Novel presence of luteinizing hormone/chorionic gonadotropin receptors in human adrenal glands.

Pabon, Jonathan; Li, X; Lei, Zhenmin; Sanfilippo, Joseph S.; Yussman, Marvin A.; Rao, C V

doi:10.1210/jcem.81.6.8964884

Cited by 73 publications

(41 citation statements)

References 20 publications

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“…Because androgens are secreted by the ovaries and the adrenals, and LH receptors have been identified in the zona reticularis and the deeper layer of the zona fasciculate of adrenal glands (48), it is possible that the lower LH levels induced by E 2 therapy reduced the production of T from both the ovary and the adrenals.…”

Section: Figurementioning

confidence: 99%

Testosterone deficiency in young women with 46,XX spontaneous premature ovarian failure

Kalantaridou

Calis

Vanderhoof

et al. 2006

Fertility and Sterility

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Section: Figurementioning

confidence: 99%

Testosterone deficiency in young women with 46,XX spontaneous premature ovarian failure

Kalantaridou

Calis

Vanderhoof

et al. 2006

Fertility and Sterility

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“…The LHCGR is normally expressed mainly in the gonads; low levels of expression have been detected in the adrenal zona reticularis [16]. Adrenal LHCGR overexpression was documented in two female patients with AIMAH and LH-responsive CS; curiously, their symptoms were not associated with pregnancy [15].…”

Section: Discussionmentioning

confidence: 94%

Case Report: Adrenal LH/hCG Receptor Overexpression and Gene Amplification Causing Pregnancy-Induced Cushing’s Syndrome

et al. 2009

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Transient pregnancy-induced Cushing's syndrome (CS) is extremely rare, with only several cases reported in the literature. Ectopic LH/hCG-receptors (LHCGR) in the adrenal gland have been suggested to be involved in the pathogenesis of this condition. We report the clinical, molecular, and genetic features of a patient with pregnancy-induced CS. A 29-year-old female patient developed CS during multiple pregnancies, leading to repeated miscarriage. Signs and symptoms of hypercortisolism resolved soon after delivery or abortion, only to recur in subsequent pregnancies. In the non-pregnant state, hCG stimulation testing resulted in elevated cortisol levels. Serum cortisol was not suppressible with dexamethasone. The adrenals exhibited bilateral adrenal cortical nodular hyperplasia. Quantitative RT-PCR revealed a 2-fold increase in LHCGR and progesterone receptor mRNA expression and decreased estrogen receptor-beta expression in the patient's adrenal tissue relative to normal adrenals. Higher intensity of immunostaining for LHCGR was observed, particularly within the nodular lesions, compared to controls. Quantitative PCR revealed a LHCGR-to-beta-actin ratio of 1.5 in genomic DNA from adrenal and peripheral leukocytes, suggesting the presence of a germline duplication of the LHCGR gene. LHCGR overexpression resulting from germline gene duplication may be a potential pathogenic mechanism underlying this case of pregnancy-induced CS.

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“…Both LHR and GnRHR can be expressed in normal adrenal tissue [5,41] , but only fetal adrenal cells secreted dehydroepiandrosterone sulphate (DHEAS) following addition of LH / hCG [45,46] . Studies involving mRNA and protein expressions have shown that in certain cases of hyperaldosteronism, LHR and / or GnRHR are markedly overexpressed [5, 39 -41] ( Table 2 ).…”

Section: Overexpression and Functionality Of Lh And Gnrh Receptors Inmentioning

confidence: 99%

Aberrant Hormone Receptors in Primary Aldosteronism

Mazzuco

Grunenwald²,

Lampron³

et al. 2010

Horm Metab Res

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The mechanisms involved in the renin-independent regulation of aldosterone secretion in primary aldosteronism are poorly understood. In ACTH-independent Cushing's syndrome, cortisol secretion can be regulated by the aberrant expression of G-protein coupled receptors (GPCRs) in unilateral tumors and bilateral macronodular adrenal hyperplasia. By analogy, some recent studies identified overexpression or function of several GPCR as a potential cause for excess aldosterone production in some aldosteronomas and in bilateral idiopathic hyperaldosteronism. Initial studies have used in vitro techniques, while the clinical aldosterone responses were not assessed. More recently, several receptors have been shown to be expressed in aldosterone-producing adrenal tumors in vitro and to regulate aberrantly renin-independent aldosterone secretion in vivo. The prevalence of aberrant hormone receptors in primary aldosteronism could be elevated, but larger systematic studies are required to establish its true frequency. The identification of aberrant adrenal GPCRs by in vivo functional studies offers the potential for novel pharmacological therapies that either suppress the endogenous ligands or block the receptor with specific antagonists.

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Novel presence of luteinizing hormone/chorionic gonadotropin receptors in human adrenal glands.

Cited by 73 publications

References 20 publications

Testosterone deficiency in young women with 46,XX spontaneous premature ovarian failure

Testosterone deficiency in young women with 46,XX spontaneous premature ovarian failure

Case Report: Adrenal LH/hCG Receptor Overexpression and Gene Amplification Causing Pregnancy-Induced Cushing’s Syndrome

Aberrant Hormone Receptors in Primary Aldosteronism

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