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An analysis of gene expression data involving examination of signaling pathways activation reveals new insights into the mechanism of action of minoxidil topical foam in men with androgenetic alopecia
Authors:
Stamatas, Georgios N.1
Wu, Jeff2
Pappas, Apostolos3
Mirmirani, Paradi4
McCormick, Thomas S.5
Cooper, Kevin D.5
Consolo, Mary5
Schastnaya, Jane6
Ozerov, Ivan V.6
Aliper, Alexander6
Zhavoronkov, Alex6
Source:
Cell Cycle; September 2017, Vol. 16 Issue: Number 17 p1578-1584, 7p
ISSN:
15384101; 15514005
Author Affiliations:
1Emerging Science & Innovation, Johnson & Johnson Santé Beauté France, Johnson & Johnson Group of Consumer Companies
2Hair Care R&D, Johnson & Johnson Consumer Worldwide, Johnson & Johnson Family of Consumer Companies, Inc.
3Emerging Science & Innovation, Johnson & Johnson Consumer Worldwide, Johnson & Johnson Family of Consumer Companies, Inc.
4Department of Dermatology, The Permanente Medical Group
5Department of Dermatology, Case Western Reserve University, University Hospitals Cleveland Medical Center
6Insilico Medicine, Inc., Emerging Technology Centers, Johns Hopkins University at Eastern
Abstract:
Androgenetic alopecia is the most common form of hair loss. Minoxidil has been approved for the treatment of hair loss, however its mechanism of action is still not fully clarified. In this study, we aimed to elucidate the effects of 5% minoxidil topical foam on gene expression and activation of signaling pathways in vertex and frontal scalp of men with androgenetic alopecia. We identified regional variations in gene expression and perturbed signaling pathways using in silicoPathway Activation Network Decomposition Analysis (iPANDA) before and after treatment with minoxidil. Vertex and frontal scalp of patients showed a generally similar response to minoxidil. Both scalp regions showed upregulation of genes that encode keratin associated proteins and downregulation of ILK, Akt, and MAPK signaling pathways after minoxidil treatment. Our results provide new insights into the mechanism of action of minoxidil topical foam in men with androgenetic alopecia.
Entry Date:
20170908
LC Classification:
20149; 10015
Accession Number:
43119896
Authors:
Stamatas, Georgios N.1
Wu, Jeff2
Pappas, Apostolos3
Mirmirani, Paradi4
McCormick, Thomas S.5
Cooper, Kevin D.5
Consolo, Mary5
Schastnaya, Jane6
Ozerov, Ivan V.6
Aliper, Alexander6
Zhavoronkov, Alex6
Source:
Cell Cycle; September 2017, Vol. 16 Issue: Number 17 p1578-1584, 7p
ISSN:
15384101; 15514005
Author Affiliations:
1Emerging Science & Innovation, Johnson & Johnson Santé Beauté France, Johnson & Johnson Group of Consumer Companies
2Hair Care R&D, Johnson & Johnson Consumer Worldwide, Johnson & Johnson Family of Consumer Companies, Inc.
3Emerging Science & Innovation, Johnson & Johnson Consumer Worldwide, Johnson & Johnson Family of Consumer Companies, Inc.
4Department of Dermatology, The Permanente Medical Group
5Department of Dermatology, Case Western Reserve University, University Hospitals Cleveland Medical Center
6Insilico Medicine, Inc., Emerging Technology Centers, Johns Hopkins University at Eastern
Abstract:
Androgenetic alopecia is the most common form of hair loss. Minoxidil has been approved for the treatment of hair loss, however its mechanism of action is still not fully clarified. In this study, we aimed to elucidate the effects of 5% minoxidil topical foam on gene expression and activation of signaling pathways in vertex and frontal scalp of men with androgenetic alopecia. We identified regional variations in gene expression and perturbed signaling pathways using in silicoPathway Activation Network Decomposition Analysis (iPANDA) before and after treatment with minoxidil. Vertex and frontal scalp of patients showed a generally similar response to minoxidil. Both scalp regions showed upregulation of genes that encode keratin associated proteins and downregulation of ILK, Akt, and MAPK signaling pathways after minoxidil treatment. Our results provide new insights into the mechanism of action of minoxidil topical foam in men with androgenetic alopecia.
Entry Date:
20170908
LC Classification:
20149; 10015
Accession Number:
43119896