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  1. Article ; Online: A brief review of in vitro models of diabetic neuropathy.

    Hattangady, Namita G / Rajadhyaksha, Medha S

    International journal of diabetes in developing countries

    2010  Volume 29, Issue 4, Page(s) 143–149

    Abstract: The neuropathies of the peripheral, central and autonomic nervous systems are known to be caused by hyperglycemia, a consequence of the deregulation of glucose in diabetes. Several in vivo models such as streptozotocin-induced diabetic rats, mice and ... ...

    Abstract The neuropathies of the peripheral, central and autonomic nervous systems are known to be caused by hyperglycemia, a consequence of the deregulation of glucose in diabetes. Several in vivo models such as streptozotocin-induced diabetic rats, mice and Chinese hamsters have been used to study the pathogenesis of diabetic neuropathy because of their resemblance to human pathology. However, these in vivo models have met with strong ethical oppositions. Further, the system complexity has inherent limitations of inconvenience of analyzing ephemeral molecular events and crosstalk of signal transduction pathways. Alternative in vitro models have been selected and put to effective use in diabetic studies. We critically review the use of these in vitro models such as primary cultures of dorsal root ganglia, Schwann cells and neural tissue as well as neural cell lines which have proved to be excellent systems for detailed study. We also assess the use of embryo cultures for the study of hyperglycemic effects on development, especially of the nervous system. These systems function as useful models to scrutinize the molecular events underlying hyperglycemia-induced stress in neuronal systems and have been very effectively used for the same. This comprehensive overview of advantages and disadvantages of in vitro systems that are currently in use will be of interest especially for comparative assessment of results and for appropriate choice of models for experiments in diabetic neuropathy.
    Language English
    Publishing date 2010-02-04
    Publishing country India
    Document type Journal Article
    ZDB-ID 2263351-0
    ISSN 1998-3832 ; 0973-3930
    ISSN (online) 1998-3832
    ISSN 0973-3930
    DOI 10.4103/0973-3930.57344
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Intestinal microbiota controls graft-versus-host disease independent of donor-host genetic disparity.

    Koyama, Motoko / Hippe, Daniel S / Srinivasan, Sujatha / Proll, Sean C / Miltiadous, Oriana / Li, Naisi / Zhang, Ping / Ensbey, Kathleen S / Hoffman, Noah G / Schmidt, Christine R / Yeh, Albert C / Minnie, Simone A / Strenk, Susan M / Fiedler, Tina L / Hattangady, Namita / Kowalsky, Jacob / Grady, Willian M / Degli-Esposti, Mariapia A / Varelias, Antiopi /
    Clouston, Andrew D / van den Brink, Marcel R M / Dey, Neelendu / Randolph, Timothy W / Markey, Kate A / Fredricks, David N / Hill, Geoffrey R

    Immunity

    2023  Volume 56, Issue 8, Page(s) 1876–1893.e8

    Abstract: Acute graft-versus-host disease (aGVHD) remains a major limitation of allogeneic stem cell transplantation (SCT), and severe intestinal manifestation is the major cause of early mortality. Intestinal microbiota control MHC class II (MHC-II) expression by ...

    Abstract Acute graft-versus-host disease (aGVHD) remains a major limitation of allogeneic stem cell transplantation (SCT), and severe intestinal manifestation is the major cause of early mortality. Intestinal microbiota control MHC class II (MHC-II) expression by ileal intestinal epithelial cells (IECs) that promote GVHD. Here, we demonstrated that genetically identical mice of differing vendor origins had markedly different intestinal microbiota and ileal MHC-II expression, resulting in discordant GVHD severity. We utilized cohousing and antibiotic treatment to characterize the bacterial taxa positively and negatively associated with MHC-II expression. A large proportion of bacterial MHC-II inducers were vancomycin sensitive, and peri-transplant oral vancomycin administration attenuated CD4
    MeSH term(s) Mice ; Animals ; Gastrointestinal Microbiome ; Vancomycin ; Graft vs Host Disease/etiology ; Hematopoietic Stem Cell Transplantation/adverse effects ; Hematopoietic Stem Cell Transplantation/methods ; Transplantation, Homologous/adverse effects
    Chemical Substances Vancomycin (6Q205EH1VU)
    Language English
    Publishing date 2023-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2023.06.024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4227: Show issues Location:
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  3. Article ; Online: Somatic

    Nanba, Kazutaka / Blinder, Amy R / Rege, Juilee / Hattangady, Namita G / Else, Tobias / Liu, Chia-Jen / Tomlins, Scott A / Vats, Pankaj / Kumar-Sinha, Chandan / Giordano, Thomas J / Rainey, William E

    Hypertension (Dallas, Tex. : 1979)

    2020  Volume 75, Issue 3, Page(s) 645–649

    Abstract: Driver somatic mutations for aldosterone excess have been found in ≈90% of aldosterone-producing adenomas (APAs) using an aldosterone synthase (CYP11B2)-guided sequencing approach. In the present study, we identified a novel ... ...

    Abstract Driver somatic mutations for aldosterone excess have been found in ≈90% of aldosterone-producing adenomas (APAs) using an aldosterone synthase (CYP11B2)-guided sequencing approach. In the present study, we identified a novel somatic
    MeSH term(s) Adenoma/complications ; Adenoma/genetics ; Adenoma/metabolism ; Adrenal Cortex Neoplasms/complications ; Adrenal Cortex Neoplasms/genetics ; Adrenal Cortex Neoplasms/metabolism ; Aldosterone/biosynthesis ; Angiotensin II/pharmacology ; Calcium Channels, T-Type/genetics ; Calcium Signaling ; Cell Line, Tumor ; Cytochrome P-450 CYP11B2/biosynthesis ; Cytochrome P-450 CYP11B2/genetics ; Doxycycline/pharmacology ; Enzyme Induction/drug effects ; Genetic Vectors/drug effects ; High-Throughput Nucleotide Sequencing ; Humans ; Hyperaldosteronism/etiology ; Lentivirus/genetics ; Mutation, Missense ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/genetics ; Whole Exome Sequencing
    Chemical Substances CACNA1H protein, human ; Calcium Channels, T-Type ; RNA, Messenger ; RNA, Neoplasm ; Recombinant Proteins ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2020-01-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.119.14349
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1488: Show issues Location:
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  4. Article ; Online: Acute and chronic regulation of aldosterone production.

    Hattangady, Namita G / Olala, Lawrence O / Bollag, Wendy B / Rainey, William E

    Molecular and cellular endocrinology

    2011  Volume 350, Issue 2, Page(s) 151–162

    Abstract: Aldosterone is the major mineralocorticoid synthesized by the adrenal and plays an important role in the regulation of systemic blood pressure through the absorption of sodium and water. Aldosterone production is regulated tightly by selective expression ...

    Abstract Aldosterone is the major mineralocorticoid synthesized by the adrenal and plays an important role in the regulation of systemic blood pressure through the absorption of sodium and water. Aldosterone production is regulated tightly by selective expression of aldosterone synthase (CYP11B2) in the adrenal outermost zone, the zona glomerulosa. Angiotensin II (Ang II), potassium (K(+)) and adrenocorticotropin (ACTH) are the main physiological agonists which regulate aldosterone secretion. Aldosterone production is regulated within minutes of stimulation (acutely) through increased expression and phosphorylation of the steroidogenic acute regulatory (StAR) protein and over hours to days (chronically) by increased expression of the enzymes involved in the synthesis of aldosterone, particularly CYP11B2. Imbalance in any of these processes may lead to several disorders of aldosterone excess. In this review we attempt to summarize the key molecular events involved in the acute and chronic phases of aldosterone secretion.
    MeSH term(s) Adrenocorticotropic Hormone/pharmacology ; Aldosterone/biosynthesis ; Aldosterone/chemistry ; Angiotensin II/pharmacology ; Animals ; Humans ; Hyperaldosteronism/enzymology ; Hyperaldosteronism/etiology ; Hyperaldosteronism/genetics ; Hyperaldosteronism/metabolism ; Metabolic Networks and Pathways/drug effects ; Metabolic Networks and Pathways/genetics ; Metabolic Networks and Pathways/physiology ; Models, Biological ; Potassium/pharmacology ; Steroids/biosynthesis ; Time Factors
    Chemical Substances Steroids ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Adrenocorticotropic Hormone (9002-60-2) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2011-08-04
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2011.07.034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1127: Show issues Location:
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  5. Article ; Online: Somatic mutations in adrenocortical carcinoma with primary aldosteronism or hyperreninemic hyperaldosteronism.

    Mouat, Isobel C / Omata, Kei / McDaniel, Andrew S / Hattangady, Namita G / Talapatra, Debnita / Cani, Andi K / Hovelson, Daniel H / Tomlins, Scott A / Rainey, William E / Hammer, Gary D / Giordano, Thomas J / Else, Tobias

    Endocrine-related cancer

    2018  Volume 26, Issue 2, Page(s) 217–225

    Abstract: Several somatic mutations specific to aldosterone-producing adenomas (APAs) have been described. A small proportion of adrenocortical carcinomas (ACCs) are associated with hyperaldosteronism, either primary aldosteronism or hyperreninemic ... ...

    Abstract Several somatic mutations specific to aldosterone-producing adenomas (APAs) have been described. A small proportion of adrenocortical carcinomas (ACCs) are associated with hyperaldosteronism, either primary aldosteronism or hyperreninemic hyperaldosteronism. However, it is unknown whether they harbor mutations of the same spectrum as APAs. The objective of this study is to describe the clinical phenotype and molecular genotype of ACCs with hyperaldosteronism, particularly the analysis for common APA-associated genetic changes. Patients were identified by retrospective chart review at a specialized referral center and by positive staining for CYP11B2 of tissue microarrays. Twenty-five patients with ACC and hyperaldosteronism were initially identified by retrospective chart review, and tissue for further analysis was available on 13 tumors. Seven patients were identified by positive staining for CYP11B2 in a tissue microarray, of which two were already identified in the initial chart review. Therefore, a total number of 18 patients with a diagnosis of ACC and features of either primary aldosteronism or hyperreninemic hyperaldosteronism were therefore included in the final study. Mutational status for a select list of oncogenes, tumor suppressor genes and genes known to carry mutations in APAs were analyzed by next-generation sequencing. Review of clinical data suggested autonomous aldosterone production in the majority of cases, while for some cases, hyperreninemic hyperaldosteronism was the more likely mechanism. The mutational landscape of ACCs associated with hyperaldosteronism was not different from ACCs with a different hormonal phenotype. None of the ACCs harbored mutations of known APA-associated genes, suggesting an alternative mechanism conferring aldosterone production.
    MeSH term(s) Adrenocortical Carcinoma/blood ; Adult ; Aged ; Female ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Hyperaldosteronism/etiology ; Male ; Middle Aged ; Mutation ; Retrospective Studies ; Young Adult
    Language English
    Publishing date 2018-11-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1218450-0
    ISSN 1479-6821 ; 1351-0088
    ISSN (online) 1479-6821
    ISSN 1351-0088
    DOI 10.1530/ERC-18-0385
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4192: Show issues Location:
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  6. Article: Acute and chronic regulation of aldosterone production

    Hattangady, Namita G / Olala, Lawrence O / Bollag, Wendy B / Rainey, William E

    Molecular and cellular endocrinology. 2012 Mar. 24, v. 350, no. 2

    2012  

    Abstract: Aldosterone is the major mineralocorticoid synthesized by the adrenal and plays an important role in the regulation of systemic blood pressure through the absorption of sodium and water. Aldosterone production is regulated tightly by selective expression ...

    Abstract Aldosterone is the major mineralocorticoid synthesized by the adrenal and plays an important role in the regulation of systemic blood pressure through the absorption of sodium and water. Aldosterone production is regulated tightly by selective expression of aldosterone synthase (CYP11B2) in the adrenal outermost zone, the zona glomerulosa. Angiotensin II (Ang II), potassium (K⁺) and adrenocorticotropin (ACTH) are the main physiological agonists which regulate aldosterone secretion. Aldosterone production is regulated within minutes of stimulation (acutely) through increased expression and phosphorylation of the steroidogenic acute regulatory (StAR) protein and over hours to days (chronically) by increased expression of the enzymes involved in the synthesis of aldosterone, particularly CYP11B2. Imbalance in any of these processes may lead to several disorders of aldosterone excess. In this review we attempt to summarize the key molecular events involved in the acute and chronic phases of aldosterone secretion.
    Keywords adrenal cortex ; agonists ; aldosterone ; angiotensin II ; blood pressure ; corticotropin ; enzymes ; phosphorylation ; potassium ; secretion ; sodium
    Language English
    Dates of publication 2012-0324
    Size p. 151-162.
    Publishing place Elsevier Ireland Ltd
    Document type Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2011.07.034
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  7. Article ; Online: Mutated KCNJ5 activates the acute and chronic regulatory steps in aldosterone production.

    Hattangady, Namita G / Karashima, Shigehiro / Yuan, Lucy / Ponce-Balbuena, Daniela / Jalife, José / Gomez-Sanchez, Celso E / Auchus, Richard J / Rainey, William E / Else, Tobias

    Journal of molecular endocrinology

    2016  Volume 57, Issue 1, Page(s) 1–11

    Abstract: Somatic and germline mutations in the inward-rectifying K(+) channel (KCNJ5) are a common cause of primary aldosteronism (PA) in aldosterone-producing adenoma and familial hyperaldosteronism type III, respectively. Dysregulation of adrenal cell calcium ... ...

    Abstract Somatic and germline mutations in the inward-rectifying K(+) channel (KCNJ5) are a common cause of primary aldosteronism (PA) in aldosterone-producing adenoma and familial hyperaldosteronism type III, respectively. Dysregulation of adrenal cell calcium signaling represents one mechanism for mutated KCNJ5 stimulation of aldosterone synthase (CYP11B2) expression and aldosterone production. However, the mechanisms stimulating acute and chronic production of aldosterone by mutant KCNJ5 have not been fully characterized. Herein, we defined the effects of the T158A KCNJ5 mutation (KCNJ5(T158A)) on acute and chronic regulation of aldosterone production using an adrenal cell line with a doxycycline-inducible KCNJ5(T158A) gene (HAC15-TRE-KCNJ5(T158A)). Doxycycline incubation caused a time-dependent increase in KCNJ5(T158A) and CYP11B2 mRNA and protein levels. Electrophysiological analyses confirm the loss of inward rectification and increased Na(+) permeability in KCNJ5(T158A)-expressing cells. KCNJ5(T158A) expression also led to the activation of CYP11B2 transcriptional regulators, NURR1 and ATF2. Acutely, KCNJ5(T158A) stimulated the expression of total and phosphorylated steroidogenic acute regulatory protein (StAR). KCNJ5(T158A) expression increased the synthesis of aldosterone and the hybrid steroids 18-hydroxycortisol and 18-oxocortisol, measured with liquid chromatography-tandem mass spectrometry (LC-MS/MS). All of these stimulatory effects of KCNJ5(T158A) were inhibited by the L-type Ca(2+) channel blocker, verapamil. Overall, KCNJ5(T158A)increases CYP11B2 expression and production of aldosterone, corticosterone and hybrid steroids by upregulating both acute and chronic regulatory events in aldosterone production, and verapamil blocks KCNJ5(T158A)-mediated pathways leading to aldosterone production.
    MeSH term(s) Adrenal Glands/metabolism ; Aldosterone/biosynthesis ; Calcium Channel Blockers/pharmacology ; Cell Line, Tumor ; Cytochrome P-450 CYP11B2/genetics ; Cytochrome P-450 CYP11B2/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/genetics ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/metabolism ; Gene Expression ; Gene Expression Regulation/drug effects ; Genetic Vectors/genetics ; Humans ; Mutation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Steroids/biosynthesis ; Transcription, Genetic ; Transduction, Genetic
    Chemical Substances Calcium Channel Blockers ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; KCNJ5 protein, human ; RNA, Messenger ; Steroids ; Aldosterone (4964P6T9RB) ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4)
    Language English
    Publishing date 2016-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 645012-x
    ISSN 1479-6813 ; 0952-5041
    ISSN (online) 1479-6813
    ISSN 0952-5041
    DOI 10.1530/JME-15-0324
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2406: Show issues Location:
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  8. Article ; Online: Aberrant gonadotropin-releasing hormone receptor (GnRHR) expression and its regulation of CYP11B2 expression and aldosterone production in adrenal aldosterone-producing adenoma (APA).

    Nakamura, Yasuhiro / Hattangady, Namita G / Ye, Ping / Satoh, Fumitoshi / Morimoto, Ryo / Ito-Saito, Takako / Sugawara, Akira / Ohba, Koji / Takahashi, Kazuhiro / Rainey, William E / Sasano, Hironobu

    Molecular and cellular endocrinology

    2014  Volume 384, Issue 1-2, Page(s) 102–108

    Abstract: Aberrant expression of gonadotropin-releasing hormone receptor (GnRHR) has been reported in human adrenal tissues including aldosterone-producing adenoma (APA). However, the details of its expression and functional role in adrenals are still not clear. ... ...

    Abstract Aberrant expression of gonadotropin-releasing hormone receptor (GnRHR) has been reported in human adrenal tissues including aldosterone-producing adenoma (APA). However, the details of its expression and functional role in adrenals are still not clear. In this study, quantitative RT-PCR analysis revealed the mean level of GnRHR mRNA was significantly higher in APAs than in human normal adrenal (NA) (P=0.004). GnRHR protein expression was detected in human NA and neoplastic adrenal tissues. In H295R cells transfected with GnRHR, treatment with GnRH resulted in a concentration-dependent increase in CYP11B2 reporter activity. Chronic activation of GnRHR with GnRH (100nM), in a cell line with doxycycline-inducible GnRHR (H295R-TR/GnRHR), increased CYP11B2 expression and aldosterone production. These agonistic effects were inhibited by blockers for the calcium signaling pathway, KN93 and calmidazolium. These results suggest GnRH, through heterotopic expression of its receptor, may be a potential regulator of CYP11B2 expression levels in some cases of APA.
    MeSH term(s) Adrenal Cortex/metabolism ; Adrenal Cortex/pathology ; Adrenal Gland Neoplasms/genetics ; Adrenal Gland Neoplasms/metabolism ; Adrenal Gland Neoplasms/pathology ; Adrenocortical Adenoma/genetics ; Adrenocortical Adenoma/metabolism ; Adrenocortical Adenoma/pathology ; Aldosterone/biosynthesis ; Benzylamines/pharmacology ; Calcium/metabolism ; Calcium Signaling/drug effects ; Cell Line, Tumor ; Cytochrome P-450 CYP11B2/genetics ; Cytochrome P-450 CYP11B2/metabolism ; Gene Expression Regulation, Neoplastic ; Gonadotropin-Releasing Hormone/genetics ; Gonadotropin-Releasing Hormone/metabolism ; Gonadotropin-Releasing Hormone/pharmacology ; Humans ; Imidazoles/pharmacology ; Receptors, LHRH/genetics ; Receptors, LHRH/metabolism ; Sulfonamides/pharmacology
    Chemical Substances Benzylamines ; GNRHR protein, human ; Imidazoles ; Receptors, LHRH ; Sulfonamides ; KN 93 (139298-40-1) ; Gonadotropin-Releasing Hormone (33515-09-2) ; Aldosterone (4964P6T9RB) ; calmidazolium (4R9H38JAWL) ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2014-01-25
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2014.01.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Aberrant gonadotropin-releasing hormone receptor (GnRHR) expression and its regulation of CYP11B2 expression and aldosterone production in adrenal aldosterone-producing adenoma (APA)

    Nakamura, Yasuhiro / Akira Sugawara / Fumitoshi Satoh / Hironobu Sasano / Kazuhiro Takahashi / Koji Ohba / Namita G. Hattangady / Ping Ye / Ryo Morimoto / Takako Ito-Saito / William E. Rainey

    Molecular and Cellular Endocrinology. 2014 Mar. 25, v. 384

    2014  

    Abstract: Aberrant expression of gonadotropin-releasing hormone receptor (GnRHR) has been reported in human adrenal tissues including aldosterone-producing adenoma (APA). However, the details of its expression and functional role in adrenals are still not clear. ... ...

    Abstract Aberrant expression of gonadotropin-releasing hormone receptor (GnRHR) has been reported in human adrenal tissues including aldosterone-producing adenoma (APA). However, the details of its expression and functional role in adrenals are still not clear. In this study, quantitative RT-PCR analysis revealed the mean level of GnRHR mRNA was significantly higher in APAs than in human normal adrenal (NA) (P=0.004). GnRHR protein expression was detected in human NA and neoplastic adrenal tissues. In H295R cells transfected with GnRHR, treatment with GnRH resulted in a concentration-dependent increase in CYP11B2 reporter activity. Chronic activation of GnRHR with GnRH (100nM), in a cell line with doxycycline-inducible GnRHR (H295R-TR/GnRHR), increased CYP11B2 expression and aldosterone production. These agonistic effects were inhibited by blockers for the calcium signaling pathway, KN93 and calmidazolium. These results suggest GnRH, through heterotopic expression of its receptor, may be a potential regulator of CYP11B2 expression levels in some cases of APA.
    Keywords adenoma ; aldosterone ; calcium signaling ; gonadotropin-releasing hormone ; hormone receptors ; humans ; messenger RNA ; protein synthesis ; reverse transcriptase polymerase chain reaction ; tissues
    Language English
    Dates of publication 2014-0325
    Size p. 102-108.
    Publishing place Elsevier Ireland Ltd
    Document type Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2014.01.016
    Database NAL-Catalogue (AGRICOLA)

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  10. Article ; Online: a Novel Y152C KCNJ5 mutation responsible for familial hyperaldosteronism type III.

    Monticone, Silvia / Hattangady, Namita G / Penton, David / Isales, Carlos M / Edwards, Michael A / Williams, Tracy A / Sterner, Christina / Warth, Richard / Mulatero, Paolo / Rainey, William E

    The Journal of clinical endocrinology and metabolism

    2013  Volume 98, Issue 11, Page(s) E1861–5

    Abstract: ... familial forms. Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein ...

    Abstract Context: Primary aldosteronism is a heterogeneous group of disorders comprising both sporadic and familial forms. Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III (FH-III) and are involved in the pathogenesis of sporadic aldosterone-producing adenomas.
    Objective: The objective of the study was to characterize the effects of a newly described KCNJ5 mutation in vitro.
    Patients and methods: The index case is a 62-year-old woman affected by primary aldosteronism, who underwent left adrenalectomy after workup for adrenal adenoma. Exon 1 of KCNJ5 was PCR amplified from adrenal tissue and peripheral blood and sequenced. Electrophysiological and gene expression studies were performed to establish the functional effects of the new mutation on the membrane potential and adrenal cell CYP11B2 expression.
    Results: KCNJ5 sequencing in the index case revealed a new p.Y152C germline mutation; interestingly, the phenotype of the patient was milder than most of the previously described FH-III families. The tyrosine-to-cysteine substitution resulted in pathological Na(+) permeability, cell membrane depolarization, and disturbed intracellular Ca(2+) homeostasis, effects similar, albeit smaller, to the ones demonstrated for other KCNJ5 mutations. Gene expression studies revealed an increased expression of CYP11B2 and its transcriptional regulator NR4A2 in HAC15 adrenal cells overexpressing KCNJ5(Y152C) compared to the wild-type channel. The effect was clearly Ca(2+)-dependent, because it was abolished by the calcium channel blocker nifedipine.
    Conclusions: Herein we describe a new germline mutation in KCNJ5 responsible for FH-III.
    MeSH term(s) Adenoma/genetics ; Adenoma/pathology ; Adenoma/surgery ; Adrenal Gland Neoplasms/genetics ; Adrenal Gland Neoplasms/pathology ; Adrenal Gland Neoplasms/surgery ; Adrenalectomy ; Calcium/metabolism ; Cytochrome P-450 CYP11B2/genetics ; Family Health ; Female ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/genetics ; HEK293 Cells ; Humans ; Hyperaldosteronism/genetics ; Hyperaldosteronism/pathology ; Hyperaldosteronism/surgery ; Middle Aged ; Point Mutation
    Chemical Substances G Protein-Coupled Inwardly-Rectifying Potassium Channels ; KCNJ5 protein, human ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-09-13
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/jc.2013-2428
    Database MEDical Literature Analysis and Retrieval System OnLINE

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