The BE (2)-M17 neuroblastoma cell line synthesizes and secretes corticotropin-releasing factor

Kasckow, John; Parkes, David G.; Owens, Michael J.; Stipetic, Mark; Han, Jin Hee; Nemeroff, Charles B.; Vale, Wylie

doi:10.1016/0006-8993(94)91583-0

Cited by 13 publications

(9 citation statements)

References 15 publications

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“…As pointed out in previous reports, both cells synthesize and secrete C R F under the conditions utilized. Our previous work with these two neuroblastoma cell lines has demonstrated that the CRF-LI produced by these cells behaves identically to synthetic C R F on reverse phase HPLC (19,20). It is difficult to compare levels of secretion and content of C R F in these two neuroblastoma cells to that in the NPLC-KC hepatoma cell line; the authors (18) expressed their data as pg CRF/8 h and did not mention the cell density.…”

Section: Discussionmentioning

confidence: 99%

“…Clonal cell lines have a distinct advantage over primary tissue culture in their biochemical homogeneity, and in this respect, the NPLC-KC cells are excellent systems with which to analyze the intracellular events needed for the processing of CRF. We have recently reported on two neuroblastoma cell lines which synthesize the CRF peptide following treatment with retinoic acid, specifically, the BE(Z)-C cells and BE(2)-M17 cells (19,20). We have demoiistrated that both secretion and intracellular content of C R F increase in response to forskolin in both cell lines.…”

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confidence: 95%

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Regulation of Corticotropin‐Releasing Factor Secretion and Synthesis in the Human Neuroblastoma Clones‐ BE(2)‐M17 and BE(2)‐C

Kasckow

Han

Parkes

et al. 1995

J Neuroendocrinology

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The BE(2)-M17 and BE(2)-C human neuroblastoma cell lines have been shown to synthesize and secrete corticotropin-releasing factor (CRF) following retinoic acid treatment. It has been demonstrated that CRF secretion and intracellular synthesis increases in response to forskolin treatment. In this report, we have further characterized these cells in response to protein kinase C activators, dexamethasone, interleukin-1 alpha, as well as various neurotransmitters and peptides. Nanomolar concentrations of the phorbol ester--phorbol 12 myristate 13--acetate (TPA), increased intracellular CRF content in both cell lines while increasing secretion only in the BE(2)-M17 cell. Nanomolar concentrations of dexamethasone were not able to alter basal levels of secretion and content in either cell type. However, in the BE(2)-M17 cell but not the BE(2)-C cell, the same concentrations of dexamethasone added to 30 microM forskolin augmented levels of CRF secretion and content. Likewise, the same augmented response in CRF secretion and content was seen only in the BE(2)-M17 cell line when nanomolar concentrations of dexamethasone were added to 20 nM TPA. Furthermore, only in the BE(2)-M17 cell line were micromolar levels of the biogenic amine serotonin able to increase levels of CRF secretion and content. No effects on CRF in both cell lines were demonstrable with picomolar levels of interleukin-1 alpha as well as micromolar levels of acetylcholine, norepinephrine, arginine-vasopressin, oxytocin, and angiotensin-II. The potential usefulness of these cells as models of central nervous system or placental CRF-containing neurons is discussed.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

Regulation of Corticotropin‐Releasing Factor Secretion and Synthesis in the Human Neuroblastoma Clones‐ BE(2)‐M17 and BE(2)‐C

Kasckow

Han

Parkes

et al. 1995

J Neuroendocrinology

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“…One particular RA regulated gene in the hypothalamus that may provide a link between RA and depression is corticotrophin-releasing hormone (CRH) 134 a key regulatory factor in the HPA axis 135 which may contribute to HPA axis hyperactivity in depression. 136, 137 Chen et al have described increased density of RARα expressing cells in the paraventricular nucleus (PVN) of patients with affective disorder 138 and this receptor colocalized with those neurons expressing CRH.…”

Section: 3 Biological Plausibilitymentioning

confidence: 99%

Retinoic Acid and Affective Disorders

Bremner¹,

Shearer²,

McCaffery³

2011

J. Clin. Psychiatry

171

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Objective Isotretinoin (13-cis-retinoic acid, or 13-cis-RA) (Accutane), approved by the FDA for the treatment of acne, carries a black box warning related to the risk of depression, suicide, and psychosis. Retinoic acid (RA), the active form of vitamin A, regulates gene expression in the brain, and isotretinoin is its 13-cis isomer. Retinoids represent a group of compounds derived from vitamin A that perform a large variety of functions in many systems, in particular the CNS, and abnormal retinoid levels can have neurological effects. Although infrequent, proper recognition and treatment of psychiatric side effects in acne patients is critical given the risk of death and disability. This paper reviews the evidence for a relationship between isotretinoin, depression and suicidality. Data Sources Evidence examined includes: 1) case reports; 2) temporal association between onset of depression and exposure to the drug; 3) challenge-rechallenge cases; 4) class effect (other compounds in the same class, like vitamin A, having similar neuropsychiatric effects); 5) dose response; and 6) biologically plausible mechanisms. Study Selection All papers in the literature related to isotretinoin, depression and suicide were reviewed, as well as papers related to class effect, dose response, and biological plausibility. Data Extraction Information from individual articles in the literature was extracted. Data Synthesis The literature reviewed is consistent with an association between isotretinoin administration, depression and suicide in some individuals. Conclusions The relationship between isotretinoin and depression may have implications for a greater understanding of the neurobiology of affective disorders.

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“…The activation of the PKA signaling also increases the CRH gene expression in rat fetal hypothalamic cultures (Emanuel et al 1992), or primary amygdalar cultures (Kasckow et al 1997). Moreover, cAMP activator stimulates the endogenous CRH mRNA expression and secretes CRH in culture medium in homologous BE(2)M17 (Kasckow et al 1994) and BE(2)C cell lines (Kasckow et al 1995). The gene expression of endogenous CRH is also up-regulated in the immortalized hypothalamic (Nikodemova et al 2003) and amygdalar (Mulchahey et al 1999) cell lines.…”

Section: Molecular Mechanisms Of Vasopressin and Crh Gene Transcriptionmentioning

confidence: 99%

Gene Regulation System of Vasopressin and Corticotoropin-Releasing Hormone

Yoshida

2008

Gene�Regul Syst Bio

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Abstract:The neurohypophyseal hormones, arginine vasopressin and corticotropin-releasing hormone (CRH), play a crucial role in the physiological and behavioral response to various kinds of stresses. Both neuropeptides activate the hypophysialpituitary-adrenal (HPA) axis, which is a central mediator of the stress response in the body. Conversely, they receive the negative regulation by glucocorticoid, which is an end product of the HPA axis. Vasopressin and CRH are closely linked to immune response; they also interact with pro-infl ammatory cytokines. Moreover, as for vasopressin, it has another important role, which is the regulation of water balance through its potent antidiuretic effect. Hence, it is conceivable that vasopressin and CRH mediate the homeostatic responses for survival and protect organisms from the external world. A tight and elaborate regulation system of the vasopressin and CRH gene is required for the rapid and fl exible response to the alteration of the surrounding environments. Several important regulatory elements have been identifi ed in the proximal promoter region in the vasopressin and CRH gene. Many transcription factors and intracellular signaling cascades are involved in the complicated gene regulation system. This review focuses on the current status of the basic research of vasopressin and CRH. In addition to the numerous known facts about their divergent physiological roles, the recent topics of promoter analyses will be discussed.

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The BE (2)-M17 neuroblastoma cell line synthesizes and secretes corticotropin-releasing factor

Cited by 13 publications

References 15 publications

Regulation of Corticotropin‐Releasing Factor Secretion and Synthesis in the Human Neuroblastoma Clones‐ BE(2)‐M17 and BE(2)‐C

Regulation of Corticotropin‐Releasing Factor Secretion and Synthesis in the Human Neuroblastoma Clones‐ BE(2)‐M17 and BE(2)‐C

Retinoic Acid and Affective Disorders

Gene Regulation System of Vasopressin and Corticotoropin-Releasing Hormone

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