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Molecular and Cellular Endocrinology
(MOL CELL ENDOCRINOL ) 《分子与细胞内分泌学 》

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分子与细胞内分泌学
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"Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.

The journal is fulfilling this aim by publishing full-length original research papers, rapid papers, invited reviews, At the Cutting Edge essays, and book reviews."
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Published 2012年11月,Volume 364,Issue 1-2

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The molecular mechanisms of pancreatic β-cell glucotoxicity: Recent findings and future research directions

 Review Article
Pages 1-27
Mohammed Bensellam, D. Ross Laybutt, Jean-Christophe Jonas
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Highlights

► Hyperglycemia exert “toxic” effects on the β-cell phenotype in type 2 diabetes. ► β-Cell “glucotoxicity” involves complex cellular and molecular mechanisms. ► ROS, UPR and loss of differentiation play major roles in β-cell glucotoxicity. ► There is an emerging role of AGEs and hypoxia in β-cell glucotoxicity. ► Manipulation of these mechanisms is protective in vitro and in animal models.
Regular Papers
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C/EBPα promotes transcription of the porcine perilipin5 gene

 Original Research Article
Pages 28-35
Lei Zhou, Lijie Zhang, Qingjie Meng, Congcong Niu, Dan Jin, An Yu, Li Gan, Zaiqing Yang
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Highlights

► C/EBPα is a crucial regulatory factor for plin5 transcription. ► C/EBPα binds to the promoter of plin5 within the −302 to −284 bp region. ► C/EBPα promotes expression of endogenous plin5. ► C/EBPα may be involved in transcriptional regulation of plin5 during fasting.
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Reduced insulin secretion correlates with decreased expression of exocytotic genes in pancreatic islets from patients with type 2 diabetes

 Original Research Article
Pages 36-45
Sofia A. Andersson, Anders H. Olsson, Jonathan L.S. Esguerra, Emilia Heimann, Claes Ladenvall, Anna Edlund, Albert Salehi, Jalal Taneera, Eva Degerman, Leif Groop, Charlotte Ling, Lena Eliasson
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Highlights

► Expression of STX1ASYT4SYT7SYT11 and SYT13 is reduced in islets from human T2D donors. ► Expression of STX1ASYT4,SYT7SYT11SYT13SNAP25 and STXBP1 correlates positively with GSIS. ► Expression of STX1ASYT4SYT7SYT11SYT13,SNAP25 and STXBP1 correlates negatively to HbA1c. ► Reduced expression of exocytotic genes contribute to impaired insulin secretion.
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GLP-2 receptors in human disease: High expression in gastrointestinal stromal tumors and Crohn’s disease

 Original Research Article
Pages 46-53
Meike Körner, Ruth Rehmann, Jean Claude Reubi
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Highlights

► GLP-2 has been linked to carcinogenesis. ► The GLP-2 analogue teduglutide reduces inflammation in Crohn’s disease patients. ► We found GLP-2 receptors in GIST tumor cells and in myenteric nerves in Crohn. ► GLP-2 receptors in GIST may be in vivo targets for radioactive GLP-2 analogs. ► The myenteric GLP-2 receptors may be teduglutide targets in Crohn’s disease.
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Regulation of CYP3A4 and CYP3A5 expression and modulation of “intracrine” metabolism of androgens in prostate cells by liganded vitamin D receptor

 Original Research Article
Pages 54-64
Orla Maguire, Catherine Pollock, Philip Martin, Andrew Owen, Thomas Smyth, Declan Doherty, Moray J. Campbell, Stephen McClean, Paul Thompson
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Highlights

► The vitamin D hormone enhances CYP3A4 and CYP3A5 expression within prostate cells. ► Vitamin D regulation of CYP3A4 andCYP3A5 was directly mediated through VDR. ► Vitamin D treatment increased CYP3A enzyme activity with LNCaP cells. ► Elevated CYP3A function increased the intracellular inactivation of testosterone.
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β-Arrestin1-mediated recruitment of c-Src underlies the proliferative action of glucagon-like peptide-1 in pancreatic β INS832/13 cells

 Original Research Article
Pages 65-70
Jason Talbot, Erik Joly, Marc Prentki, Jean Buteau
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Highlights

► GLP-1 enhances c-Src activity. ► GLP-1 triggers the formation of a signaling complex comprising β-arrestin1 and c-Src. ► β-Arrestin1 and c-Src mediates the action of GLP-1 on β-cell proliferation.
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Normal testicular function without detectable follicle-stimulating hormone. A novel mutation in the follicle-stimulating hormone receptor gene leading to apparent constitutive activity and impaired agonist-induced desensitization and internalization

 Original Research Article
Pages 71-82
Patricia Casas-González, Hugo E. Scaglia, Marco A. Pérez-Solís, Guillaume Durand, Javier Scaglia, Teresa Zariñán, James A. Dias, Eric Reiter, Alfredo Ulloa-Aguirre
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Highlights

► We report a novel mutation in the follicle-stimulating hormone receptor. ► The N431I mutation in the FSHR leads to constitutive activation. ► The N431I mutation in the FSHR leads to impaired desensitization. ► The N431I mutation in the FSHR leads to impaired internalization. ► The mutation (N431I) was detected in an asyntomatic man with normal spermatogenesis.
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Estrogen and telomerase in human peripheral blood mononuclear cells

 Original Research Article
Pages 83-88
Ann L. Benko, Nancy J. Olsen, William J. Kovacs
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Highlights

► We evaluated a postulated role for estrogens in regulation of telomerase in T lymphocytes. ► T cells from females showed slightly greater telomerase induction with T cell receptor engagement. ► Estradiol did not directly change telomerase activity in resting or activated T cells. ► Our experiments exclude a direct effect of estradiol on telomerase induction in peripheral T cells.
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Experimental and computational study of inter- and intra- species specificity of gonadotropins for various gonadotropin receptors

 Original Research Article
Pages 89-100
Joseph Aizen, Noga Kowalsman, Makito Kobayashi, Lian Hollander, Young Chang Sohn, Goro Yoshizaki, Masha Y. Niv, Berta Levavi-Sivan
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Highlights

► The article presents molecular modeling of GTHs and GTHRs of tilapia, trout and eel. ► Each of the gonadotropins of eel, trout tilapia and human activated its own cognate receptors. ► Tilapia LHR was activated by hCG and eel LHR was activated by hFSH, hCG, and trout FSH. ► For FSHR, the only cross-reactivity detected was for hFSHR, which was activated by pFSH and bFSH.
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Efficacy of the novel dual PI3-kinase/mTOR inhibitor NVP-BEZ235 in a preclinical model of adrenocortical carcinoma

 Original Research Article
Pages 101-104
Mabrouka Doghman, Enzo Lalli
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Highlights

► Current therapies for advanced adrenocortical cancer are insufficient. ► The dual PI3K/mTOR inhibitor NVP-BEZ235 efficiently inhibits ACC cell proliferation. ► Concomitant inhibition of Erk may be required to potentiate the NVP-BEZ235 effect.
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AU-rich elements in the 3′-UTR regulate the stability of the 141 amino acid isoform of parathyroid hormone-related protein mRNA

 Original Research Article
Pages 105-112
Alexander I. Luchin, Murali V.P. Nadella, Nanda K. Thudi, Wessel P. Dirksen, Parul Gulati, Soledad A. Fernandez, Thomas J. Rosol
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Highlights

► The instability of PTHrP 1-141 mRNA is determined by four AREs in its 3′-UTR. ► Effects of these AREs are potentially mediated by the tristetraproline (TTP) ARE-binding protein. ► Additional proteins (60–80 kDa) bind specifically to the AREs in HARA cell extracts.
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Cortisol regulates Na+ uptake in zebrafish, Danio rerio, larvae via the glucocorticoid receptor

Original Research Article
Pages 113-125
Yusuke Kumai, Dinushan Nesan, Mathilakath M. Vijayan, Steve F. Perry
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Highlights

► Cortisol stimulates Na+ uptake and ammonia excretion in zebrafish larvae through glucocorticoid receptor. ► The stimulation of Na+ uptake in larvae during acid-exposure is at least partially mediated by increased cortisol level. ► Cortisol stimulates Na+ uptake by stimulating the recently proposed NHE3b–Rhcg1 functional metabolon. ► Glucocorticoid receptor is highly expressed in ionocytes responsible for Na+ uptake.
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Estrogens promote cell–cell adhesion of normal and malignant mammary cells through increased desmosome formation

 Original Research Article
Pages 126-133
Marie Maynadier, Monique Chambon, Ilaria Basile, Michel Gleizes, Philippe Nirde, Magali Gary-Bobo, Marcel Garcia
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Highlights

► We proved that estrogens increase cell–cell adhesion in breast cancer cell lines. ► Estrogen increases desmosomes number in normal and breast cancer cells. ► Expression of several desmosomal proteins is increased by estrogen treatment. ► Silencing of the estrogen receptor α expression prevents cell–cell adhesion. ► Silencing of a key desmosomal protein impairs estrogen-induced adhesion.
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