Featured Research

from universities, journals, and other organizations

Metabolic Disease: The Protein Cd36 Helps Trap Macrophages In The Wall Of Arterial Blood Vessels

Date:
December 8, 2008
Source:
Journal of Clinical Investigation
Summary:
One of the most common causes of death in the developed world is a disease of the major arterial blood vessels that can cause heart attacks and stroke. A critical step in this disease (which is known as atherosclerosis, or hardening of the arteries) is the trapping of cells known as macrophages in the innermost layer of arteries, but the mechanism by which this occurs has not been well defined.

One of the most common causes of death in the developed world is a disease of the major arterial blood vessels that can cause heart attacks and stroke. A critical step in this disease (which is known as atherosclerosis, or hardening of the arteries) is the trapping of cells known as macrophages in the innermost layer of arteries, but the mechanism by which this occurs has not been well defined.

Now, however, Roy Silverstein and colleagues, at the Cleveland Clinic Foundation, Cleveland, have provided insight into this event by studying mice and human macrophages in vitro.

In the study, both in vivo and in vitro assays indicated that a molecule known as oxLDL, which is an important trigger of atherosclerosis, inhibited the migration of mouse macrophages. Importantly, this inhibitory effect was not observed if the macrophages came from mice lacking the protein CD36.

A similar role was also observed for CD36 in modulating the in vitro migratory response of human macrophages to oxLDL.

Further analysis revealed the molecular changes that occur after oxLDL interaction with CD36 to modulate macrophage migration. The authors speculate that the interaction of oxLDL and CD36 on macrophages might inhibit their migration in vivo and lead to them becoming trapped in the innermost layer of the arterial wall.


Story Source:

The above story is based on materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


Journal Reference:

  1. CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima. Journal of Clinical Investigation, Dec 8, 2008

Cite This Page:

Journal of Clinical Investigation. "Metabolic Disease: The Protein Cd36 Helps Trap Macrophages In The Wall Of Arterial Blood Vessels." ScienceDaily. ScienceDaily, 8 December 2008. <www.sciencedaily.com/releases/2008/12/081208180234.htm>.
Journal of Clinical Investigation. (2008, December 8). Metabolic Disease: The Protein Cd36 Helps Trap Macrophages In The Wall Of Arterial Blood Vessels. ScienceDaily. Retrieved July 23, 2014 from www.sciencedaily.com/releases/2008/12/081208180234.htm
Journal of Clinical Investigation. "Metabolic Disease: The Protein Cd36 Helps Trap Macrophages In The Wall Of Arterial Blood Vessels." ScienceDaily. www.sciencedaily.com/releases/2008/12/081208180234.htm (accessed July 23, 2014).

Share This




More Health & Medicine News

Wednesday, July 23, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

Courts Conflicted Over Healthcare Law

Courts Conflicted Over Healthcare Law

AP (July 22, 2014) Two federal appeals courts issued conflicting rulings Tuesday on the legality of the federally-run healthcare exchange that operates in 36 states. (July 22) Video provided by AP
Powered by NewsLook.com
Why Do People Believe We Only Use 10 Percent Of Our Brains?

Why Do People Believe We Only Use 10 Percent Of Our Brains?

Newsy (July 22, 2014) The new sci-fi thriller "Lucy" is making people question whether we really use all our brainpower. But, as scientists have insisted for years, we do. Video provided by Newsy
Powered by NewsLook.com
Scientists Find New Way To Make Human Platelets

Scientists Find New Way To Make Human Platelets

Newsy (July 22, 2014) Boston scientists have discovered a new way to create fully functioning human platelets using a bioreactor and human stem cells. Video provided by Newsy
Powered by NewsLook.com
Gilead's $1000-a-Pill Drug Could Cure Hep C in HIV-Positive People

Gilead's $1000-a-Pill Drug Could Cure Hep C in HIV-Positive People

TheStreet (July 21, 2014) New research shows Gilead Science's drug Sovaldi helps in curing hepatitis C in those who suffer from HIV. In a medical study, the combination of Gilead's Hep C drug with anti-viral drug Ribavirin cured 76% of HIV-positive patients suffering from the most common hepatitis C strain. Hepatitis C and related complications have been a top cause of death in HIV-positive patients. Typical medication used to treat the disease, including interferon proteins, tended to react badly with HIV drugs. However, Sovaldi's %1,000-a-pill price tag could limit the number of patients able to access the treatment. TheStreet's Keris Lahiff reports from New York. Video provided by TheStreet
Powered by NewsLook.com

Search ScienceDaily

Number of stories in archives: 140,361

Find with keyword(s):
Enter a keyword or phrase to search ScienceDaily for related topics and research stories.

Save/Print:
Share:

Breaking News:
from the past week

In Other News

... from NewsDaily.com

Science News

Health News

Environment News

Technology News



Save/Print:
Share:

Free Subscriptions


Get the latest science news with ScienceDaily's free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Get Social & Mobile


Keep up to date with the latest news from ScienceDaily via social networks and mobile apps:

Have Feedback?


Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?
Mobile: iPhone Android Web
Follow: Facebook Twitter Google+
Subscribe: RSS Feeds Email Newsletters
Latest Headlines Health & Medicine Mind & Brain Space & Time Matter & Energy Computers & Math Plants & Animals Earth & Climate Fossils & Ruins