Nitric oxide: a key mediator in cutaneous physiology

Weller, R.

Oxford, UK : Blackwell Science Ltd
Published 2003
ISSN:
1365-2230
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
Type of Medium:
Electronic Resource
URL:
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autor Weller, R.
book_url http://dx.doi.org/10.1046/j.1365-2230.2003.01365.x
datenlieferant nat_lic_papers
hauptsatz hsatz_simple
identnr NLZ242588921
insertion_date 2012-04-27
issn 1365-2230
journal_name Clinical and experimental dermatology
materialart 1
notes Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
package_name Blackwell Publishing
publikationsjahr_anzeige 2003
publikationsjahr_facette 2003
publikationsjahr_intervall 7999:2000-2004
publikationsjahr_sort 2003
publikationsort Oxford, UK
publisher Blackwell Science Ltd
reference 28 (2003), S. 0
search_space articles
shingle_author_1 Weller, R.
shingle_author_2 Weller, R.
shingle_author_3 Weller, R.
shingle_author_4 Weller, R.
shingle_catch_all_1 Weller, R.
Nitric oxide: a key mediator in cutaneous physiology
Blackwell Science Ltd
Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
1365-2230
13652230
shingle_catch_all_2 Weller, R.
Nitric oxide: a key mediator in cutaneous physiology
Blackwell Science Ltd
Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
1365-2230
13652230
shingle_catch_all_3 Weller, R.
Nitric oxide: a key mediator in cutaneous physiology
Blackwell Science Ltd
Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
1365-2230
13652230
shingle_catch_all_4 Weller, R.
Nitric oxide: a key mediator in cutaneous physiology
Blackwell Science Ltd
Summary Nitric oxide (NO) is a free radical synthesized from l-arginine by a family of NO synthase (NOS) enzymes, all of which are present in the skin, and also by reduction of sweat nitrate. NO synthesis is regulated by NOS activation (eNOS and nNOS) or synthesis (iNOS) and by substrate availability. Elevated arginase concentrations in psoriatic skin suggest that substrate competition may affect NO production. The balance of NO and reactive oxygen species is probably also important in regulating the biological actions of NO. The physiological functions of NO in the skin are being elaborated. NO release is increased following exposure to ultraviolet radiation (UVR); in eNOS null mice, dermal and epidermal apoptosis following UVR exposure is increased. Experiments in which keratinocytes and melanocytes were cocultured show melanogenesis being dependent on keratinocyte-generated NO, and UVR-induced guinea pig pigmentation is delayed following application of a NOS antagonist to the skin. Wound healing is delayed in eNOS and iNOS null mice.
1365-2230
13652230
shingle_title_1 Nitric oxide: a key mediator in cutaneous physiology
shingle_title_2 Nitric oxide: a key mediator in cutaneous physiology
shingle_title_3 Nitric oxide: a key mediator in cutaneous physiology
shingle_title_4 Nitric oxide: a key mediator in cutaneous physiology
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titel Nitric oxide: a key mediator in cutaneous physiology
titel_suche Nitric oxide: a key mediator in cutaneous physiology
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