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Public release date: 22-Feb-2013[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
How to mend a broken heart: advances in parthenogenic stem cells
Parthenogenesis is a form of asexual reproduction during which unfertilized eggs begin to develop as if they had been fertilized. It occurs naturally in many plants and a few invertebrate (some bees, scorpions, parasitic wasps) and vertebrate animals (some fish, reptiles, and amphibians), but does not occur naturally in mammals. In 2007, researchers were able to chemically induce human egg cells to undergo parthenogenesis. The resulting parthenogenote has properties similar to an embryo, but cannot develop further. In this issue of the Journal of Clinical Investigation, Wolfram Zimmerman and colleagues at Georg-August-Universitt Gttingen in Gttingen, Germany, demonstrated that cells from the parthenogenote function as embryonic stem cells and maintain the capacity to develop into different types of tissue. Further, they used parthenogenic stem cells to make cardiomyocytes and engineered heart muscle (myocardium) that exhibited the structural and functional properties of normal myocardium. The engineered myocardium could then be used to engraft the mice that had contributed the eggs for parthenogenesis. These studies demonstrate that parthenogenic stem cells can be used for tissue engineering. In a companion commentary, Michael Schneider of the Imperial College of London discusses how these findings could impact the development of cell replacement therapies.
TITLE:
Parthenogenetic stem cells for tissue engineered heart repair
AUTHOR CONTACT:
Wolfram Zimmermann
Georg-August-Universitt Gttingen, Gttingen, DEU
Phone: +49 (0) 551 39-57 81; E-mail: w.zimmermann@med.uni-goettingen.de
View this article at: http://www.jci.org/articles/view/66854?key=31d6143cd2894a5b80d5
ACCOMPANYING COMMENTARY
TITLE:
Virgin birth: engineered heart muscle from parthenogenic stem cells
AUTHOR CONTACT:
Michael D. Schneider
Imperial College London, London, UNK, GBR
Phone: 011 44 20 7594 3027; Fax: 011 44 20 7594 3190; E-mail: m.d.schneider@imperial.ac.uk
View this article at: http://www.jci.org/articles/view/67961?key=a07301e0e8f34e261854
Pulmonary fibrosis: between a ROCK and a hard place
Pulmonary fibrosis is a scarring or thickening of the lungs that causes shortness of breath, a dry cough, fatigue, chest discomfort, weight loss, a decrease in the ability of the lungs to transmit oxygen to the blood stream, and, eventually, heart failure. Cells known as myofibroblasts normally secrete materials that are required for wound healing; once the wound has closed, the cells disappear. In pulmonary fibrosis, the myofibroblasts stick around, continuing to secrete wound healing factors that cause fibrosis in the lungs. In this issue of the Journal of Clinical Investigation, Yong Zhou and colleagues at the University of Alabama at Birmingham identified a mechanosensitive cellular signaling pathway in myofibroblasts that is activated by the hardening of tissue that has become fibrotic. Activation of this pathway promotes myofibroblast survival and prevents the normal disappearance of these cells after completion of wound healing. The pathway is dependent on a protein known as ROCK. Zhou and colleagues found that a drug that inhibits ROCK, fasudil, attenuates the pro-survival pathway and causes myofibroblasts to die. Further, fasudil treatment protected mice from injury-induced lung fibrosis. These studies suggest that ROCK inhibitors could be used to treat pulmonary fibrosis. In a companion Attending Physician article, Dean Sheppard of the University of California, San Francisco, discusses the feasibility of using ROCK inhibitors in a clinical setting.
TITLE:
Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis
AUTHOR CONTACT:
Yong Zhou
University of Alabama at Birmingham, Birmingham, AL, USA
Phone: 2059752216; E-mail: yzhou@uab.edu
View this article at: http://www.jci.org/articles/view/66700?key=1e6504f3d5e43afe19fb
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE:
ROCKing pulmonary fibrosis
AUTHOR CONTACT:
Dean Sheppard
UCSF, San Francisco, CA, USA
Phone: 415-514-4269; Fax: 415-514-4278; E-mail: dean.sheppard@ucsf.edu
View this article at: http://www.jci.org/articles/view/68417?key=3482e828788968b30192
Epigenetic alterations reprogram pancreatic cells to secrete insulin
Epigenetic modification is a change to gene expression or cellular phenotype that is caused by alterations that don't involve the underlying DNA sequence. Because all cells in your body contain the exact same genes, these epigenetic changes help determine which genes different cells express, allowing them to develop specialized functions. The pancreas consists of insulin-secreting beta cells and glucagon-secreting alpha cells. Insulin serves as a signal for cells in the body to take up glucose, while glucagon opposes this effect; malfunction of these cells leads to the development of diabetes. In this issue of the Journal of Clinical Investigation, Klaus Kaestner and colleagues at the University of Pennsylvania identified epigenetic modifications that distinguish pancreatic beta cells from alpha cells. Additionally, Kaestner and colleagues found that they could reprogram alpha cells to function as beta cells by mimicking the epigenetic modifications found in beta cells through treatment with a drug known as a histone methyltransferase inhibitor. These studies suggest that epigenetic manipulation could be used to generate replacement cells for diseases such as diabetes, in which patients lack functional beta cells. In a companion commentary, Larry Moss of Duke University discusses how these cells might serve as an important resource in both research and therapeutic development.
TITLE:
Epigenomic plasticity enables human pancreatic ?- to ?-cell reprogramming
AUTHOR CONTACT:
Klaus Kaestner
University of Pennsylvania, Perelman School of Medicine, Philadeplhia, PA, USA
Phone: 215.898.8759; Fax: 215.573.5892; E-mail: kaestner@mail.med.upenn.edu
View this article at: http://www.jci.org/articles/view/66514?key=e4b199f5a3826369a938
ACCOMPANYING COMMENTARY
TITLE:
Creating new beta cells: Cellular transmutation by genomic alchemy
AUTHOR CONTACT:
Larry G. Moss
Duke University Medical Center, Durham, NC, USA
Phone: 617-479-2310; E-mail: larry.moss@duke.edu
View this article at: http://www.jci.org/articles/view/68348?key=11aa06302a250850c4ef
Brain "clean-up crew" captured by MRI
All parts of the body generate waste that must be flushed out in order to remove harmful materials, old proteins, and other cellular detritus. Most tissues utilize the lymphatic system to keep clean, but the central nervous system (CNS) does not have lymphatic vasculature and relies instead on a waste clearance pathway known as the glymphatic system. The glymphatic system cleans the cerebrospinal fluid (CSF) that surround the brain and spinal cord and relies on specialized CNS support cells known as glia. In this issue of the Journal of Clinical Investigation, researchers led by Helene Benveniste at Stony Brook University used MRI to visualize the glymphatic system in rats that had been given a fluorescent tracer. The whole brain images allowed Benveniste and colleagues to identify two key influx nodes in the brain. Additionally, they could measure the rate at which the fluorescent tracer was removed by the glymphatic system. Currently, amyloid plaques and other molecules that accumulate in diseases such as Alzheimer's and Huntington's disease cannot be visualized in live patients. In a companion commentary, Warren Strittmatter of Duke University discusses how this new technology could be used to track the development or progression of diseases in which the clearance of specific proteins is impaired.
TITLE:
Brain-wide pathway for waste clearance captured by contrast enhanced MRI
AUTHOR CONTACT:
Helene Benveniste
Stony Brook University Medical Center, Stony Brook, NY, USA
Phone: 631-624-7018; Fax: 631-444-2907; E-mail: helene.benveniste@stonybrookmedicine.edu
View this article at: http://www.jci.org/articles/view/67677?key=e3d4b4a78599273ea579
ACCOMPANYING COMMENTARY
TITLE:
Bathing the brain
AUTHOR CONTACT:
Warren James Strittmatter
Duke University Medical Center, Durham, NC, USA
Phone: 919-684-0053; Fax: 919-681-7198; E-mail: warren@neuro.duke.edu
View this article at: http://www.jci.org/articles/view/68241?key=808d2caf308ec46730fb
ALSO IN THIS ISSUE
Smap1 deficiency perturbs receptor trafficking and predisposes mice to myelodysplasia
HDAC4 controls histone methylation in response to elevated cardiac load
Sprouty2, PTEN and PP2A interact to regulate prostate cancer progression
Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility | Back to top
TITLE:
Smap1 deficiency perturbs receptor trafficking and predisposes mice to myelodysplasia
AUTHOR CONTACT:
Masanobu Satake
Institute of Development, Aging and Cancer, Tohoku University, Sendai, UNK, JPN
Phone: (81)22-717-8477; E-mail: satake@idac.tohoku.ac.jp
View this article at: http://www.jci.org/articles/view/63711?key=81fb94bf3f59a4902e5b
TITLE:
HDAC4 controls histone methylation in response to elevated cardiac load
AUTHOR CONTACT:
Christoph Maack
Universittsklinikum des Saarlandes, Homburg, DEU
Phone: +49-6841-1623000; Fax: +49-6841-1623434; E-mail: christoph.maack@uks.eu
View this article at: http://www.jci.org/articles/view/61084?key=3b2f824d313bb1325d7a
TITLE:
Sprouty2, PTEN and PP2A interact to regulate prostate cancer progression
AUTHOR CONTACT:
Hing Leung
The Beatson Institute for Cancer Research, Glasgow, , GBR
Phone: 441413303658; E-mail: h.leung@beatson.gla.ac.uk
View this article at: http://www.jci.org/articles/view/63672?key=c51d70b1b0cef75eae44
TITLE:
Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility
AUTHOR CONTACT:
Tsang-Chih Kuo
Graduate Institute of Toxicology, College of Medicine, National Taiwan Univ, Taipei, TWN
Phone: 886-2-23123456#88649; E-mail: f95447013@ntu.edu.tw
View this article at: http://www.jci.org/articles/view/64044?key=48ac6b9d93d7fc1ccb38
###
[ | 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: 22-Feb-2013[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
How to mend a broken heart: advances in parthenogenic stem cells
Parthenogenesis is a form of asexual reproduction during which unfertilized eggs begin to develop as if they had been fertilized. It occurs naturally in many plants and a few invertebrate (some bees, scorpions, parasitic wasps) and vertebrate animals (some fish, reptiles, and amphibians), but does not occur naturally in mammals. In 2007, researchers were able to chemically induce human egg cells to undergo parthenogenesis. The resulting parthenogenote has properties similar to an embryo, but cannot develop further. In this issue of the Journal of Clinical Investigation, Wolfram Zimmerman and colleagues at Georg-August-Universitt Gttingen in Gttingen, Germany, demonstrated that cells from the parthenogenote function as embryonic stem cells and maintain the capacity to develop into different types of tissue. Further, they used parthenogenic stem cells to make cardiomyocytes and engineered heart muscle (myocardium) that exhibited the structural and functional properties of normal myocardium. The engineered myocardium could then be used to engraft the mice that had contributed the eggs for parthenogenesis. These studies demonstrate that parthenogenic stem cells can be used for tissue engineering. In a companion commentary, Michael Schneider of the Imperial College of London discusses how these findings could impact the development of cell replacement therapies.
TITLE:
Parthenogenetic stem cells for tissue engineered heart repair
AUTHOR CONTACT:
Wolfram Zimmermann
Georg-August-Universitt Gttingen, Gttingen, DEU
Phone: +49 (0) 551 39-57 81; E-mail: w.zimmermann@med.uni-goettingen.de
View this article at: http://www.jci.org/articles/view/66854?key=31d6143cd2894a5b80d5
ACCOMPANYING COMMENTARY
TITLE:
Virgin birth: engineered heart muscle from parthenogenic stem cells
AUTHOR CONTACT:
Michael D. Schneider
Imperial College London, London, UNK, GBR
Phone: 011 44 20 7594 3027; Fax: 011 44 20 7594 3190; E-mail: m.d.schneider@imperial.ac.uk
View this article at: http://www.jci.org/articles/view/67961?key=a07301e0e8f34e261854
Pulmonary fibrosis: between a ROCK and a hard place
Pulmonary fibrosis is a scarring or thickening of the lungs that causes shortness of breath, a dry cough, fatigue, chest discomfort, weight loss, a decrease in the ability of the lungs to transmit oxygen to the blood stream, and, eventually, heart failure. Cells known as myofibroblasts normally secrete materials that are required for wound healing; once the wound has closed, the cells disappear. In pulmonary fibrosis, the myofibroblasts stick around, continuing to secrete wound healing factors that cause fibrosis in the lungs. In this issue of the Journal of Clinical Investigation, Yong Zhou and colleagues at the University of Alabama at Birmingham identified a mechanosensitive cellular signaling pathway in myofibroblasts that is activated by the hardening of tissue that has become fibrotic. Activation of this pathway promotes myofibroblast survival and prevents the normal disappearance of these cells after completion of wound healing. The pathway is dependent on a protein known as ROCK. Zhou and colleagues found that a drug that inhibits ROCK, fasudil, attenuates the pro-survival pathway and causes myofibroblasts to die. Further, fasudil treatment protected mice from injury-induced lung fibrosis. These studies suggest that ROCK inhibitors could be used to treat pulmonary fibrosis. In a companion Attending Physician article, Dean Sheppard of the University of California, San Francisco, discusses the feasibility of using ROCK inhibitors in a clinical setting.
TITLE:
Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis
AUTHOR CONTACT:
Yong Zhou
University of Alabama at Birmingham, Birmingham, AL, USA
Phone: 2059752216; E-mail: yzhou@uab.edu
View this article at: http://www.jci.org/articles/view/66700?key=1e6504f3d5e43afe19fb
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE:
ROCKing pulmonary fibrosis
AUTHOR CONTACT:
Dean Sheppard
UCSF, San Francisco, CA, USA
Phone: 415-514-4269; Fax: 415-514-4278; E-mail: dean.sheppard@ucsf.edu
View this article at: http://www.jci.org/articles/view/68417?key=3482e828788968b30192
Epigenetic alterations reprogram pancreatic cells to secrete insulin
Epigenetic modification is a change to gene expression or cellular phenotype that is caused by alterations that don't involve the underlying DNA sequence. Because all cells in your body contain the exact same genes, these epigenetic changes help determine which genes different cells express, allowing them to develop specialized functions. The pancreas consists of insulin-secreting beta cells and glucagon-secreting alpha cells. Insulin serves as a signal for cells in the body to take up glucose, while glucagon opposes this effect; malfunction of these cells leads to the development of diabetes. In this issue of the Journal of Clinical Investigation, Klaus Kaestner and colleagues at the University of Pennsylvania identified epigenetic modifications that distinguish pancreatic beta cells from alpha cells. Additionally, Kaestner and colleagues found that they could reprogram alpha cells to function as beta cells by mimicking the epigenetic modifications found in beta cells through treatment with a drug known as a histone methyltransferase inhibitor. These studies suggest that epigenetic manipulation could be used to generate replacement cells for diseases such as diabetes, in which patients lack functional beta cells. In a companion commentary, Larry Moss of Duke University discusses how these cells might serve as an important resource in both research and therapeutic development.
TITLE:
Epigenomic plasticity enables human pancreatic ?- to ?-cell reprogramming
AUTHOR CONTACT:
Klaus Kaestner
University of Pennsylvania, Perelman School of Medicine, Philadeplhia, PA, USA
Phone: 215.898.8759; Fax: 215.573.5892; E-mail: kaestner@mail.med.upenn.edu
View this article at: http://www.jci.org/articles/view/66514?key=e4b199f5a3826369a938
ACCOMPANYING COMMENTARY
TITLE:
Creating new beta cells: Cellular transmutation by genomic alchemy
AUTHOR CONTACT:
Larry G. Moss
Duke University Medical Center, Durham, NC, USA
Phone: 617-479-2310; E-mail: larry.moss@duke.edu
View this article at: http://www.jci.org/articles/view/68348?key=11aa06302a250850c4ef
Brain "clean-up crew" captured by MRI
All parts of the body generate waste that must be flushed out in order to remove harmful materials, old proteins, and other cellular detritus. Most tissues utilize the lymphatic system to keep clean, but the central nervous system (CNS) does not have lymphatic vasculature and relies instead on a waste clearance pathway known as the glymphatic system. The glymphatic system cleans the cerebrospinal fluid (CSF) that surround the brain and spinal cord and relies on specialized CNS support cells known as glia. In this issue of the Journal of Clinical Investigation, researchers led by Helene Benveniste at Stony Brook University used MRI to visualize the glymphatic system in rats that had been given a fluorescent tracer. The whole brain images allowed Benveniste and colleagues to identify two key influx nodes in the brain. Additionally, they could measure the rate at which the fluorescent tracer was removed by the glymphatic system. Currently, amyloid plaques and other molecules that accumulate in diseases such as Alzheimer's and Huntington's disease cannot be visualized in live patients. In a companion commentary, Warren Strittmatter of Duke University discusses how this new technology could be used to track the development or progression of diseases in which the clearance of specific proteins is impaired.
TITLE:
Brain-wide pathway for waste clearance captured by contrast enhanced MRI
AUTHOR CONTACT:
Helene Benveniste
Stony Brook University Medical Center, Stony Brook, NY, USA
Phone: 631-624-7018; Fax: 631-444-2907; E-mail: helene.benveniste@stonybrookmedicine.edu
View this article at: http://www.jci.org/articles/view/67677?key=e3d4b4a78599273ea579
ACCOMPANYING COMMENTARY
TITLE:
Bathing the brain
AUTHOR CONTACT:
Warren James Strittmatter
Duke University Medical Center, Durham, NC, USA
Phone: 919-684-0053; Fax: 919-681-7198; E-mail: warren@neuro.duke.edu
View this article at: http://www.jci.org/articles/view/68241?key=808d2caf308ec46730fb
ALSO IN THIS ISSUE
Smap1 deficiency perturbs receptor trafficking and predisposes mice to myelodysplasia
HDAC4 controls histone methylation in response to elevated cardiac load
Sprouty2, PTEN and PP2A interact to regulate prostate cancer progression
Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility | Back to top
TITLE:
Smap1 deficiency perturbs receptor trafficking and predisposes mice to myelodysplasia
AUTHOR CONTACT:
Masanobu Satake
Institute of Development, Aging and Cancer, Tohoku University, Sendai, UNK, JPN
Phone: (81)22-717-8477; E-mail: satake@idac.tohoku.ac.jp
View this article at: http://www.jci.org/articles/view/63711?key=81fb94bf3f59a4902e5b
TITLE:
HDAC4 controls histone methylation in response to elevated cardiac load
AUTHOR CONTACT:
Christoph Maack
Universittsklinikum des Saarlandes, Homburg, DEU
Phone: +49-6841-1623000; Fax: +49-6841-1623434; E-mail: christoph.maack@uks.eu
View this article at: http://www.jci.org/articles/view/61084?key=3b2f824d313bb1325d7a
TITLE:
Sprouty2, PTEN and PP2A interact to regulate prostate cancer progression
AUTHOR CONTACT:
Hing Leung
The Beatson Institute for Cancer Research, Glasgow, , GBR
Phone: 441413303658; E-mail: h.leung@beatson.gla.ac.uk
View this article at: http://www.jci.org/articles/view/63672?key=c51d70b1b0cef75eae44
TITLE:
Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility
AUTHOR CONTACT:
Tsang-Chih Kuo
Graduate Institute of Toxicology, College of Medicine, National Taiwan Univ, Taipei, TWN
Phone: 886-2-23123456#88649; E-mail: f95447013@ntu.edu.tw
View this article at: http://www.jci.org/articles/view/64044?key=48ac6b9d93d7fc1ccb38
###
[ | 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/2013-02/joci-jet021513.php
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