulin-induced tyrosine phosphorylation of the insulin receptors, IRS-1, IRS-2, and ERK, and higher insulin-induced IRS-1 and IRS-2/PI3-kinase association. Except for the regulation of ERK, SR59230A abolished all the cold-induced effects upon the insulin signal transduction pathway. However, this antagonist only partially inhibited the cold-induced increase of glucose uptake. Thus, the sympathetic tonus generated during cold-exposure acts, in brown adipose tissue, through the beta3-adrenergic receptor and modulates insulin signal transduction, with the exception of ERK. However, insulin-independent mechanisms other than beta3-adrenergic activation participate in cold-induced glucose uptake in brown adipose tissue of rats.

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“…The major autoantigen in the adrenal cortex and gonads is P450 scc (side‐chain cleavage enzyme) [14, 15]. In the pancreatic β‐cells glutamic acid decarboxylase (GAD) [16, 17]and aromatic l ‐amino acid decarboxylase (AADC) [18]have been identified as autoantigens. AADC is an enzyme known to be involved in the biosynthesis of catecholamine and indolamine neurotransmitters [19].…”

Section: Introductionmentioning

confidence: 99%

Cytochrome P450IA2 and aromatic l‐amino acid decarboxylase are hepatic autoantigens in autoimmune polyendocrine syndrome type I

Gebre-Medhin¹,

Husebye²,

Gustafsson³

et al. 1997

FEBS Letters

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Autoimmune chronic active hepatitis (AI-CAH) is a feared component of autoimmune polyendocrine syndrome type I (APS I). In this study, immunoreactivity was assessed in sera from eight APS I patients, of whom three had AI-CAH, in an attempt to identify hepatic autoantigens. We performed indirect immunofluorescence staining of human and rat liver sections, Western blots on subcellular fractions of human and rat liver, immunoprecipitations of labelled aromatic L-amino acid decarboxylase (AADC) and cytochrome P450IA2 (CYP IA2) expressed by an in vitro transcription and translation system and studies of enzymatic activity. Autoantibodies against AADC were present in sera from all eight APS I patients, while immunoreactivity against CYP IA2 was only found in sera from the three APS I patients with AI-CAH. Enzymatic activity of CYP IA2 was inhibited by sera from APS I patients with AI-CAH but not by control sera. Our results show that CYP IA2 and AADC constitute hepatic autoantigens in patients with APS I and that immunoreactivity against CYP IA2 is associated with the presence of AI-CAH.

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Autoantibodies against a novel 51 kDa islet antigen and glutamate decarboxylase isoforms in autoimmune polyendocrine syndrome type I

Cited by 8 publications

References 22 publications

Autoimmune Polyglandular Syndrome Type 1

Autoimmune Polyglandular Syndrome Type 1

β3-Adrenergic-dependent and -independent mechanisms participate in cold-induced modulation of insulin signal transduction in brown adipose tissue of rats

Cytochrome P450IA2 and aromatic l‐amino acid decarboxylase are hepatic autoantigens in autoimmune polyendocrine syndrome type I

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