Electron Microscopic Study of Subcapsular Cell Hyperplasia in the Adrenal Glands of IQI/Jic Mice

Kim, Jong-Soo; Kubota, Hisayo; Sakai, Toshio; Doi, Kunio; Saegusa, Junzo

doi:10.1538/expanim.54.107

Cited by 4 publications

(4 citation statements)

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“…The adrenal glands, the main peripheral source of glucocorticoids, have a remarkable tissue plasticity that allows their remodeling with age (Bland et al, 2003). SCH, one of the characteristics of adrenal tissue remodeling, is histologically distinct from tumors and dysplasia (Kim et al, 2005;Kovatch et al, 1986;Yoshida et al, 1986). We have now demonstrated that SCH is functionally different as well.…”

Section: Discussionmentioning

confidence: 72%

“…The adrenal gland is a highly plastic tissue that remodels with age (Bland et al, 2003). Development of subcapsular cell hyperplasia (SCH), a common histological change distinct from tumors and dysplasia, is known as one of the characteristics of adrenal tissue remodeling in rodents and humans (Aiba and Fujibayashi, 2011;Kim et al, 2005;Kovatch et al, 1986;Yoshida et al, 1986). In this report, we describe the unexpected effects of adrenal SCH on circulating glucocorticoid levels and anxiety-like behaviors.…”

Section: Introductionmentioning

confidence: 91%

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Modulation of Circadian Glucocorticoid Oscillation via Adrenal Opioid-CXCR7 Signaling Alters Emotional Behavior

Ikeda

Kumagai

Skach

et al. 2013

Cell

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Circulating glucocorticoid levels oscillate with a robust circadian rhythm, yet the physiological relevance of this rhythmicity remains unclear. Here, we show that modulation of circadian glucocorticoid oscillation by enhancing its amplitude leads to anxiolytic-like behavior. We observed that mice with adrenal subcapsular cell hyperplasia (SCH), a common histological change in the adrenals, are less anxious than mice without SCH. This behavioral change was found to be dependent on the higher amplitude of glucocorticoid oscillation, although the total glucocorticoid secretion is not increased in these mice. Genetic and pharmacologic experiments demonstrated that intermediate opioid peptides secreted from SCH activate CXCR7, a β-arrestin-biased G-protein-coupled receptor (GPCR), to augment circadian oscillation of glucocorticoid levels in a paracrine manner. Furthermore, recapitulating this paracrine axis by subcutaneous administration of a synthetic CXCR7 ligand is sufficient to induce anxiolytic-like behavior. Adrenocortical β-arrestin-biased GPCR signaling is a potential target for modulating circadian glucocorticoid oscillation and emotional behavior.

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Section: Discussionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 91%

Modulation of Circadian Glucocorticoid Oscillation via Adrenal Opioid-CXCR7 Signaling Alters Emotional Behavior

Ikeda

Kumagai

Skach

et al. 2013

Cell

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“…In addition, lymphocytic infiltration can occur in multiple exocrine and non-exocrine organs, such as pancreas, kidneys, and lungs [104]. As such, this strain has been used for the study of other diseases, such as dermatitis [105], colitis [106] and adrenal cell hyperplasia [107]. Of note, ANA were detected but neither anti-SSA/Ro nor anti-SSB/La autoantibodies were detected from their sera [103].…”

Section: Mouse Modelsmentioning

confidence: 99%

Mouse Models of Primary Sjogren’s Syndrome

Park¹,

Gauna²,

Cha

2015

CPD

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Sjögren’s syndrome (SjS) is a chronic autoimmune disorder characterized by immune cell infiltration and progressive injury to the salivary and lacrimal glands. As a consequence, patients with SjS develop xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes). SjS is the third most common rheumatic autoimmune disorder, affecting 4 million Americans with over 90% of patients being female. Current diagnostic criteria for SjS frequently utilize histological examinations of minor salivary glands for immune cell foci, serology for autoantibodies, and dry eye evaluation by corneal or conjunctival staining. SjS can be classified as primary or secondary SjS, depending on whether it occurs alone or in association with other systemic rheumatic conditions, respectively. Clinical manifestations typically become apparent when the disease is relatively advanced in SjS patients, which poses a challenge for early diagnosis and treatment of SjS. Therefore, SjS mouse models, because of their close resemblance to the human SjS, have been extremely valuable to identify early disease markers and to investigate underlying biological and immunological dysregulations. However, it is important to bear in mind that no single mouse model has duplicated all aspects of SjS pathogenesis and clinical features, mainly due to the multifactorial etiology of SjS that includes numerous susceptibility genes and environmental factors. As such, various mouse models have been developed in the field to try to recapitulate SjS. In this review, we focus on recent mouse models of primary SjS and describe them under three categories of spontaneous, genetically engineered, and experimentally induced development of SjS-like disease. In addition, we discuss future perspectives of SjS mouse models highlighting pros and cons of utilizing mouse models and demands for improved models.

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“…The proliferation may occur in a focal or diffuse pattern and it may progress to subcapsular tumor (Taylor 2012; Bernichtein, Peltoketo, and Huhtaniemi 2009). In IQI/Jic female mice, it has been suggested that based on their ultrastructural features (e.g., elongated mitochondria with lamellar cristae and round mitochondria with tubular cristae), hyperplastic cells in subcapsular hyperplasia might be adrenal pluripotent progenitor cells that are located in the zona glomerulosa or in the junction of the zona glomerulosa/fasciculata (Kim et al 2005). In our study, it was the most common proliferative lesion in both sexes, with a much higher incidence in females.…”

Section: Discussionmentioning

confidence: 99%

Adrenal Gland Background Findings in CD-1 (Crl:CD-1(ICR)BR) Mice from 104-week Carcinogenicity Studies

et al. 2015

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The authors performed a retrospective study to determine the incidences of spontaneous findings in the adrenal glands of control CD-1 mice. Data were collected from 2,163 mice from control dose groups in 104-week carcinogenicity studies carried out between 2000 and 2010. Adrenal gland nonproliferative lesions were more common in males than in females. In males, the most common nonproliferative lesions were cortical hypertrophy, cortical atrophy, pigment deposition/pigmentation, cysts, and extramedullary hematopoiesis. In females, the most common nonproliferative lesions were pigment deposition/pigmentation, extramedullary hematopoiesis, and cortical atrophy. Proliferative lesions were more common in females than in males. In both sexes, the most common proliferative lesions were subcapsular cell hyperplasia, focal cortical hyperplasia, and subcapsular cell tumor. Pheochromocytomas were uncommon in both sexes, with a slightly higher incidence in females, and the benign type was more frequent than the malignant type. Lymphoma was the most common metastatic tumor in both males and females, followed by histiocytic sarcoma and erythroid/myeloid leukemia. To the best knowledge of the authors, there are no recent reports on spontaneous pathological findings in the adrenal glands of CD-1 mice, and these results will facilitate the interpretation of background findings in carcinogenicity studies.

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Electron Microscopic Study of Subcapsular Cell Hyperplasia in the Adrenal Glands of IQI/Jic Mice

Abstract: Hyperplastic cells in subcapsular cell hyperplasia (SCH) lesion in adrenal glands

Cited by 4 publications

References 10 publications

Modulation of Circadian Glucocorticoid Oscillation via Adrenal Opioid-CXCR7 Signaling Alters Emotional Behavior

Modulation of Circadian Glucocorticoid Oscillation via Adrenal Opioid-CXCR7 Signaling Alters Emotional Behavior

Mouse Models of Primary Sjogren’s Syndrome

Adrenal Gland Background Findings in CD-1 (Crl:CD-1(ICR)BR) Mice from 104-week Carcinogenicity Studies

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