Post by Max on Jun 12, 2005 5:30:11 GMT -5
Isolating effects in the skin and disregarding severe effects in various parts of the brain, pituitary gland and organs such as the liver is current dermatological practise.
Hoffman la Roche itself has reported "abnormal wound healing, delayed healing of exuberant granulation tissue with crusting" in association with (Ro)accutane exposure in human subjects [0]. A dogmatic, non-scientifically proven view held as a truth is that Roaccutane decreases scar-formation in the skin, but does not necessarily have to be correct and needs clarification. Some evidence is pointing rather at the opposite direction. An increased scar-formation in subjects exposed to retinoic acid in doses over 1 microM is here suggested to be possible due to retinoic acid induced changes in the extracellular matrix affecting the cell migration in the healing process.
Integrin Alpha5 beta1 was found to be increased in various human cell lines exposed to retinoic acid in low and high doses [1 and 4]. Integrins are cell membrane structures that link the cell membrane to the extracellular matrix [3].
Increased levels of the alpha5 beta1 integrin appears to have close relation to the formation and development of abnormal scars, and was found to be higher in hypertrophic scars than normal skin. To find a way to decrease the expression level of alpha5 beta1 integrin in fibroblasts may be a new approach to inhibit scar hypertrophy [2]. Furthermore, effects in the scar formation depending of the arrangement in the extracellular matrix during a continous proteolytic cleavage of integrin alpha5 beta1 induced by retinoic acid, as is suggested to be an early phase of the atra-induced apoptotic process, are not clarified. [5]
Hoffman la Roche itself has reported "abnormal wound healing, delayed healing of exuberant granulation tissue with crusting" in association with (Ro)accutane exposure in human subjects [0]. A dogmatic, non-scientifically proven view held as a truth is that Roaccutane decreases scar-formation in the skin, but does not necessarily have to be correct and needs clarification. Some evidence is pointing rather at the opposite direction. An increased scar-formation in subjects exposed to retinoic acid in doses over 1 microM is here suggested to be possible due to retinoic acid induced changes in the extracellular matrix affecting the cell migration in the healing process.
Integrin Alpha5 beta1 was found to be increased in various human cell lines exposed to retinoic acid in low and high doses [1 and 4]. Integrins are cell membrane structures that link the cell membrane to the extracellular matrix [3].
Increased levels of the alpha5 beta1 integrin appears to have close relation to the formation and development of abnormal scars, and was found to be higher in hypertrophic scars than normal skin. To find a way to decrease the expression level of alpha5 beta1 integrin in fibroblasts may be a new approach to inhibit scar hypertrophy [2]. Furthermore, effects in the scar formation depending of the arrangement in the extracellular matrix during a continous proteolytic cleavage of integrin alpha5 beta1 induced by retinoic acid, as is suggested to be an early phase of the atra-induced apoptotic process, are not clarified. [5]