A shortcut to blood progenitor cells?

Biotechnology: Gauging the behaviour of nanoparticles in the lung; Medicine: Taming prostate cancer aggressiveness; Geoscience: Tropical rainfall in a changing climate; Genetics: RNAs regulate reprogramming; Immunology: Natural signaling blocker identified; Neuroscience: Genes regulating neuronal sprouting after stroke

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 07 November 2010

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Nature: A shortcut to blood progenitor cells?

Biotechnology: Gauging the behaviour of nanoparticles in the lung

Medicine: Taming prostate cancer aggressiveness

Geoscience: Tropical rainfall in a changing climate

Genetics: RNAs regulate reprogramming

Immunology: Natural signaling blocker identified

And finally… Neuroscience: Genes regulating neuronal sprouting after stroke

· Mention of papers to be published at the same time with the same embargo

· Geographical listing of authors

PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.

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[1] Nature: A shortcut to blood progenitor cells?
DOI: 10.1038/nature09591

Researchers have converted human fibroblasts directly into blood progenitors for the first time, without the need for the cells to go through a pluripotent stage. The findings are published this week in Nature.

The ability to reprogram cells to a pluripotent state has been limited by a lack of understanding of the process by which these cells specialise. Mickie Bhatia and colleagues use the transcription factor OCT4 together with specific cytokine treatment to generate progenitors that can give rise to a full range of mature blood cells in the laboratory, directly from human dermal fibroblasts—without first establishing pluripotency. The findings could lead to a useful source of cells for clinical applications.

Author contact:
Mickie Bhatia (McMaster University, Hamilton, Canada)

Please contact via:
Veronica McGuire (Media Relations, McMaster University, Hamilton, Canada)
Tel: +1 905 525 9140, ext. 22169; E-mail: [email protected]

[2] Biotechnology: Gauging the behaviour of nanoparticles in the lung
DOI: 10.1038/nbt.1696

The behaviour of nanoparticles in the body after they are deposited in the lungs is reported online in Nature Biotechnology this week. The findings may have implications for future drug delivery, and in the study of air pollution and cancer development.

John Frangioni, Akira Tsuda, and colleagues used near-infrared fluorescent imaging to track nanoparticles administered to the lungs of rats. They varied the chemical composition, size and surface charge of the nanoparticles in order to determine which properties affect the transport of nanoparticles into tissues and their subsequent clearance from the body. The team shows that non-positively charged particles smaller than 34 nanometres in diameter are rapidly transported to lymph nodes, and that nanoparticles smaller than six nanometres with equal positive and negative charge are quickly cleared from the body via the kidneys.

With regard to the health effects of environmental pollutants, this work helps to explain why certain nanoparticles are more toxic than others. It also suggests that the toxicity of nanoparticle pollutants could be reduced by chemical strategies to alter their size and charge.

Author contact:
John Frangioni (Beth Israel Deaconess Medical Center, Boston, MA, USA)
Tel: +1 617 667 0692; E-mail: [email protected]

Akira Tsuda (Harvard School of Public Health, Boston, MA, USA)
Tel: + 1 617 432 0127; E-mail: [email protected]

[3] Medicine: Taming prostate cancer aggressiveness
DOI: 10.1038/nm.2236

The cell-adhesion molecule N-cadherin is critical for the tumour transition from a relatively benign to a very aggressive form of prostate cancer, reports an article published online this week in Nature Medicine. Therapeutic targeting of this adhesion molecule may have future clinical benefits for the treatment of prostate cancer.

Men with prostate cancer tend to respond to castration therapy, as prostate tumours are often dependent on androgenic hormones to grow. If, on the other hand, the tumour becomes androgen-independent and resistant to castration, the disease becomes lethal. What controls the transition to the castration-resistant state has been unknown.

Robert Reiter and his colleagues found that the expression of N-cadherin, a protein that acts as molecular glue between cells, is increased in tumours of people with castration-resistant prostate cancer. They found that forced expression of N-cadherin in androgen-dependent prostate cancer cells made them resistant to castration and promoted cancer metastasis. Monoclonal antibodies against N-cadherin reduced proliferation, adhesion and metastasis of prostate cancer cells transplanted into mice, leading in some cases to complete tumour regression.

Author contact:
Robert Reiter (University of California, Los Angeles, CA, USA)
Tel: +1 310 794 7224; E-mail: [email protected]

[4] Geoscience: Tropical rainfall in a changing climate
DOI: 10.1038/ngeo1008

The sea surface temperature threshold above which the tropical atmosphere becomes unstable and open to the formation of deep thunderclouds has risen in line with surface ocean warming, suggests a study published online this week in Nature Geoscience.

Nathaniel Johnson and Shang-Ping Xie analysed satellite data recording rainfall and sea surface temperatures in the tropics, and found that sea surface temperatures have risen by 0.1°C per decade over the past 30 years. They went on to estimate the sea surface temperature threshold for deep convection which affects the regions of cyclone formation, tropical atmospheric temperature and rainfall. This threshold had risen at the same rate, suggesting that the stability of the tropical atmosphere has been unaffected by climate change.

Author contact:
Nathaniel Johnson (University of Hawaii at Manoa, Honolulu, HI, USA)
Tel: +1 808 956 2375; E-mail: [email protected]

[5] Genetics: RNAs regulate reprogramming
DOI: 10.1038/ng.710

Long noncoding RNAs (lincRNAs) regulate somatic cell reprogramming—the process used to convert cells committed to one fate into induced pluripotent stem cells. These findings, published online this week in Nature Genetics, are the first demonstration of a function for lincRNAs in somatic cell reprogramming.

LincRNAs are encoded in the mammalian genome and are evolutionarily conserved. The biological roles of lincRNAs, which don’t encode proteins but rather have functions carried out by the RNA molecule are known for only a few of the many known lincRNAs.

George Daley and colleagues report that one such region, the lincRNA-RoR, regulates reprogramming of fibroblasts and blood cells into induced pluripotent stem cells. The authors further show that increased levels of lincRNA-RoR improves reprogramming efficiency.

Author contact:
George Daley (Harvard Medical School, Cambridge, MA, USA)
Tel: +1 617 919 2013; E-mail: [email protected]

[6] Immunology: Natural signaling blocker identified
DOI: 10.1038/ni.1957

Identification of a molecule that can halt immune cell signaling through the surface receptor gp130 is reported in this week’s online edition of Nature Immunology.

Certain mediators of inflammation and heightened antibody responses signal via gp130-linked receptors, marking these pathways as potential targets for therapeutic intervention in some autoimmune or inflammatory conditions, such as rheumatoid arthritis or inflammatory bowel disease.

Chris Hunter and colleagues show that the protein subunit p28 of interleukin 27 binds to gp130, preventing other molecules from interacting with the receptor and thus blunts the ability of gp130 to transmit signals. As a proof-of-principle, they show mice transiently expressing p28 show less severe disease manifestation in an experimental autoimmune encephalomyelitis (EAE) model, which mimics aspects of the human disease multiple sclerosis.

Author contact:
Chris Hunter (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 573 7772; E-mail: [email protected]

[7] And finally…Neuroscience: Genes regulating neuronal sprouting after stroke
DOI: 10.1038/nn.2674

Gene expression differences between neurons that show recovery-associated growth after stroke and neurons that don’t show such growth are reported in a study published online this week in Nature Neuroscience. These findings have the potential to identify novel therapeutic targets for the treatment of stroke in humans.

Recovery from stroke had been associated with the brain’s ability to reorganize by having spared regions assume functions carried out by the compromised tissue. This reorganization is thought to be sub-served, in part, by axonal growth or “sprouting” of spared neurons, which allows them to make new connections in the recovering brain. However, only a subset of spared neurons show sprouting and what makes these neurons “special” is unknown.

Thomas Carmichael and colleagues developed a technique that allowed them to selectively label and then isolate sprouting and non-sprouting neurons from the same rats after stroke. They then compared gene expression profiles of these two neuronal groups to identify differences. Because the majority of human stroke victims are older adults, they also compared gene expression differences between young and aged rats. Because stroke is an age-related disease, they also compared gene expression differences between young and aged rats and found a number of significant differences.

As proof of concept, the authors selected a set of the genes which were highly activated in sprouting neurons from aged rats and studied these further. They report that an epigenetic regulatory protein and a growth factor acted to promote sprouting, whereas up-regulated inhibitory myelin receptors acted to limit sprouting.

Author contact:
S. Thomas Carmichael (University of California, Los Angeles, CA, USA)
Tel: +1 310 206 0550; E-mail: [email protected]

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Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (http://www.nature.com/nature)

[8] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2
DOI: 10.1038/nature09586

NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)

[9] Suppressing resistance to Bt cotton with sterile insect releases
DOI: 10.1038/nbt.1704

NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)

[10] Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence
DOI: 10.1038/ncb2123

NATURE CHEMISTRY (http://www.nature.com/nchem)

[11] Surface-assisted cyclodehydrogenation provides a synthetic route towards easily processable and chemically tailored nanographenes
DOI: 10.1038/nchem.891

[12] Mutual modulation between membrane-embedded receptor clustering and ligand binding in lipid membranes
DOI: 10.1038/nchem.892

NATURE GENETICS (http://www.nature.com/naturegenetics)

[13] Exome sequencing identifies ACAD9 mutations as a cause of complex I deficiency
DOI: 10.1038/ng.706

[14] Fine-mapping at three loci known to affect fetal hemoglobin levels explains additional genetic variation
DOI: 10.1038/ng.707

[15] Targets and dynamics of promoter DNA methylation during early mouse development
DOI: 10.1038/ng.708

[16] miR-212 and miR-132 are required for epithelial stromal interactions and mouse mammary gland development
DOI: 10.1038/ng.709

NATURE GEOSCIENCE (http://www.nature.com/ngeo)

[17] Skilful multi-year predictions of Atlantic hurricane frequency
DOI: 10.1038/ngeo1004

[18] Sedimentary membrane lipids recycled by deep-sea benthic archaea
DOI: 10.1038/ngeo983

NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)

[19] Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria
DOI: 10.1038/ni.1960

NATURE MATERIALS (http://www.nature.com/naturematerials)

[20] Flexible organic transistors and circuits with extreme bending stability
DOI: 10.1038/nmat2896

NATURE METHODS (http://www.nature.com/nmeth)

[21] Analysis and design of RNA sequencing experiments for identifying mRNA isoform regulation
DOI: 10.1038/nmeth.1528

[22] FragSeq: transcriptome-wide RNA structure probing using high-throughput sequencing
DOI: 10.1038/nmeth.1529

Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)

[23] Otx2 controls neuron subtype identity in the ventral tegmental area and antagonizes vulnerability to the Parkinsonian toxin MPTP by suppressing Dopamine transporter
DOI: 10.1038/nn.2661

[24] When size matters: attention affects performance by contrast or response gain
DOI: 10.1038/nn.2669

[25] Yy1: a molecular link between neuregulin and transcriptional modulation of peripheral myelination
DOI: 10.1038/nn.2686

Nature PHYSICS (http://www.nature.com/naturephysics)

[26] A holey structured metamaterial for acoustic deep subwavelength imaging
DOI: 10.1038/nphys1804

[27] Giant Faraday rotation in single- and multilayer graphene
DOI: 10.1038/nphys1816

[28] Quantum memory for entangled continuous variable states
DOI: 10.1038/nphys1819

[29] Accessing the dark exciton with light
DOI: 10.1038/nphys1812

Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)

[30] Reduced Rif2 and lack of Mec1 target short telomeres for elongation rather than double-strand break repair
DOI: 10.1038/nsmb.1947

[31] H2A.Z nucleosomes enriched over active genes are homotypic
DOI: 10.1038/nsmb.1926

[32] Correlated conformational events in EF-G and the ribosome regulate translocation
DOI: 10.1038/nsmb.1925

[33] Reciprocal intronic and exonic histone modification regions in humans
DOI: 10.1038/nsmb.1924

***************************************************************************************************************

GEOGRAPHICAL LISTING OF AUTHORS

The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.

CANADA:
Hamilton: 1
Montreal: 14
Vancouver: 3

CZECH REPUBLIC
Brno: 10

DENMARK
Aalborg Ost: 26
Copenhagen: 28

FRANCE
Montpellier: 15
Strasbourg: 11

GERMANY
Berlin: 27
Bremen: 18
Erlangen: 27
Frankfurt: 13, 16
Goettingen: 16
Hannover: 16
Heidelberg: 16
Kiel: 6
Mainz: 11
Munich: 2, 13, 23
Neuherberg: 2, 13, 23
Stuttgart: 20
Tuebingen: 13
Ulm: 28

ISRAEL
Haifa: 29

ITALY
Benevento: 23
Milan: 13
Naples: 23

JAPAN
Fukuoka: 15
Nangoku: 18
Tokyo: 3, 18, 20
Yokohama: 18
Yokosuka: 18

POLAND
Warsaw: 28

SINGAPORE
Singapore: 10

SPAIN
Madrid: 26
Zaragoza: 26

SWITZERLAND
Basel: 15
Bern: 11
Dubendorf: 11
Geneva: 27
Rueschlikon: 11
Zurich: 11

UNITED KINGDOM
Cardiff: 6
Cambridge: 21
Dundee: 10
Edinburgh: 29
Exeter: 17
London: 12, 28
Nottingham: 28
Oxford: 13

UNITED STATES OF AMERICA

Arizona
Maricopa: 9
Phoenix: 9
Tucson: 9

California
Berkeley: 26, 27
La Jolla: 8
Los Angeles: 3, 7
Menlo Park: 22
Palo Alto: 6
Parlier: 9
Pasadena: 29
San Francisco: 33
Santa Barbara: 29
Santa Cruz: 22
Thousand Oaks: 6

Connecticut
New Haven: 5

Hawaii
Honolulu: 4

Maryland
Bethesda: 8, 10
Chevy Chase: 5
Frederick: 7

Massachusetts
Boston: 2, 5, 8, 14
Cambridge: 2, 5, 14

Michigan
Ann Arbor: 7

Missouri
St Louis: 9

New Jersey
Princeton: 30

New York
New York: 24, 25, 32
Rochester: 22

Ohio
Cleveland: 8
Columbus: 19

Pennsylvania
Philadelphia: 6, 7
Radnor: 6
Warwick: 6

Virginia
Richmond: 25

Washington
Seattle: 3, 6, 19, 31

Wisconsin
Madison: 25

PRESS CONTACTS…

For media inquiries relating to embargo policy for all the Nature Research Journals:

Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]

Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]

Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]

For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:

Nature Biotechnology (New York)
Michael Francisco
Tel: +1 212 726 9288; E-mail: [email protected]

Nature Cell Biology (London)
Sowmya Swaminathan
Tel: +44 20 7843 4656; E-mail: [email protected]

Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]

Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]

Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail: [email protected]

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: [email protected]

Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]

Nature Structural & Molecular Biology (New York)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]

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Published: 07 Nov 2010

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Reference: 

Nature and Nature Research Journal

Medicine