NGF-p75 and neuropsin/KLK8 pathways stimulate each other to cause hyperkeratosis and acanthosis in inflamed skin

J Dermatol Sci. 2012 Jul;67(1):71-3. doi: 10.1016/j.jdermsci.2012.03.008. Epub 2012 Mar 30.
No abstract available

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Dermatitis / etiology
  • Dermatitis / genetics
  • Dermatitis / metabolism*
  • Dermatitis / pathology
  • Disease Models, Animal
  • Epidermis / metabolism*
  • Epidermis / pathology
  • Gene Expression Regulation
  • Humans
  • Kallikreins / deficiency
  • Kallikreins / genetics
  • Kallikreins / metabolism*
  • Keratinocytes / metabolism
  • Keratosis / chemically induced
  • Keratosis / genetics
  • Keratosis / metabolism*
  • Keratosis / pathology
  • Melanosis / chemically induced
  • Melanosis / genetics
  • Melanosis / metabolism*
  • Melanosis / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nerve Growth Factor / metabolism*
  • RNA Interference
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Receptors, Nerve Growth Factor / deficiency
  • Receptors, Nerve Growth Factor / genetics
  • Receptors, Nerve Growth Factor / metabolism*
  • Sodium Dodecyl Sulfate
  • Transfection

Substances

  • NGF protein, human
  • RNA, Messenger
  • Receptors, Nerve Growth Factor
  • Ngfr protein, mouse
  • Sodium Dodecyl Sulfate
  • Nerve Growth Factor
  • KLK8 protein, human
  • Kallikreins
  • Prss19 protein, mouse