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Public release date: 15-Oct-2013
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Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Sound preconditioning prevents ototoxic drug-induced hearing loss in mice
The death of sensory hair cells in the ear results in irreversible hearing loss. Several classes of drugs, including aminoglycoside antibiotics and chemotherapy drugs are known to kill hair cells; however, in many cases the benefit of using the drug outweighs the potential for hearing loss. Previous research has shown that a class of proteins induced in response to cell stress, the heat shock proteins (HSPs), can protect against sensory hair cell death in response to ototoxic drugs. Despite understanding how HSPs protect the hair cells of the inner ear, there are no current therapies to induce expression of or deliver HSP directly to the inner ear. In this issue of the Journal of Clinical Investigation, Lisa Cunningham and colleagues at the National Institutes of Health developed a sound preconditioning protocol in mice that did not damage hearing, but induced HSP expression in the ear. They found that sound conditioning prior to treatment with ototoxic drugs, protected mice from drug-induced hearing loss. Furthermore, sound preconditioning resulted in increased expression of HSPs in the inner ear. Together, these data indicate that sound therapy may protect hearing in patients that require treatment with ototoxic drugs.
TITLE: Sound preconditioning therapy inhibits ototoxic hearing loss in mice
AUTHOR CONTACT: Lisa L. Cunningham
NIH/NIDCD, Rockville, MD, USA
Phone: 3014432766; E-mail: lisa.cunningham@nih.gov
View this article at: http://www.jci.org/articles/view/71353?key=a2b6f7687aa43c459a9f
Bone loss associated with increased production of ROS
Bone is constantly being broken down and remodeled. Osteoporosis results when bone resorption outpaces bone regeneration. Production of reactive oxygen species, a form of oxidative stress, has been predicted to promote bone loss, but a source of reactive oxygen is unknown. In this issue of the Journal of Clinical Investigation, Katrin Schrder and colleagues at Goethe-University identify a relationship between NADPH oxidase 4 (NOX4), an enzyme that promotes reactive oxygen species formation, and bone resorption. In a mouse model of osteoporosis, genetic disruption or drug-induced loss of NOX4 protected the mice from bone loss. Additionally, the authors identify a small nuclear polymorphism in NOX4 in human patients that associated with increased bone turnover. Together, these data suggest treatments targeting NOX4 activity may benefit osteoporosis patients.
TITLE: NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis
AUTHOR CONTACT: Katrin Schrder
Klinikum der Johann-Wolfgang-Goethe-Universitt, Frankfurt, UNK, DEU
Phone: 004969630183660; E-mail: schroeder@vrc.uni-frankfurt.de
View this article at: http://www.jci.org/articles/view/67603?key=b63670ba8b7f0b31366d
ALSO IN THIS ISSUE
TITLE: Type III TGF-β receptor promotes FGF2-mediated neuronal differentiation in neuroblastoma
AUTHOR CONTACT: Gerard C. Blobe
Duke University, Durham, NC, USA
Phone: (919) 668-1352; Fax: (919) 681-6906; E-mail: blobe001@mc.duke.edu
View this article at: http://www.jci.org/articles/view/69657?key=3c48ae0c7412e1ff480c
TITLE: Induction of myelodysplasia by myeloid-derived suppressor cells
AUTHOR CONTACT: Sheng Wei
Moffitt Cancer Center, Tampa, FL, USA
Phone: 813-745-3934; Fax: 813-745-7264; E-mail: sheng.wei@moffitt.org
View this article at: http://www.jci.org/articles/view/67580?key=e7fd55be719d248e14af
TITLE: Hirschsprung-like disease is exacerbated by reduced de novo GMP synthesis
AUTHOR CONTACT: Robert Heuckeroth
Washington University School of Medicine, St. Louis, MO, USA
Phone: 314-286-2853; Fax: 314-286-2893; E-mail: heuckeroth@kids.wustl.edu
View this article at: http://www.jci.org/articles/view/69781?key=97ac79dd1a6d6863ae84
TITLE: Allogeneic T-cell responses are regulated by a specific miRNA-mRNA network
AUTHOR CONTACT: Pavan Reddy
University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA
Phone: 734-647-5954; Fax: 734-647-9647; E-mail: reddypr@umich.edu
View this article at: http://www.jci.org/articles/view/70013?key=adfdfe15de70ef021fe7
TITLE: Chronic itch development in sensory neurons requires BRAF signaling pathways
AUTHOR CONTACT: Zhou-Feng Chen
Washington University, St. Louis, MO, USA
Phone: (314) 747-5093; E-mail: chenz@wustl.edu
View this article at: http://www.jci.org/articles/view/70528?key=99f7ee0c59d277305044
TITLE: A recurrent dominant-negative E47 mutation causes agammaglobulinemia and BCR- B-cells
AUTHOR CONTACT: Mary Ellen Conley
LeBonheur Children's Hospital, Memphis, TN, USA
Phone: 901-287-4657; Fax: 901-287-5036; E-mail: maryellen.conley@stjude.org
View this article at: http://www.jci.org/articles/view/71927?key=d30fff619706f0ada145
###
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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: 15-Oct-2013
[
|
Share]
Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Sound preconditioning prevents ototoxic drug-induced hearing loss in mice
The death of sensory hair cells in the ear results in irreversible hearing loss. Several classes of drugs, including aminoglycoside antibiotics and chemotherapy drugs are known to kill hair cells; however, in many cases the benefit of using the drug outweighs the potential for hearing loss. Previous research has shown that a class of proteins induced in response to cell stress, the heat shock proteins (HSPs), can protect against sensory hair cell death in response to ototoxic drugs. Despite understanding how HSPs protect the hair cells of the inner ear, there are no current therapies to induce expression of or deliver HSP directly to the inner ear. In this issue of the Journal of Clinical Investigation, Lisa Cunningham and colleagues at the National Institutes of Health developed a sound preconditioning protocol in mice that did not damage hearing, but induced HSP expression in the ear. They found that sound conditioning prior to treatment with ototoxic drugs, protected mice from drug-induced hearing loss. Furthermore, sound preconditioning resulted in increased expression of HSPs in the inner ear. Together, these data indicate that sound therapy may protect hearing in patients that require treatment with ototoxic drugs.
TITLE: Sound preconditioning therapy inhibits ototoxic hearing loss in mice
AUTHOR CONTACT: Lisa L. Cunningham
NIH/NIDCD, Rockville, MD, USA
Phone: 3014432766; E-mail: lisa.cunningham@nih.gov
View this article at: http://www.jci.org/articles/view/71353?key=a2b6f7687aa43c459a9f
Bone loss associated with increased production of ROS
Bone is constantly being broken down and remodeled. Osteoporosis results when bone resorption outpaces bone regeneration. Production of reactive oxygen species, a form of oxidative stress, has been predicted to promote bone loss, but a source of reactive oxygen is unknown. In this issue of the Journal of Clinical Investigation, Katrin Schrder and colleagues at Goethe-University identify a relationship between NADPH oxidase 4 (NOX4), an enzyme that promotes reactive oxygen species formation, and bone resorption. In a mouse model of osteoporosis, genetic disruption or drug-induced loss of NOX4 protected the mice from bone loss. Additionally, the authors identify a small nuclear polymorphism in NOX4 in human patients that associated with increased bone turnover. Together, these data suggest treatments targeting NOX4 activity may benefit osteoporosis patients.
TITLE: NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis
AUTHOR CONTACT: Katrin Schrder
Klinikum der Johann-Wolfgang-Goethe-Universitt, Frankfurt, UNK, DEU
Phone: 004969630183660; E-mail: schroeder@vrc.uni-frankfurt.de
View this article at: http://www.jci.org/articles/view/67603?key=b63670ba8b7f0b31366d
ALSO IN THIS ISSUE
TITLE: Type III TGF-β receptor promotes FGF2-mediated neuronal differentiation in neuroblastoma
AUTHOR CONTACT: Gerard C. Blobe
Duke University, Durham, NC, USA
Phone: (919) 668-1352; Fax: (919) 681-6906; E-mail: blobe001@mc.duke.edu
View this article at: http://www.jci.org/articles/view/69657?key=3c48ae0c7412e1ff480c
TITLE: Induction of myelodysplasia by myeloid-derived suppressor cells
AUTHOR CONTACT: Sheng Wei
Moffitt Cancer Center, Tampa, FL, USA
Phone: 813-745-3934; Fax: 813-745-7264; E-mail: sheng.wei@moffitt.org
View this article at: http://www.jci.org/articles/view/67580?key=e7fd55be719d248e14af
TITLE: Hirschsprung-like disease is exacerbated by reduced de novo GMP synthesis
AUTHOR CONTACT: Robert Heuckeroth
Washington University School of Medicine, St. Louis, MO, USA
Phone: 314-286-2853; Fax: 314-286-2893; E-mail: heuckeroth@kids.wustl.edu
View this article at: http://www.jci.org/articles/view/69781?key=97ac79dd1a6d6863ae84
TITLE: Allogeneic T-cell responses are regulated by a specific miRNA-mRNA network
AUTHOR CONTACT: Pavan Reddy
University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA
Phone: 734-647-5954; Fax: 734-647-9647; E-mail: reddypr@umich.edu
View this article at: http://www.jci.org/articles/view/70013?key=adfdfe15de70ef021fe7
TITLE: Chronic itch development in sensory neurons requires BRAF signaling pathways
AUTHOR CONTACT: Zhou-Feng Chen
Washington University, St. Louis, MO, USA
Phone: (314) 747-5093; E-mail: chenz@wustl.edu
View this article at: http://www.jci.org/articles/view/70528?key=99f7ee0c59d277305044
TITLE: A recurrent dominant-negative E47 mutation causes agammaglobulinemia and BCR- B-cells
AUTHOR CONTACT: Mary Ellen Conley
LeBonheur Children's Hospital, Memphis, TN, USA
Phone: 901-287-4657; Fax: 901-287-5036; E-mail: maryellen.conley@stjude.org
View this article at: http://www.jci.org/articles/view/71927?key=d30fff619706f0ada145
###
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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/2013-10/joci-et100813.php
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