J Invest Dermatol. 2003 Dec; 121(6): 1544-51. Related Articles, Links
Click here to read
Expression and activity of arginase isoenzymes during normal and
diabetes-impaired skin repair.
Kampfer H, Pfeilschifter J, Frank S.
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang
Goethe-Universitat, Frankfurt am Main, Germany.
Within the past years, an important role for nitric oxide (NO) in
skin repair has been well defined. As NO is synthesized from L-arginine
by NO synthases (NOS), the availability of L-arginine might be one
rate-limiting factor of NO production at the wound site. Upon injury,
arginase-1 and -2 mRNA, protein, and activity were strongly induced
reaching a maximum between day 3 and day 7 postwounding.
Immunohistochemistry colocalized both arginases and the inducible NOS
(iNOS) at epithelial sites at the margins of the wound. Notably,
diabetes-impaired skin repair in leptin-deficient mice
(diabetes/diabetes, db/db; and obese/obese, ob/ob) was characterized by
an abnormally elevated arginase activity in wound tissue in the absence
of an expression of iNOS. Expression analyses demonstrated that
arginase-1 contributed to increased arginase activities in impaired
repair. Interestingly, an improved healing of chronic wound situations
in leptin-supplemented ob/ob mice was strongly associated with an
adjustment of the dysregulated expression of L-arginine-converting
enzymes: an attenuated iNOS expression was upregulated early in repair
and an augmented arginase-1 expression and activity was downregulated in
the presence of markedly elevated numbers of macrophages during late
repair. These data suggest a coordinated consumption of L-arginine by
the NOS and arginase enzymatic pathways at the wound site as a
prerequisite for a balanced NO (via iNOS) and polyamine (via arginases)
synthesis that drives a normal skin repair.
PMID: 14675208 [PubMed - in process]
Altern Med Rev. 2003 Nov; 8(4): 359-77. Related Articles, Links
Nutritional support for wound healing.
MacKay D, Miller AL.
Thorne Research, Inc., PO Box 25, Dover, ID 83825, USA.
duffy@thorne.com
Healing of wounds, whether from accidental injury or surgical
intervention, involves the activity of an intricate network of blood
cells, tissue types, cytokines, and growth factors. This results in
increased cellular activity, which causes an intensified metabolic
demand for nutr
Click here to read
Expression and activity of arginase isoenzymes during normal and
diabetes-impaired skin repair.
Kampfer H, Pfeilschifter J, Frank S.
Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang
Goethe-Universitat, Frankfurt am Main, Germany.
Within the past years, an important role for nitric oxide (NO) in
skin repair has been well defined. As NO is synthesized from L-arginine
by NO synthases (NOS), the availability of L-arginine might be one
rate-limiting factor of NO production at the wound site. Upon injury,
arginase-1 and -2 mRNA, protein, and activity were strongly induced
reaching a maximum between day 3 and day 7 postwounding.
Immunohistochemistry colocalized both arginases and the inducible NOS
(iNOS) at epithelial sites at the margins of the wound. Notably,
diabetes-impaired skin repair in leptin-deficient mice
(diabetes/diabetes, db/db; and obese/obese, ob/ob) was characterized by
an abnormally elevated arginase activity in wound tissue in the absence
of an expression of iNOS. Expression analyses demonstrated that
arginase-1 contributed to increased arginase activities in impaired
repair. Interestingly, an improved healing of chronic wound situations
in leptin-supplemented ob/ob mice was strongly associated with an
adjustment of the dysregulated expression of L-arginine-converting
enzymes: an attenuated iNOS expression was upregulated early in repair
and an augmented arginase-1 expression and activity was downregulated in
the presence of markedly elevated numbers of macrophages during late
repair. These data suggest a coordinated consumption of L-arginine by
the NOS and arginase enzymatic pathways at the wound site as a
prerequisite for a balanced NO (via iNOS) and polyamine (via arginases)
synthesis that drives a normal skin repair.
PMID: 14675208 [PubMed - in process]
Altern Med Rev. 2003 Nov; 8(4): 359-77. Related Articles, Links
Nutritional support for wound healing.
MacKay D, Miller AL.
Thorne Research, Inc., PO Box 25, Dover, ID 83825, USA.
duffy@thorne.com
Healing of wounds, whether from accidental injury or surgical
intervention, involves the activity of an intricate network of blood
cells, tissue types, cytokines, and growth factors. This results in
increased cellular activity, which causes an intensified metabolic
demand for nutr