Posters
Fatty acid accumulation in hair follicle induce Alopecia
Presentation Type
Poster
Discipline Track
Clinical Science
Abstract Type
Research/Clinical
Abstract
Background: Hair is an essential indicator of individual characteristics such as self-image, identity, ethnicity, and health. Loss of hair from any part of the body for any reason is called alopecia. The alopecia is of two kinds, scarring alopecia and non-scarring alopecia. The scarring alopecia is divided into three types depending upon the inflammatory cell presence: lymphocytic, neutrophilic, and mixed. Scarring alopecia’s is typically caused by inflammation, resulting in the hair follicle's destruction leading to irreversible hair loss. The etiology and pathogenesis of PCA remain unclear, but PCA is currently treated as an inflammatory disorder. The treatment options for PCA are limited and are not very effective in controlling the disease progression.
Methods: One of the previous studies elucidated that sterol intermediate of cholesterol biosynthesis initiates inflammation. At an earlier study, the gene expression profile identified that abnormalities of lipid metabolism and sterol intermediates accumulation underlie the pathogenesis of PCA. Here we performed a metabolomics approach to identify metabolites unique to the lymphocytic PCA, frontal fibrosing alopecia (FFA), and the K14-aryl hydrocarbon receptor (K14-AhR-CA) mouse model.
Results: Global metabolomics profiles of unaffected and affected FFA scalp biopsies and skin biopsies from K14-AhR-CA mice and wild-type littermates (Week 0-9) were generated on GC/MS and LC/MS/MS platforms. The earliest change in the K14 –AhR mouse was the accumulation of fatty acids like behenate, lignoceric, and hexacosanaoate. Interestingly, a pile of fatty acid caproate and laurate were more in scalp biopsies. This revealed the changes in mitochondrial metabolism in the FFA patients and the transgenic mice. Decreased glutathione (GSH) and elevated levels of oxidized glutathione (GSSG) were also observed in FFA samples and the K14-AhR mice, suggesting that mitochondrial impairment and lowered energy metabolism an indicators of early disease pathogenesis. The accumulation of fatty acid and the oxidative stress response were observed before the loss of stem cells and the onset of inflammation in the K14-AhR mouse model and FFA samples.
Conclusion: Our data suggest that the accumulation of fatty acids evokes oxidative stress, promotes inflammation and cell death in the hair follicle and leads to alopecia.
Academic/Professional Position
Faculty
Recommended Citation
Panicker, Sreejith Parameswara, "Fatty acid accumulation in hair follicle induce Alopecia" (2023). Research Symposium. 115.
https://scholarworks.utrgv.edu/somrs/theme1/posters/115
Fatty acid accumulation in hair follicle induce Alopecia
Background: Hair is an essential indicator of individual characteristics such as self-image, identity, ethnicity, and health. Loss of hair from any part of the body for any reason is called alopecia. The alopecia is of two kinds, scarring alopecia and non-scarring alopecia. The scarring alopecia is divided into three types depending upon the inflammatory cell presence: lymphocytic, neutrophilic, and mixed. Scarring alopecia’s is typically caused by inflammation, resulting in the hair follicle's destruction leading to irreversible hair loss. The etiology and pathogenesis of PCA remain unclear, but PCA is currently treated as an inflammatory disorder. The treatment options for PCA are limited and are not very effective in controlling the disease progression.
Methods: One of the previous studies elucidated that sterol intermediate of cholesterol biosynthesis initiates inflammation. At an earlier study, the gene expression profile identified that abnormalities of lipid metabolism and sterol intermediates accumulation underlie the pathogenesis of PCA. Here we performed a metabolomics approach to identify metabolites unique to the lymphocytic PCA, frontal fibrosing alopecia (FFA), and the K14-aryl hydrocarbon receptor (K14-AhR-CA) mouse model.
Results: Global metabolomics profiles of unaffected and affected FFA scalp biopsies and skin biopsies from K14-AhR-CA mice and wild-type littermates (Week 0-9) were generated on GC/MS and LC/MS/MS platforms. The earliest change in the K14 –AhR mouse was the accumulation of fatty acids like behenate, lignoceric, and hexacosanaoate. Interestingly, a pile of fatty acid caproate and laurate were more in scalp biopsies. This revealed the changes in mitochondrial metabolism in the FFA patients and the transgenic mice. Decreased glutathione (GSH) and elevated levels of oxidized glutathione (GSSG) were also observed in FFA samples and the K14-AhR mice, suggesting that mitochondrial impairment and lowered energy metabolism an indicators of early disease pathogenesis. The accumulation of fatty acid and the oxidative stress response were observed before the loss of stem cells and the onset of inflammation in the K14-AhR mouse model and FFA samples.
Conclusion: Our data suggest that the accumulation of fatty acids evokes oxidative stress, promotes inflammation and cell death in the hair follicle and leads to alopecia.