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Public release date: 9-Jan-2013[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Small peptide ameliorates autoimmune skin blistering disease in mice
Pemphigus vulgaris is a life-threatening autoimmune skin disease that is occurs when the body's immune system generates antibodies that target proteins in the skin known as desomogleins. Desmogleins help to form the adhesive bonds that hold skin cells together and keep the skin intact. Currently, pemphigus vulgaris is treated by long-term immune suppression; however, this can leave the patient susceptible to infection. In this issue of the Journal of Clinical Investigation, researchers led by Jens Waschke at the Institute of Anatomy and Cell Biology in Munich, Germany, report on a small peptide that blocked antibody recognition of desmogleins. Importantly, the peptide could prevent antibody-mediated skin blistering when applied topically to mice. At the cellular level, the peptide improved cell-cell adhesion and attenuated signaling pathways that are activated by antibody binding. These results suggest that this peptide could serve as a treatment option for pemphigus vulgaris.
TITLE:
Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering
AUTHOR CONTACT:
Jens Waschke
Ludwig-Maximilians-University Munich, Munich, , DEU
Phone: 0049-89-5160-4811; Fax: 0049-89-5160-4802; E-mail: jens.waschke@med.uni-muenchen.de
View this article at: http://www.jci.org/articles/view/60139?key=b333192372ea9937c9be
A new treatment for kidney disease-associated heart failure?
Chronic kidney disease (CKD) patients frequently suffer from mineral bone disorder, which causes vascular calcification and, eventually, chronic heart failure. Similar to patients with CKD, mice with low levels of the protein klotho (klotho hypomorphic mice) also develop vascular calcification and have shorter life spans compared to normal mice. In this issue of the Journal of Clinical Investigation, Florian Lang and colleagues at the University of Tbingen in Germany, found that treatment with the mineralocorticoid receptor antagonist spironolactone reduced vascular calcification in klotho hypomorphic mice and increased their life span. In a companion Attending Physician article, Darryl Quarles of the University of Tennessee discusses the implications of these findings for the treatment of CKD patients.
TITLE:
Spironolactone-sensitive vascular calcification and Pit-1-dependent osteoblastic differentiation in klotho-hypomorphic mice
AUTHOR CONTACT:
Florian Lang
Dept. of Physiology, Tuebingen, NULL, DEU
Phone: +4970712972194; Fax: +497071295618; E-mail: florian.lang@uni-tuebingen.de
View this article at: http://www.jci.org/articles/view/64093?key=3010c850d2f970ad6617
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE:
Reducing cardiovascular mortality in chronic kidney disease: something borrowed, something new
AUTHOR CONTACT:
Darryl Quarles
University of Tennessee Health Science Center, memphis, TN, USA
Phone: 901-448-1459; Fax: 901-448-1188; E-mail: dquarles@uthsc.edu
View this article at: http://www.jci.org/articles/view/67203?key=054ae63743c930253936
New fusion gene contributes to glioblastoma progression
Fusion genes are common chromosomal aberrations in many cancers, and can be used as prognostic markers and drug targets in clinical practice. In this issue of the Journal of Clinical Investigation, researchers led by Matti Annala at Tampere University of Technology in Finland identified a fusion between the FGFR3 and TACC3 genes in human glioblastoma samples. The protein produced by this fusion gene promoted tumor growth and progression in a mouse model of glioblastoma, while increased expression of either of the normal genes did not alter tumor progression. Ivan Babic and Paul Mischel of the University of California, San Diego, explain in the accompanying commentary that it remains unclear how this fusion protein mediates tumorigenesis.
TITLE:
The tumorigenic fusion FGFR3-TACC3 escapes miR-99a regulation in glioblastoma
AUTHOR CONTACT:
Matti Annala
Tampere University of Technology, Tampere, FIN
Phone: +358415079885; E-mail: matti.annala@tut.fi
View this article at: http://www.jci.org/articles/view/67144?key=b644a26bcc8a516cd41d
ACCOMPANYING COMMENTARY
TITLE:
Multiple functions of a glioblastoma fusion oncogene
AUTHOR CONTACT:
Paul Mischel
UCSD, La Jolla, CA, USA
Phone: (858) 534-6080; Fax: ; E-mail: pmischel@ucsd.edu
View this article at: http://www.jci.org/articles/view/67658?key=0186fce1cd2ddde6082f
ALSO IN THIS ISSUE
TITLE:
Type 1 diabetes patients exhibit altered cerebral metabolism during hypoglycemia
AUTHOR CONTACT:
Bastiaan de Galan
Radboud University Nijmegen Medical Centre, Nijmegen, UNK, NLD
Phone: +31243618819; Fax: +31243541734; E-mail: b.degalan@aig.umcn.nl
View this article at: http://www.jci.org/articles/view/62742?key=9b86666385df6bd2593b
TITLE:
Regulation of dendritic cell activation by microRNA let-7c and BLIMP1
AUTHOR CONTACT:
Betty Diamond
The Feinstein Institute for Medical Research, Manhasset, NY, USA
Phone: 516-562-3830; Fax: 516-562-2953; E-mail: bdiamond@nshs.edu
View this article at: http://www.jci.org/articles/view/64712?key=6599e97537112226049c
TITLE:
Liver acid sphingomyelinase inhibits growth of metastatic colon cancer
AUTHOR CONTACT:
Yosuke Osawa
Gifu University Graduate School of Medicine, Gifu, JPN
Phone: 81-58-230-6217; Fax: 81-58-230-6218; E-mail: osawa-gif@umin.ac.jp
View this article at: http://www.jci.org/articles/view/65188?key=4dc45a19d2e16fb3b7c9
TITLE:
Specialized role of migratory dendritic cells in peripheral tolerance induction
AUTHOR CONTACT:
Juliana Idoyaga
The Rockefeller University, New York, NY, USA
Phone: 212-327-7863; Fax: 212-327-8875; E-mail: ijuliana@rockefeller.edu
View this article at: http://www.jci.org/articles/view/65260?key=843f605de298ce5048b3
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 9-Jan-2013[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Small peptide ameliorates autoimmune skin blistering disease in mice
Pemphigus vulgaris is a life-threatening autoimmune skin disease that is occurs when the body's immune system generates antibodies that target proteins in the skin known as desomogleins. Desmogleins help to form the adhesive bonds that hold skin cells together and keep the skin intact. Currently, pemphigus vulgaris is treated by long-term immune suppression; however, this can leave the patient susceptible to infection. In this issue of the Journal of Clinical Investigation, researchers led by Jens Waschke at the Institute of Anatomy and Cell Biology in Munich, Germany, report on a small peptide that blocked antibody recognition of desmogleins. Importantly, the peptide could prevent antibody-mediated skin blistering when applied topically to mice. At the cellular level, the peptide improved cell-cell adhesion and attenuated signaling pathways that are activated by antibody binding. These results suggest that this peptide could serve as a treatment option for pemphigus vulgaris.
TITLE:
Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering
AUTHOR CONTACT:
Jens Waschke
Ludwig-Maximilians-University Munich, Munich, , DEU
Phone: 0049-89-5160-4811; Fax: 0049-89-5160-4802; E-mail: jens.waschke@med.uni-muenchen.de
View this article at: http://www.jci.org/articles/view/60139?key=b333192372ea9937c9be
A new treatment for kidney disease-associated heart failure?
Chronic kidney disease (CKD) patients frequently suffer from mineral bone disorder, which causes vascular calcification and, eventually, chronic heart failure. Similar to patients with CKD, mice with low levels of the protein klotho (klotho hypomorphic mice) also develop vascular calcification and have shorter life spans compared to normal mice. In this issue of the Journal of Clinical Investigation, Florian Lang and colleagues at the University of Tbingen in Germany, found that treatment with the mineralocorticoid receptor antagonist spironolactone reduced vascular calcification in klotho hypomorphic mice and increased their life span. In a companion Attending Physician article, Darryl Quarles of the University of Tennessee discusses the implications of these findings for the treatment of CKD patients.
TITLE:
Spironolactone-sensitive vascular calcification and Pit-1-dependent osteoblastic differentiation in klotho-hypomorphic mice
AUTHOR CONTACT:
Florian Lang
Dept. of Physiology, Tuebingen, NULL, DEU
Phone: +4970712972194; Fax: +497071295618; E-mail: florian.lang@uni-tuebingen.de
View this article at: http://www.jci.org/articles/view/64093?key=3010c850d2f970ad6617
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE:
Reducing cardiovascular mortality in chronic kidney disease: something borrowed, something new
AUTHOR CONTACT:
Darryl Quarles
University of Tennessee Health Science Center, memphis, TN, USA
Phone: 901-448-1459; Fax: 901-448-1188; E-mail: dquarles@uthsc.edu
View this article at: http://www.jci.org/articles/view/67203?key=054ae63743c930253936
New fusion gene contributes to glioblastoma progression
Fusion genes are common chromosomal aberrations in many cancers, and can be used as prognostic markers and drug targets in clinical practice. In this issue of the Journal of Clinical Investigation, researchers led by Matti Annala at Tampere University of Technology in Finland identified a fusion between the FGFR3 and TACC3 genes in human glioblastoma samples. The protein produced by this fusion gene promoted tumor growth and progression in a mouse model of glioblastoma, while increased expression of either of the normal genes did not alter tumor progression. Ivan Babic and Paul Mischel of the University of California, San Diego, explain in the accompanying commentary that it remains unclear how this fusion protein mediates tumorigenesis.
TITLE:
The tumorigenic fusion FGFR3-TACC3 escapes miR-99a regulation in glioblastoma
AUTHOR CONTACT:
Matti Annala
Tampere University of Technology, Tampere, FIN
Phone: +358415079885; E-mail: matti.annala@tut.fi
View this article at: http://www.jci.org/articles/view/67144?key=b644a26bcc8a516cd41d
ACCOMPANYING COMMENTARY
TITLE:
Multiple functions of a glioblastoma fusion oncogene
AUTHOR CONTACT:
Paul Mischel
UCSD, La Jolla, CA, USA
Phone: (858) 534-6080; Fax: ; E-mail: pmischel@ucsd.edu
View this article at: http://www.jci.org/articles/view/67658?key=0186fce1cd2ddde6082f
ALSO IN THIS ISSUE
TITLE:
Type 1 diabetes patients exhibit altered cerebral metabolism during hypoglycemia
AUTHOR CONTACT:
Bastiaan de Galan
Radboud University Nijmegen Medical Centre, Nijmegen, UNK, NLD
Phone: +31243618819; Fax: +31243541734; E-mail: b.degalan@aig.umcn.nl
View this article at: http://www.jci.org/articles/view/62742?key=9b86666385df6bd2593b
TITLE:
Regulation of dendritic cell activation by microRNA let-7c and BLIMP1
AUTHOR CONTACT:
Betty Diamond
The Feinstein Institute for Medical Research, Manhasset, NY, USA
Phone: 516-562-3830; Fax: 516-562-2953; E-mail: bdiamond@nshs.edu
View this article at: http://www.jci.org/articles/view/64712?key=6599e97537112226049c
TITLE:
Liver acid sphingomyelinase inhibits growth of metastatic colon cancer
AUTHOR CONTACT:
Yosuke Osawa
Gifu University Graduate School of Medicine, Gifu, JPN
Phone: 81-58-230-6217; Fax: 81-58-230-6218; E-mail: osawa-gif@umin.ac.jp
View this article at: http://www.jci.org/articles/view/65188?key=4dc45a19d2e16fb3b7c9
TITLE:
Specialized role of migratory dendritic cells in peripheral tolerance induction
AUTHOR CONTACT:
Juliana Idoyaga
The Rockefeller University, New York, NY, USA
Phone: 212-327-7863; Fax: 212-327-8875; E-mail: ijuliana@rockefeller.edu
View this article at: http://www.jci.org/articles/view/65260?key=843f605de298ce5048b3
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2013-01/joci-jet010213.php
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