JCI online early table of contents: Nov. 16, 2009

Many biological processes are controlled by small molecules known as microRNAs, which work by suppressing the expression of specific sets of genes. Xiang-Hang Luo and colleagues, at Second Xiangya Hospital of Central South University, People's Republic of China, have now identified a previously unknown microRNA (miR-2861) as crucial to bone maintenance in mice and humans. Of clinical importance, expression of functional miR-2861 was absent in two related adolescents with primary osteoporosis.

Several lines of evidence determined the key role of miR-2861 in maintaining bone. First, miR-2861 promoted the in vitro development of a mouse stromal cell line into the cells responsible for bone formation. Second, in mice, in vivo silencing of miR-2861 inhibited bone formation and decreased bone mass. Last, analysis of ten patients with primary osteoporosis revealed two related adolescents in whom disease was caused by a mutation in the miR-2861 precursor (pre-miR-2861) that blocked expression of miR-2861. These data led the authors to conclude that miR-2861 has an important role in controlling the generation of the cells responsible for bone formation and that defects in the processing of its precursor can cause osteoporosis.

TITLE: A novel microRNA targeting HDAC5 regulates osteoblast differentiation in mice and contributes to primary osteoporosis in humans

AUTHOR CONTACT:
Xiang-Hang Luo
Second Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Phone: 86-731-85292152; Fax: 86-731-85533525; E-mail: xianghangluo@21cn.com.

View this article at: http://www.jci.org/articles/view/39832?key=wTvdY50uyZkh8Uji59Po

Lyme disease is caused by the microbe Borrelia burgdorferi, which is transmitted to humans from feeding ticks. Justin Radolf and colleagues, at the University of Connecticut Health Center, Farmington, have now visualized the microbe moving through the feeding tick and determined that it has a biphasic mode of dissemination. These data provide new insight into the transmission process, detailed understanding of which is essential if new methods of preventing human infection with the Lyme disease–causing microbe are to be developed.

In this study, the midguts and salivary glands of ticks before, during, and after feeding were isolated, and the live Borrelia burgdorferi microbes imaged in real time. In the first phase of dissemination, replicating microbes formed networks of nonmotile organisms that moved by adhering to the cells lining the tick midgut. In the second phase of dissemination, the microbes became motile invasive organisms that ultimately entered the salivary glands. These data challenge the conventional viewpoint that Lyme disease–causing microbes are always motile within ticks and that this drives their dissemination.

TITLE: Live imaging reveals a biphasic mode of dissemination of Borrelia burgdorferi within ticks

AUTHOR CONTACT:
Justin D. Radolf
University of Connecticut Health Center, Farmington, Connecticut, USA.
Phone: (860) 679-8480; Fax: (860) 679-1358; E-mail: jradolf@up.uchc.edu.

View this article at: http://www.jci.org/articles/view/39401?key=HnLk45JRxih3aqbS4YCQ

TITLE: Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion

AUTHOR CONTACT:
Lawrence H. Young
Yale University School of Medicine, New Haven, Connecticut, USA.
Phone: (203) 785-4102; Fax: (203) 785-7567; E-mail: lawrence.young@yale.edu.

View this article at: http://www.jci.org/articles/view/39738?key=8h26RuTn7HM7U213N81F

TITLE: Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling

AUTHOR CONTACT:
Carsten B. Schmidt-Weber
National Heart and Lung Institute, Imperial College, London, United Kingdom.
Phone: 44-78-26-743-578; E-mail: c.schmidt-weber@imperial.ac.uk.

View this article at: http://www.jci.org/articles/view/40202?key=94Ifno0iLjDPD54ZjN6W

TITLE: MAPK phosphatase-1 facilitates the loss of oxidative myofibers associated with obesity in mice

AUTHOR CONTACT:
Anton M. Bennett
Yale University School of Medicine, New Haven, Connecticut, USA.
Phone: (203) 737-2441; Fax: (203) 737-2738; E-mail: anton.bennett@yale.edu.

View this article at: http://www.jci.org/articles/view/39054?key=72bc5PqjImjVhlo44k05

TITLE: Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice

AUTHOR CONTACT:
Ellen Puré
The Wistar Institute, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-1570; Fax: (215) 898-3937; E-mail: pure@wistar.org.

Angélica M. Santos
The Wistar Institute, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-1570; Fax: (215) 898-3937; E-mail: asantos@wistar.org.

View this article at: http://www.jci.org/articles/view/38988?key=yZdblFdKB7BdGZeviwjj

TITLE: An adventitial IL-6/MCP1 amplification loop accelerates macrophage-mediated vascular inflammation leading to aortic dissection in mice

AUTHOR CONTACT:
Allan R. Brasier
University of Texas Medical Branch, Galveston, Texas, USA.
Phone: (409) 772-2824; Fax: (409) 772-8709; E-mail: arbrasie@utmb.edu.

View this article at: http://www.jci.org/articles/view/38308?key=Z4esMx0R2w90OrPJDZ3u

TITLE: alpha-1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice

AUTHOR CONTACT:
Jeffery D. Molkentin
Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Phone: (513) 636-3557; Fax (513) 636-5958; E-mail: jeff.molkentin@cchmc.org.

View this article at: http://www.jci.org/articles/view/39724?key=z9O2wDK4PVNLyd0m471e