JCI online early table of contents: April 15, 2008

The protein KIM-1 (also known as TIM-1) is upregulated on the surface of injured kidney epithelial cells. In the study, it was found that upregulation of KIM-1 enabled rat, pig, and dog kidney epithelial cells to take up cells that had died by a process known as apoptosis. The uptake of the apoptotic cells, by a process known as phagocytosis, occurred after KIM-1 bound molecules on the surface of the apoptotic cells, specifically phosphatidylserine and oxidized lipoproteins. These data suggest a role for KIM-1 in repair of the lining of the kidney tubules following injury.

TITLE: Kidney injury molecule–1 is a phosphatidylserine receptor that confers a phagocytic phenotype on epithelial cells

AUTHOR CONTACT:

Takaharu Ichimura
Brigham and Women's Hospital, Harvard Institute of Medicine, Boston, Massachusetts, USA.
Phone: (617) 525-5961; Fax: (617) 525-5965; E-mail: .

Jeremy S. Duffield
Brigham and Women's Hospital, Harvard Institute of Medicine, Boston, Massachusetts, USA.
Phone: (617) 525-5914; Fax: (617) 525-5830; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=34487

CARDIOVASCULAR DISEASE

ROCK solid: A key role for the protein ROCK1 in vessel wall damage

Diseases that affect the heart and/or blood vessels are known as cardiovascular diseases and they include high blood pressure (also known as hypertension), stroke, and atherosclerosis. The disease-causing changes to blood vessels in some cardiovascular diseases occur as a result of a damaging inflammatory response to blood vessel injury, and increased activity of members of the ROCK family of proteins has been linked to this process. However, several cell types are involved in the blood vessel–damaging inflammatory response to injury and it has not been determined which specific ROCK protein is involved in which specific cell type. In a new study, using mice expressing only one of the genes containing the information for making ROCK1 (Rock1+/– mice) and mice expressing only one of the genes containing the information for making ROCK2 (Rock2+/– mice), James Liao and colleagues at Brigham and Women’s Hospital and Harvard Medical School, Boston, have shown that ROCK1, and not ROCK2, mediates damaging changes to blood vessels after they have been injured by being closed off. The lack of damaging changes to blood vessels in Rock1+/– mice was associated with decreased inflammatory cell mobilization to the site of injury. Further analysis indicated that ROCK1 expression in bone marrow–derived cells, most probably inflammatory cells, was important for mediating the damaging changes to blood vessels after injury. The authors therefore concluded that ROCK1 might provide a useful target for treating inflammatory diseases of blood vessels.