[ Back to EurekAlert! ] Public release date: 24-Sep-2012
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Contact: Jillian Hurst
Journal of Clinical Investigation

JCI early table of contents for September 24, 2012

Small proteins in the cornea protect against bacterial infection

Exposed tissue surfaces, including skin and mucous membranes, are under constant threat of attack by microorganisms in the environment. The layer of cells that line these areas, known as epithelial cells, are the first line of defense against these pathogens, but the underlying molecular mechanisms that allow them to repel microbes are unknown. In this issue of the Journal of Clinical Investigation, researchers at the University of California, Berkeley, report that epithelial cells in the cornea, which is highly resistant to bacterial infection, express small antimicrobial peptides, portions of human cytokeratin 6A, that defend the eye against infection. Using mass spectrometry, Suzanne Fleiszig and colleagues determined that these peptides protect against multiple bacterial pathogens by preventing the bacteria from binding to the epithelial cells. Additionally, they found that mice lacking cytokeratin 6A were more susceptible to eye infections. In an accompanying commentary, Michael Zasloff of Georgetown University School of Medicine discusses the implications of these findings for the development of antimicorbial therapeutics.


Cytokeratins mediate epithelial innate defense through their antimicrobial properties


Suzanne Fleiszig

University of California at Berkeley, Berkeley, CA, USA

Phone: 510 643-0990; Fax: 510 643-5109; E-mail: fleiszig@berkeley.edu

View this article at: http://www.jci.org/articles/view/64416?key=ede08273cbaa5718b658



Defending the cornea with antibacterial fragments of keratin


Michael A. Zasloff

Georgetown University Medical Center, Washington, DC, USA

Phone: 202-687-8962; Fax: 202-687-2792; E-mail: maz5@georgetown.edu

View this article at: http://www.jci.org/articles/view/65380?key=44a31f9a7987a1f6fd5e

New insight into hyperporlactinemia-associated infertility

Hyperprolactinemia, the presence of abnormally high levels of the hormone prolactin, is a well-established cause of infertility in women in their 20s and 30s. This hormone imbalance is frequently associated with low levels of gonadotrophic-releasing hormone (GnRH), a lack of ovulation, and a decrease in menstruation; however, the molecular mechanisms by which excess prolactin causes infertility are unclear. In this issue of the Journal of Clinical Investigation, researchers led by Nadine Binart at the University of Paris report that high levels of prolactin block expression of kisspeptin, a protein hormone that induces secretion of GnRH. By administering kisspeptin, Binart and colleagues restored ovulation in mice with high levels of prolactin. In an accompanying article, Ursula Kaiser of Brigham and Women's Hospital in Boston discusses the implications of this research for the clinical treatment of infertility in patients with hyperprolactinemia.


Hyperprolactinemia-induced ovarian acyclicity is reversed by kisspeptin administration


Nadine Binart

Inserm U 693, Le Kremlin Bicetre, UNK, FRA

Phone: 331-49596701; Fax: 331-49596732; E-mail: nadine.binart@inserm.fr

View this article at: http://www.jci.org/articles/view/63937?key=280ce0bc284f919d41a1



Hyperprolactinemia and infertility: new insights


Ursula Kaiser

Brigham and Women's Hospital, Boston, MA, USA

Phone: 617-732-5768; Fax: 617-582-6193; E-mail: ukaiser@partners.org

View this article at: http://www.jci.org/articles/view/64455?key=bfeda7b4e5e1fa11a4b3

GATA transcription factors regulate pancreas development

Type 1 diabetes is caused by the autoimmune destruction of insulin-producing pancreatic β islets. Efforts to reverse the disease are focused on replacing these cells and current research is focused on identifying the factors that contribute to islet generation during embryonic development. In this issue of the Journal of Clinical Investigation two research teams led by Anabel Rojas at the Andalusian Center for Molecular Biology and Regenerative Medicine in Seville, Spain and Lori Sussel at Columbia University report that GATA4 and GATA6 transcription factors are required for development of the pancreas in mice. Mice deficient in both genes failed to develop a pancreas, exhibited hyperglycemia, and died shortly after birth, while mice deficient in only one of the genes had very minor defects. Mutations in GATA6 and GATA4 are frequently found in neonatal diabetic patients. In a companion commentary, Jorge Ferrer and colleagues at the Hospital Clinic of Barcelona, Spain discusses the transcriptional mechanisms that underlie pancreas formation and their relation to new regenerative therapies for type 1 diabetes.


GATA4 and GATA6 control mouse pancreas organogenesis


Anabel Rojas

CABIMER, Sevilla, , ESP

Phone: +34 956467427; Fax: +34 954 461 464; E-mail: anabel.rojas@cabimer.es

View this article at: http://www.jci.org/articles/view/63240?key=c8a6bd31c727e2d3b763



Pancreas-specific deletion of mouse Gata4 and Gata6 causes pancreatic agenesis


Lori Sussel

Columbia University, New York, NY, USA

Phone: 212-851-5115; E-mail: lgs2@columbia.edu

View this article at: http://www.jci.org/articles/view/63352?key=fb768d6ab25676b91c54



GATA believe it: new essential regulators of pancreas development


Jorge Ferrer

Hospital Clinic de Barcelona, Barcelona, , ESP

Phone: Tel +34 932275400 (office ext 3; Fax: +34 93 4516638; E-mail: jferrer@clinic.ub.es

View this article at: http://www.jci.org/articles/view/65751?key=af40e461737fe0703fce

MicroRNA links oncogenic signaling pathways in glioblastoma

Glioblastomas, the most prevalent primary brain tumor, frequently exhibit alterations in a number of signaling pathways that promote growth and metastasis; however, targeting of single elements has been clinically disappointing as the cancer cells simply reduce their reliance on targeted pathway. In this issue of the Journal of Clinical Investigation researchers at the Zhongshan School of Medicine in Ghuangzhou, China report on a microRNA, miR-182, that links two oncogenic signaling pathways in glioblastoma. MicroRNAs are molecules that suppress the expression of target genes. Jun Li and colleagues found that miR-182 was over-expressed in human glioblastoma patients and was correlated with the hyperactivation of two different oncogenic signaling pathways. Expression of miR-182 repressed expression of multiple negative regulators of these pathways, leading to sustained activation and enhanced malignancy. In a companion commentary, Christine Eyler of Brigham and Women's Hospital in Boston and Jeremy Rich of the Cleveland Clinic discuss the necessity of identifying multiple molecular targets within a given cancer to develop effective therapies.


TGF-β induces miR-182 to sustain NF-κB activation in glioma subsets


Jun Li

Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, , CHN

Phone: +86(20)87335828; E-mail: lijun37@mail.sysu.edu.cn

View this article at: http://www.jci.org/articles/view/62339?key=f349f446cf2044913393



Looking in the miR-ror: TGF-β–mediated activation of NF-κB in glioma


Jeremy Rich

College of Medicine at Case Western Reserve University, Cleveland, OH, USA

Phone: 216.636.0790; Fax: 216.636.5454; E-mail: richj@ccf.org

View this article at: http://www.jci.org/articles/view/66058?key=e2a0f7a4caee9492bf27


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