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trkA and trkC expression is increased in human diabetic skin
G Terenghi1, D Mann, P G Kopelman
1Blond McIndoe Centre, Queen Victoria Hospital, Sussex, UK. terenghi@dial.pipex.com
Neuroscience Letters
|May 30, 1997
Summary
Nerve growth factor (NGF) is reduced in diabetic skin, leading to sensory fiber dysfunction. Diabetic skin shows increased expression of trkA and trkC receptors in epidermal keratinocytes, possibly as a compensatory mechanism.
Area of Science:
- Dermatology
- Neuroscience
- Molecular Biology
Background:
- Nerve growth factor (NGF) reduction in diabetic skin keratinocytes is linked to sensory fiber dysfunction.
- Keratinocytes express NGF and trkA receptors, potentially via an autocrine loop.
- In vivo trkA expression in normal and diabetic skin keratinocytes remains uncharacterized.
Purpose of the Study:
- To quantify in vivo trkA and trkC receptor expression in epidermal keratinocytes of normal and diabetic human skin.
- To investigate potential changes in neurotrophin receptor expression in early subclinical diabetic neuropathy.
Main Methods:
- In situ hybridization was used to measure trkA and trkC mRNA expression in calf skin biopsies.
- Image analysis quantification determined the density of hybridization signals.
- Biopsies were obtained from patients with early subclinical diabetic neuropathy and control subjects.
Main Results:
- Both trkA and trkC receptors were detected throughout the epidermis in control skin.
- Diabetic epidermis showed a significant increase in trkA expression (P < 0.001).
- Diabetic epidermis also exhibited a significant increase in trkC expression (P < 0.001).
Conclusions:
- Epidermal trkA and trkC receptor expression is upregulated in diabetic skin.
- This upregulation may be a compensatory response to decreased autocrine neurotrophin signaling.
- Findings suggest a complex neurotrophin-keratinocyte interaction in diabetic neuropathy.