References: Hair growth and hair loss
Genetics. 1997 Aug;146(4):1407-15.
Genetic studies of the mouse mutations mahogany and mahoganoid.
Miller KA, Gunn TM, Carrasquillo MM, Lamoreux ML, Galbraith DB, Barsh GS.
Department of Pediatrics, Stanford University School of Medicine, California 94305-5428, USA.
The mouse mutations mahogany (mg) and mahoganoid (md) are negative modifiers of the Agouti coat color gene, which encodes a paracrine signaling molecule that induces a swithc in melanin synthesis from eumelanin to pheomelanin. Animals mutant for md or mg synthesize very little or no pheomelanin depending on Agouti gene background. The Agouti protein is normally expressed in the skin and acts as an antagonist of the melanocyte receptor for alpha-MSH (Mc1r); however, ectopic expression of Agouti causes obesity, possibly by antagonizing melanocortin receptors expressed in the brain. To investigate where md and mg lie in a genetic pathway with regard to Agouti and Mc1r signaling, we determined the effects of these mutations in animals that carried either a loss-of-function Mc1r mutation (recessive yellow, Mc1re) or a gain-of-function Agouti mutation (lethal yellow, Ay). We found that the Mc1re mutation suppressed the effects of md and mg, but that md and mg suppressed the effects of Ay on both coat color and obesity. Plasma levels of alpha-MSH and of ACTH were unaffected by md or mg. These results suggest that md and mg interfere directly with Agouti signaling, possibly at the level of protein production or receptor regulation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9258683&dopt=Abstract
kids.wustl.edu
A technique has been developed for preparing the mouse temporal bone for histopathological examination: first, as a whole mount to detect any gross malformations of the bony or membranous labyrinths; second, in dissected segments to localize damage in the different sensory organs and to quantify sensory- and supporting-cell losses; and finally, in semi-thick and thin sections to identify and characterize subcellular pathology. Examples are given of the successful application of this technique to mice with very different inner-ear problems, including those with an abnormally short cochlear spiral, a defective lateral semicircular canal, abnormal otoliths over the saccular macula, an increased susceptibility to noise damage and those which lack fibroblast growth factor receptor 3.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9259234&dopt=Abstract
Int J Dev Neurosci. 1997 Jul;15(4-5):417-32.
Calbindin and parvalbumin are early markers of non-mitotically regenerating hair cells in the bullfrog vestibular otolith organs.
Steyger PS, Burton M, Hawkins JR, Schuff NR, Baird RA.
R. S. Dow Neurological Sciences Institute, Legacy Good Samaritan Hospital, Portland, OR 97209, USA.
Earlier studies have demonstrated hair cell regeneration in the absence of cell proliferation, and suggested that supporting cells could phenotypically convert into hair cells following hair cell loss. Because calcium-binding proteins are involved in gene up-regulation, cell growth, and cell differentiation, we wished to determine if these proteins were up-regulated in scar formations and regenerating hair cells following gentamicin treatment. Calbindin and parvalbumin immunolabeling was examined in control or gentamicin-treated (GT) bullfrog saccular and utricular explants cultured for 3 days in amphibian culture medium or amphibian culture medium supplemented with aphidicolin, a blocker of nuclear DNA replication in eukaryotic cells. In control cultures, calbindin and parvalbumin immunolabeled the hair bundles and, less intensely, the cell bodies of mature hair cells. In GT or mitotically-blocked GT (MBGT) cultures, calbindin and parvalbumin immunolabeling was also seen in the hair bundles, cuticular plates, and cell bodies of hair cells with immature hair bundles. Thus, these antigens were useful markers for both normal and regenerating hair cells. Supporting cell immunolabeling was not seen in control cultures nor in the majority of supporting cells in GT cultures. In MBGT cultures, calbindin and parvalbumin immunolabeling was up-regulated in the cytosol of single supporting cells participating in scar formations and in supporting cells with hair cell-like characteristics. These data provide further evidence that non-mitotic hair cell regeneration in cultures can be accomplished by the conversion of supporting cells into hair cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9263023&dopt=Abstract
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