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JCI table of contents: April 25, 2011

EDITOR'S PICK: Pelvic organs given the slip by the protein fibulin-5

Pelvic organ prolapse (POP) is a disabling condition that affects almost 50% of women over the age of 50. It occurs when the muscles and ligaments supporting a woman's pelvic organs weaken such that the pelvic organs slip out of place, often protruding into the vagina. For many affected women, treatment involves surgery. Defining the molecular mechanisms underlying POP could provide targets for nonsurgical approaches to treating the condition. In this context, a team of researchers, led by Hiromi Yanagisawa, at the University of Texas Southwestern Medical Center, Dallas, has now identified a key role for the protein fibulin-5 in preventing the development of POP in mice.

The team found that fibulin-5 prevents the development of POP in mice in two ways. First, it facilitates the assembly of normal elastic fibers that help keep pelvic organs in place. Second, it inhibits the activity of MMP9, a protein that degrades the elastic fibers that help keep pelvic organs in place. As vaginal tissue samples from women with POP also showed increased levels of MMP-9, the authors suggest that therapies targeting elastic fiberdegrading proteins may help prevent, or even ameliorate, POP in women.

Gina Northington, at the University of Pennsylvania School of Medicine, Philadelphia, discusses in detail the importance of this study in an accompanying commentary.

TITLE: Extracellular matrix proteases contribute to progression of pelvic organ prolapse in mice and humans

Hiromi Yanagisawa
University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Phone: 214.648.7723; Fax: 214.648.1488; E-mail:

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TITLE: Fibulin-5: two for the price of one maintaining pelvic support

Gina M. Northington
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: 215.662.6361; Fax: 215.662.7929; E-mail:

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INFECTIOUS DISEASE: Targeting tissue destruction in tuberculosis

Infection with the bacterium Mycobacterium tuberculosis can cause tuberculosis. In most people, however, the bacteria do not cause disease but are sequestered in the lung in walled off compartments known as granulomas. By studying both human samples and mice expressing the human form of the protein MMP-1, a team of researchers, led by Paul Elkington, at Imperial College London, United Kingdom, has now generated data indicating that MMP-1 drives lung tissue destruction in granulomas. The team therefore suggests that targeting MMP-1 might provide a way to limit the damage caused by infection with Mycobacterium tuberculosis. This and other data indicating that MMPs represent viable therapeutic targets to control Mycobacterium tuberculosis infections are discussed in an accompanying commentary by Padmini Salgame, at the University of Medicine and Dentistry of New Jersey, Newark.

TITLE: MMP-1 drives immunopathology in human tuberculosis and transgenic mice

Paul Elkington
Imperial College London, London, United Kingdom.
Phone: +44.20.8383.2733; Fax: +44.20.8383.3394; E-mail:

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TITLE: MMPs in tuberculosis: granuloma creators and tissue destroyers

Padmini Salgame
University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey, USA.
Phone: 973.972.8647; Fax: 973.972.0713; E-mail:

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ONCOLOGY: On the origin of the tumor

It is, in general, very hard to cure a cancer once it has become clinically apparent. By identifying the cells from which a cancer arises researchers hope that it might be possible to detect cancerous lesions at much earlier stages and treat them more successfully. With this in mind, Andrzej Dlugosz and colleagues, at the University of Michigan Medical School, Ann Arbor, have now identified in mice the cells from which two forms of basal cell carcinoma arise.

Basal cell carcinomas are the most common human cancers. Although uncontrolled Hedgehog signaling drives almost all basal cell carcinomas, it is not clear why they differ in appearance and can be divided into different types. In this study, Dlugosz and colleagues used engineered mouse models of basal cell carcinoma to determine that superficial basal cell carcinomalike tumors arise from interfollicular epidermis and nodular basal cell carcinomalike tumors from hair follicle stem cells, thereby generating data that indicate that the cell of origin influences the type of basal cell carcinoma that develops.

In an accompanying commentary, Ervin Epstein Jr., at Children's Hospital of Oakland Research Institute, Oakland, discusses how these data fit with other recent studies on the origin of basal cell carcinomas and open doors for further investigation.

TITLE: Basal cell carcinomas in mice arise from hair follicle stem cells and multiple epithelial progenitor populations

Andrzej A. Dlugosz
University of Michigan Medical School, Ann Arbor, Michigan, USA.
Phone: 734.647.9482; Fax: 734.763.4575; E-mail:

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TITLE: Mommy where do tumors come from?

Ervin H. Epstein Jr.
Children's Hospital of Oakland Research Institute, Oakland, California, USA.
Phone: 510.502.6144; Fax: 510.597.7096; E-mail:

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INFLAMMATION: New role for energy generators in controlling inflammation

The inflammatory response is initiated as a protective response but if the response is sustained or excessive it leads to tissue damage. A team of researchers, led by Jahar Bhattacharya, at Columbia University College of Physicians and Surgeons, New York, has now identified in mice a new molecular mechanism that curbs excessive inflammation. Specifically, the team found that mitochondria (the energy generating compartments of a cell) in cells lining blood vessels in the lungs are key regulators of inflammation. As highlighted by both the authors and, in an accompanying commentary, Laura A. Dada and Jacob I. Sznajder, these data provide potential new therapeutic targets for the treatment of the deleterious effects of the inflammatory response.

TITLE: Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels

Jahar Bhattacharya
Columbia University College of Physicians and Surgeons, New York, New York, USA.
Phone: 212.305.7093; Fax: 212.305.6724; E-mail:

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TITLE: Mitochondrial Ca2+ and ROS take center stage to orchestrate TNF-alphamediated inflammatory responses

Jacob I. Sznajder
Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Phone: 312.908.7737; Fax: 312.908.4650; E-mail:

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GASTROENTEROLOGY: Cellular connection between inflammatory bowel disease and colon cancers

Individuals with the inflammatory bowel disease ulcerative colitis are at high risk for developing colon cancer, but the mechanisms underlying this are not completely understood. A team of researchers, led by Stefan Fichtner-Feigl, at the University of Regensburg, Germany, has now identified a defined population of immune cells known as macrophages that facilitate the development of colon cancer in a mouse model of ulcerative colitis. These cells were marked by expression of F4/80, high levels of CD11b, and low levels of Gr1 and promoted tumor development, in part, via the production of the tumor-promoting factors IL-6 and TGF-beta-1. The authors plan to investigate whether individuals with ulcerative colitis also have increased numbers of these macrophages and whether their presence can be used to predict the development of colon cancer.

TITLE: Tumor development in murine ulcerative colitis depends on MyD88 signaling of colonic F4/80+CD11bhighGr1low macrophages

Stefan Fichtner-Feigl
University of Regensburg, Regensburg, Germany.
Phone: 49.941.944.6868; Fax: 49.941.944.6802; E-mail:

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Contact: Karen Honey
Journal of Clinical Investigation

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