References: Hair growth and hair loss
J Invest Dermatol. 1999 May;112(5):788-95.
Spatial and temporal expression of parathyroid hormone-related protein during wound healing.
Blomme EA, Zhou H, Kartsogiannis V, Capen CC, Rosol TJ.
Department of Veterinary Biosciences, The Ohio State University, Columbus 43210, USA.
Parathyroid hormone-related protein is produced by many normal tissues including the skin, where it regulates growth and differentiation of keratinocytes. To define better the role of parathyroid hormone-related protein in the skin, we investigated the spatial and temporal expression of parathyroid hormone-related protein and mRNA by immunohistochemistry and in situ hybridization during the healing of skin wounds, and the effects of topical administration of a parathyroid hormone-related protein agonist [parathyroid hormone-related protein (1-36)] and a parathyroid hormone-related protein antagonist [parathyroid hormone (7-34)] on the healing rate and morphology of the wounds. Wounds were produced on the back of guinea pigs with a 4 mm punch, and wound sites were collected at different time points during the healing process. Parathyroid hormone-related protein was expressed in normal skin by all viable keratinocyte layers, hair follicles, and adnexae. Following injury, migratory keratinocytes at wound margins and the newly restored epidermis expressed increased levels of parathyroid hormone-related protein. The remodeling phase was associated with progressive restoration of the pattern of parathyroid hormone-related protein expression in normal epidermis. Granulation tissue myofibroblasts and infiltrating macrophages also expressed parathyroid hormone-related protein. In vitro studies using THP-1 cells (a promonocytic cell line) confirmed that macrophages expressed parathyroid hormone-related protein, especially after activation. Topical application of parathyroid hormone related protein (1-36) or parathyroid hormone (7-34) did not result in significant changes in the healing rate and morphology of the wounds. These findings demonstrated that, in addition to keratinocytes, myofibroblasts and macrophages also represent sources of parathyroid hormone-related protein during the healing of skin wounds. Although the data suggest a role for parathyroid hormone-related protein in the healing of skin and in the restoration of epidermal homeostasis, parathyroid hormone-related protein does not appear to be required for proper re-epithelialization in response to injury, potentially because of redundancy in epidermal growth and wound healing, as has been shown for other paracrine and autocrine growth factors of the epidermis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233773&dopt=Abstract
Genetics. 1990 Jun;125(2):421-30.
Interaction of the murine dilute suppressor gene (dsu) with fourteen coat color mutations.
Moore KJ, Swing DA, Copeland NG, Jenkins NA.
Mammalian Genetics Laboratory, NCI-Frederick Cancer Research Facility, Maryland 21701.
The murine dilute suppressor gene, dsu, was previously shown to suppress the dilute coat color phenotypes of mice homozygous for the dilute (d), leaden (ln), and ashen (ash) mutations. Each of these mutations produce adendritic melanocytes, which results in an abnormal transportation of pigment granules into the hair shaft and a diluted coat color. The suppression of each mutation is associated with the restoration of near normal melanocyte morphology, indicating that dsu can compensate for the absence of normal d, ln and ash gene products. In experiments described here, we have determined whether dsu can suppress the coat color phenotype of 14 additional mutations, at 11 loci, that affect coat color by mechanisms other than alterations in melanocyte morphology. In no case was dsu able to suppress the coat color phenotype of these 14 mutations. This suggests that dsu acts specifically on coat color mutations that result from an abnormal melanocyte morphology. Unexpectedly, dsu suppressed the ruby eye color of ruby-eye (ru) and ruby-eye-2 (ru-2) mice, to black. The exact nature of the defect producing these two mutant phenotypes is unknown. Histological examination of the pigmented tissues of the eyes of these mice indicated that dsu suppresses the eye color by increasing the overall level of pigmentation in the choroid but not the retinal pigmented epithelium. Choroid melanocytes, like those in the skin, are derived from the neural crest while melanocytes in the retinal pigmented epithelium are derived from the optic cup. This suggests that dsu may act specifically on neural crest-derived melanocytes. These studies have thus identified a second group of genes whose phenotypes are suppressed by dsu and have provided new insights into the mechanism of action of dsu.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2379821&dopt=Abstract
Vestn Dermatol Venerol. 1990;(5):44-7.
[The clinico-dermatological and morphological characteristics of the hair involvement in children with chemical poisoning]
[Article in Russian]
Pavlov IuV, Alisievich VI, Grebeniuk VN, Mazitova LP.
A syndromal condition, transitory neuropsychic symptoms and signs of catarrhal inflammation of upper respiratory tract mucosae and alopecia, develop in children with symptoms of chemical poisoning due to exposure to heavy metal salts. Electron microscopy shows changes that evidence a high incidence of dying and dead hair. Alopecia was more frequently subtotal and there was a tendency to hair growth restoration after the cause of the condition was removed and prophylactic measures carried out.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2402942&dopt=Abstract
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