Proteomic profiling reveals candidate markers for arsenic-induced skin keratosis

Zhiling Guo, Qin Hu, Jijing Tian, Li Yan, Chuanyong Jing, Heidi Qunhui Xie, Wenjun Bao, Robert H. Rice, Bin Zhao, Guibin Jiang

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Proteomics technology is an attractive biomarker candidate discovery tool that can be applied to study large sets of biological molecules. To identify novel biomarkers and molecular targets in arsenic-induced skin lesions, we have determined the protein profile of arsenic-affected human epidermal stratum corneum by shotgun proteomics. Samples of palm and foot sole from healthy subjects were analyzed, demonstrating similar protein patterns in palm and sole. Samples were collected from the palms of subjects with arsenic keratosis (lesional and adjacent non-lesional samples) and arsenic-exposed subjects without lesions (normal). Samples from non-exposed healthy individuals served as controls. We found that three proteins in arsenic-exposed lesional epidermis were consistently distinguishably expressed from the unaffected epidermis. One of these proteins, the cadherin-like transmembrane glycoprotein, desmoglein 1 (DSG1) was suppressed. Down-regulation of DSG1 may lead to reduced cell-cell adhesion, resulting in abnormal epidermal differentiation. The expression of keratin 6c (KRT6C) and fatty acid binding protein 5 (FABP5) were significantly increased. FABP5 is an intracellular lipid chaperone that plays an essential role in fatty acid metabolism in human skin. This raises a possibility that overexpression of FABP5 may affect the proliferation or differentiation of keratinocytes by altering lipid metabolism. KRT6C is a constituent of the cytoskeleton that maintains epidermal integrity and cohesion. Abnormal expression of KRT6C may affect its structural role in the epidermis. Our findings suggest an important approach for future studies of arsenic-mediated toxicity and skin cancer, where certain proteins may represent useful biomarkers of early diagnoses in high-risk populations and hopefully new treatment targets. Further studies are required to understand the biological role of these markers in skin pathogenesis from arsenic exposure.

Original languageEnglish (US)
Pages (from-to)34-38
Number of pages5
JournalEnvironmental Pollution
Volume218
DOIs
StatePublished - Nov 1 2016

Fingerprint

Keratosis
Arsenic
Proteomics
Skin
Keratin
Fatty acids
Fatty Acid-Binding Proteins
Proteins
Biomarkers
Keratins
Desmoglein 1
Epidermis
Glycoproteins
Cell adhesion
Firearms
Skin Neoplasms
Cadherins
Cytoskeleton
Keratinocytes
Lipid Metabolism

Keywords

  • Arsenic
  • Biomarker
  • Human epidermis
  • Proteomic
  • Skin keratosis

ASJC Scopus subject areas

  • Toxicology
  • Pollution
  • Health, Toxicology and Mutagenesis

Cite this

Proteomic profiling reveals candidate markers for arsenic-induced skin keratosis. / Guo, Zhiling; Hu, Qin; Tian, Jijing; Yan, Li; Jing, Chuanyong; Xie, Heidi Qunhui; Bao, Wenjun; Rice, Robert H.; Zhao, Bin; Jiang, Guibin.

In: Environmental Pollution, Vol. 218, 01.11.2016, p. 34-38.

Research output: Contribution to journalArticle

Guo, Z, Hu, Q, Tian, J, Yan, L, Jing, C, Xie, HQ, Bao, W, Rice, RH, Zhao, B & Jiang, G 2016, 'Proteomic profiling reveals candidate markers for arsenic-induced skin keratosis', Environmental Pollution, vol. 218, pp. 34-38. https://doi.org/10.1016/j.envpol.2016.08.035
Guo, Zhiling ; Hu, Qin ; Tian, Jijing ; Yan, Li ; Jing, Chuanyong ; Xie, Heidi Qunhui ; Bao, Wenjun ; Rice, Robert H. ; Zhao, Bin ; Jiang, Guibin. / Proteomic profiling reveals candidate markers for arsenic-induced skin keratosis. In: Environmental Pollution. 2016 ; Vol. 218. pp. 34-38.
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AU - Xie, Heidi Qunhui

AU - Bao, Wenjun

AU - Rice, Robert H.

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AB - Proteomics technology is an attractive biomarker candidate discovery tool that can be applied to study large sets of biological molecules. To identify novel biomarkers and molecular targets in arsenic-induced skin lesions, we have determined the protein profile of arsenic-affected human epidermal stratum corneum by shotgun proteomics. Samples of palm and foot sole from healthy subjects were analyzed, demonstrating similar protein patterns in palm and sole. Samples were collected from the palms of subjects with arsenic keratosis (lesional and adjacent non-lesional samples) and arsenic-exposed subjects without lesions (normal). Samples from non-exposed healthy individuals served as controls. We found that three proteins in arsenic-exposed lesional epidermis were consistently distinguishably expressed from the unaffected epidermis. One of these proteins, the cadherin-like transmembrane glycoprotein, desmoglein 1 (DSG1) was suppressed. Down-regulation of DSG1 may lead to reduced cell-cell adhesion, resulting in abnormal epidermal differentiation. The expression of keratin 6c (KRT6C) and fatty acid binding protein 5 (FABP5) were significantly increased. FABP5 is an intracellular lipid chaperone that plays an essential role in fatty acid metabolism in human skin. This raises a possibility that overexpression of FABP5 may affect the proliferation or differentiation of keratinocytes by altering lipid metabolism. KRT6C is a constituent of the cytoskeleton that maintains epidermal integrity and cohesion. Abnormal expression of KRT6C may affect its structural role in the epidermis. Our findings suggest an important approach for future studies of arsenic-mediated toxicity and skin cancer, where certain proteins may represent useful biomarkers of early diagnoses in high-risk populations and hopefully new treatment targets. Further studies are required to understand the biological role of these markers in skin pathogenesis from arsenic exposure.

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