JCI table of contents: Nov. 23, 2009
EDITOR'S PICK: Gene implicated in stress-induced high blood pressure Do stressful situations make your blood pressure rise? If so, your phosducin gene could be to blame according to a team of researchers, at the University of Freiburg, Germany, and the Medical College of Wisconsin, Milwaukee, that has identified a role for the protein generated by the phosducin gene in modulating blood pressure in response to stress in both mice and humans.
The team, led by Lutz Hein and Ulrich Broeckel, generated mice lacking phosducin and found that they had increased baseline blood pressure when compared with normal mice and that they showed enhanced increases in blood pressure in response to post-operative stress. Analysis in humans indicated that a number of phosducin gene variants were associated with certain stress-dependent blood pressure responses. Further, one gene variant in particular was associated with elevated baseline blood pressure. These data led the authors to suggest that phosducin might be a good target for drugs designed to alleviate stress-induced high blood pressure. In an accompanying commentary, however, Guido Grassi, at Clinica Medica, Italy, notes that further studies are needed before the therapeutic implications of these data can really be determined.
TITLE: Phosducin influences sympathetic activity and prevents stress-induced hypertension in humans and mice
AUTHOR CONTACT:
Lutz Hein
University of Freiburg, Freiburg, Germany.
Phone: 49-761-2035314; Fax: 49-761-2035318; E-mail: lutz.hein@pharmakol.uni-freiburg.de.
Ulrich Broeckel
Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Phone: (414) 955-2369; Fax: (414) 456-6516; E-mail: broeckel@mcw.edu.
View this article at: http://www.jci.org/articles/view/38433?key=ch6PLgvm06ENhpLnhy41
ACCOMPANYING COMMENTARY
TITLE: Phosducin – a candidate gene for stress-dependent hypertension
AUTHOR CONTACT:
Guido Grassi
Clinica Medica, Monza, Milan, Italy.
Phone: 39-039-233-357; Fax: 39-039-322-274; Email: guido.grassi@unimib.it.
View this article at: http://www.jci.org/articles/view/41508?key=JtWzBvLn9C3r9GYN8BN8
EDITOR'S PICK: Lessons for HIV learned from monkey control of SIV infection
SIV is a virus related to HIV that can infect monkeys. In some strains of monkey (which are known as natural hosts) SIV does not cause disease, whereas it does in others (which are known as susceptible hosts). It is hoped that understanding why SIV does not cause disease in natural hosts will provide insight into how to control HIV infection of humans. Two independent research teams, one led by Michaela C. Müller-Trutwin, and the other led by Guido Silvestri, Ashley Haase, and David Kelvin, have now determined that SIV induces vigorous activation of the immune system, in particular upregulation of genes stimulated by immune molecules known as IFNs, in both natural and susceptible hosts, but strikingly, the responses are later brought under control only in the former. In an accompanying commentary, Nina Bhardwaj and Olivier Manches, at New York University Langone Medical Center, New York, discuss how the lessons learned from these studies might impact HIV vaccine design and therapy.
TITLE: Global genomic analysis reveals rapid control of a robust innate response in SIV-infected sooty mangabeys
AUTHOR CONTACT:
Guido Silvestri
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-5363; Fax: (215) 573-5369; E-mail: gsilvest@mail.med.upenn.edu.
Ashley T. Haase,
University of Minnesota, Minneapolis, Minnesota, USA.
Phone: (612) 624-4442; Fax: (612) 626-0623; E-mail: haase001@umn.edu.
David J. Kelvin
University Health Network, Toronto, Ontario, Canada.
Phone: (416) 581-7605; Fax: (416) 581-7606; E-mail: dkelvin@uhnresearch.ca.
View this article at: http://www.jci.org/articles/view/40115?key=oNmMSIkn4H9JdUJ72v6a
ACCOMPANYING ARTICLE
TITLE: Nonpathogenic SIV infection of African green monkeys induces a strong but rapidly controlled type I IFN response
AUTHOR CONTACT:
Michaela C. Müller-Trutwin
Institut Pasteur, Paris, France.
Phone: 33-1-40-61-39-69; Fax: 33-1-45-68-89-57; E-mail: michaela.muller-trutwin@pasteur.fr.
View this article at: http://www.jci.org/articles/view/40093?key=8rqR89T5BZYeJ7KuHW55
ACCOMPANYING COMMENTARY
TITLE: Resolution of immune activation defines nonpathogenic SIV infection
AUTHOR CONTACT:
Nina Bhardwaj
The New York University Langone Medical Center, New York, New York, USA.
Phone: (212) 263-5814; Fax: (212) 263-6729; Email: Nina.Bhardwaj@med.nyu.edu.
View this article at: http://www.jci.org/articles/view/41509?key=YH73bnLajqEZK6CETk0O
HEMATOLOGY: Double trouble: the protein GSK-3 controls self-renewal and commitment of blood stem cells
TITLE: Pivotal role for glycogen synthase kinase-3 in hematopoietic stem cell homeostasis in mice
AUTHOR CONTACT:
Peter S. Klein
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-2179; Fax: (215) 573-4320; E-mail: pklein@mail.med.upenn.edu.
View this article at: http://www.jci.org/articles/view/40572?key=JnYgR1FfQ3JoB2G24T0j
Source: Journal of Clinical Investigation
Articles on the same topic
- New stress-related gene modulates high blood pressure in mice and menWed, 25 Nov 2009, 23:04:04 UTC
- Gene implicated in stress-induced high blood pressureTue, 24 Nov 2009, 0:31:50 UTC
Other sources
- New stress-related gene modulates high blood pressure in mice and menfrom Science BlogThu, 26 Nov 2009, 15:49:28 UTC
- New stress-related gene modulates high blood pressure in mice and menfrom Science BlogThu, 26 Nov 2009, 0:14:31 UTC
- Gene implicated in stress-induced high blood pressurefrom Science DailyTue, 24 Nov 2009, 19:21:32 UTC
- Gene implicated in stress-induced high blood pressurefrom PhysorgTue, 24 Nov 2009, 0:28:13 UTC