Health & Medicine
Molecule Critical to Healing Wounds May Help Speed Healing Process
Catherine Griffin
First Posted: Nov 16, 2013 09:41 AM EST
When you're injured, an open wound can leave you vulnerable to viruses, bacteria and parasites. That's why wound healing is so crucial; it seals off the area that might leave you open for further infection. Now, scientists have discovered a clearer explanation of the role of one of the players in the wound-healing process, providing researchers with a possible new target for drugs that could help speed up the process.
The major player in question is a molecule called FOX01. A critical element of healing is the movement of keratinocytes, the primary cells comprising the epidermis, which is the outer layer of skin. Since FOX01 is found in much higher levels in wounds, scientists decided to investigate its role a bit more closely.
The scientists bred mice that lacked FOX01 in their keratinocytes. They then watched the wound healing process in these mice compared to mice with normal FOX01. Although they thought that deleting FOX01 would speed up the wound-healing process, since it's been previously associated with interfering with cell reproduction, it seemed to have the opposite effect.
The mice that lacked FOX01 showed significant delays in healing. All of the wounds in the control mice, in contrast, were healed after just one week. Needless to say, the researchers decided to delve a bit further.
The scientists examined the effect of reducing FOX01 levels on other genes known to play a role in cell migration. They found that many of these genes were significantly reduced, notably TGF-β1, a critical growth factor in wound repair. When the researchers added TGF-β1 to cells lacking FOX01, the cells behaved normally and healed normally. This seemed to show that FOX01 acts upstream of TGF-β1 in the signaling pathway triggered during a healing process. In addition, the researchers found that mice lacking FOX01 had evidence of increased oxidative stress, which is detrimental to wound healing.
"The wound healing environment is a stressful environment for the cell," said Dana Graves, one of the researchers, in a news release. "It appears that upregulation of FOX01 helps protect the cell against oxidative stress."
The findings reveal a little bit more about the wound healing process. More specifically, the findings could help with stimulating wound healing in patients.
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First Posted: Nov 16, 2013 09:41 AM EST
When you're injured, an open wound can leave you vulnerable to viruses, bacteria and parasites. That's why wound healing is so crucial; it seals off the area that might leave you open for further infection. Now, scientists have discovered a clearer explanation of the role of one of the players in the wound-healing process, providing researchers with a possible new target for drugs that could help speed up the process.
The major player in question is a molecule called FOX01. A critical element of healing is the movement of keratinocytes, the primary cells comprising the epidermis, which is the outer layer of skin. Since FOX01 is found in much higher levels in wounds, scientists decided to investigate its role a bit more closely.
The scientists bred mice that lacked FOX01 in their keratinocytes. They then watched the wound healing process in these mice compared to mice with normal FOX01. Although they thought that deleting FOX01 would speed up the wound-healing process, since it's been previously associated with interfering with cell reproduction, it seemed to have the opposite effect.
The mice that lacked FOX01 showed significant delays in healing. All of the wounds in the control mice, in contrast, were healed after just one week. Needless to say, the researchers decided to delve a bit further.
The scientists examined the effect of reducing FOX01 levels on other genes known to play a role in cell migration. They found that many of these genes were significantly reduced, notably TGF-β1, a critical growth factor in wound repair. When the researchers added TGF-β1 to cells lacking FOX01, the cells behaved normally and healed normally. This seemed to show that FOX01 acts upstream of TGF-β1 in the signaling pathway triggered during a healing process. In addition, the researchers found that mice lacking FOX01 had evidence of increased oxidative stress, which is detrimental to wound healing.
"The wound healing environment is a stressful environment for the cell," said Dana Graves, one of the researchers, in a news release. "It appears that upregulation of FOX01 helps protect the cell against oxidative stress."
The findings reveal a little bit more about the wound healing process. More specifically, the findings could help with stimulating wound healing in patients.
See Now: NASA's Juno Spacecraft's Rendezvous With Jupiter's Mammoth Cyclone