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JCI early table of contents for Aug. 1, 2013

JCI Journals

Prolactin reduces arthritis inflammation

Inflammatory joint diseases such as rheumatoid arthritis are the result of cartilage damage and loss. Chondrocytes are the only cells that are found in cartilage and their death is linked to decreased cartilage health. In this issue of the Journal of Clinical Investigation, Carmen Clapp and colleagues at the National University of Mexico identify prolactin as a potential treatment for inflammatory joint disease. Prolactin treatment prevented chondrocyte death and associated cartilage degradation. In a rat model of inflammatory arthritis, prolactin treatment reduced inflammation, bone erosion, joint swelling, and pain. This study indicates that prolactin therapy has the potential to relieve many symptoms associated with rheumatoid arthritis and other inflammatory-related diseases.

TITLE: Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

Carmen Clapp
National University of Mexico, Queretaro, , MEX
Phone: 52442 2381028; Fax: 52442 2340344; E-mail:

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Identification of a molecule linking bone loss and bone formation

Bone integrity requires skeletal remodeling, which involves both bone formation and resorption. It has been previously shown that the formation of new bone is triggered by degradation of older bone. However, it is unknown how these two processes coordinate for skeletal maintenance. In this issue of the Journal of Clinical Investigation, Sunao Takeshita and colleagues at the National Center for Geriatrics and Gerontology identify a protein, CTHRC1 that is secreted by bone adsorbing cells (osteoclasts) and helps initiate bone formation. The authors found that CTHRC1 secretion in bone coincided with bone remodeling and an increase in bone-producing cells. Mice with osteoclasts that did not produce CTHRC1 had lower bone mass than normal animals. This group also found that as animals aged, Cthrch1 expression decreased, suggesting a role for this molecule in age related bone loss. Together these data imply CTHRC1 as a target for treatment and diagnosis of bone diseases such as osteoporosis.

TITLE: Osteoclast-secreted Cthrc1 in the coupling of bone resorption to formation

Sunao Takeshita
National Center for Geriatrics and Gerontology, Obu, UNK, JPN
Phone: 81-562-44-5651 ext5047; Fax: 81-562-44-6595; E-mail:

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Defense against bacterial infection in chronic granulomatous disease

Patients suffering from chronic granulomatous disease (CGD) are prone to recurrent and potentially life threatening bouts of infection due to the inability of phagocytic cells to kill invading microorganisms. Normal phagocytes release reactive oxygen compounds in response to infection, but this defense is lacking in phagocytes of people with CGD. In the current issue of the Journal of Clinical Investigation, Griffin Rodgers and colleagues at the National Institutes of Health identify a neutrophil granule protein, OLFM4 as a potential therapeutic target for CGD patients. In a mouse model of CGD, deletion of Olfm4 protected the mice from infection with Staphylococcus aureus. The protective effect of Olmf4 deletion in CGD mice extended to multiple strains of S. aureus, including a community-associated strain of MRSA. This study suggests that targeting OLMF4 in CGD patients may enhance their ability to fight off bacterial infection.

TITLE: Olfm4 deletion enhances defense against Staphylococcus aureus in CGD mice

Griffin Platt Rodgers
National Institutes of Health, Bethesda, MD, USA
Phone: 301-496-5741; E-mail:

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TITLE: Congenital amegakaryotic thrombocytopenia iPS cells exhibit defective MPL-mediated signaling

Koji Eto
Center for iPS Cell Research and Application, Kyoto University, Kyoto, JPN
Phone: +81-75-366-7075; Fax: +81-76-366-7095; E-mail:

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TITLE: Myeloperoxidase, paraoxonase-1 and HDL form a functional ternary complex

Stanley L. Hazen
Cleveland Clinic, Cleveland, OH, USA
Phone: 216-445-9763; Fax: 216-444-9404; E-mail:

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TITLE: Mobilizing monocytes to cross-present circulating viral antigen in chronic infection

Adam Gehring
Saint Louis University, School of Medicine, Saint Louis, MO, USA
Phone: +1 (314) 977-8711; Fax: +1 (314) 977-8717; E-mail:

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