Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle...

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Published inAustralasian journal of dermatology Vol. 62; no. 1; pp. e29 - e34
Main Authors Marie, Radwa El‐ Sayed Mahmoud, Abd El‐ Fadeal, Noha M, Atef, Lina M
Format Journal Article
LanguageEnglish
Published Australia Wiley Subscription Services, Inc 01.02.2021
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Abstract Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self‐reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild‐type p53. Aim The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients. Methods The mRNA tissue expression of survivin and p53 was measured by quantitative real‐time polymerase chain reaction in lesional and non‐lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects. Results The study showed higher mRNA expression of survivin in lesional biopsies compared to non‐lesional (P < 0.001) and control biopsies (P = 0.001). In non‐lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non‐lesional biopsies relative to control biopsies. However, the difference was only significant in non‐lesional biopsies (P = 0.017). Conclusion Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.
AbstractList Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self‐reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild‐type p53. Aim The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients. Methods The mRNA tissue expression of survivin and p53 was measured by quantitative real‐time polymerase chain reaction in lesional and non‐lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects. Results The study showed higher mRNA expression of survivin in lesional biopsies compared to non‐lesional (P < 0.001) and control biopsies (P = 0.001). In non‐lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non‐lesional biopsies relative to control biopsies. However, the difference was only significant in non‐lesional biopsies (P = 0.017). Conclusion Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.
Alopecia areata is a common non-scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self-reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild-type p53. The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients. The mRNA tissue expression of survivin and p53 was measured by quantitative real-time polymerase chain reaction in lesional and non-lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects. The study showed higher mRNA expression of survivin in lesional biopsies compared to non-lesional (P < 0.001) and control biopsies (P = 0.001). In non-lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non-lesional biopsies relative to control biopsies. However, the difference was only significant in non-lesional biopsies (P = 0.017). Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.
Alopecia areata is a common non-scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self-reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild-type p53.BACKGROUNDAlopecia areata is a common non-scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self-reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild-type p53.The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients.AIMThe aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients.The mRNA tissue expression of survivin and p53 was measured by quantitative real-time polymerase chain reaction in lesional and non-lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects.METHODSThe mRNA tissue expression of survivin and p53 was measured by quantitative real-time polymerase chain reaction in lesional and non-lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects.The study showed higher mRNA expression of survivin in lesional biopsies compared to non-lesional (P < 0.001) and control biopsies (P = 0.001). In non-lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non-lesional biopsies relative to control biopsies. However, the difference was only significant in non-lesional biopsies (P = 0.017).RESULTSThe study showed higher mRNA expression of survivin in lesional biopsies compared to non-lesional (P < 0.001) and control biopsies (P = 0.001). In non-lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non-lesional biopsies relative to control biopsies. However, the difference was only significant in non-lesional biopsies (P = 0.017).Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.CONCLUSIONOur results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.
BackgroundAlopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self‐reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild‐type p53.AimThe aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients.MethodsThe mRNA tissue expression of survivin and p53 was measured by quantitative real‐time polymerase chain reaction in lesional and non‐lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects.ResultsThe study showed higher mRNA expression of survivin in lesional biopsies compared to non‐lesional (P < 0.001) and control biopsies (P = 0.001). In non‐lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non‐lesional biopsies relative to control biopsies. However, the difference was only significant in non‐lesional biopsies (P = 0.017).ConclusionOur results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.
Author Abd El‐ Fadeal, Noha M
Atef, Lina M
Marie, Radwa El‐ Sayed Mahmoud
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2020 The Australasian College of Dermatologists.
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Keywords alopecia areata
survivin
p53
Language English
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Notes Conflicts of Interest: none. The study was conducted in accordance with the guidelines of the Helsinki Declaration. The study had the approval of the local Institutional Review board and the Research Ethical Committee of Faculty of Medicine, Suez Canal University. All participants filled a written informed consent prior to participation in the study.
Funding Statement: none.
Radwa E M Marie, MD. Noha M Abd El‐Fadeal, MD. Lina M Atef, MD.
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Snippet Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune...
Alopecia areata is a common non-scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack...
BackgroundAlopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune...
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wiley
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SubjectTerms Alopecia
alopecia areata
Apoptosis
Autoimmune diseases
Baldness
Biopsy
Cell cycle
Follicles
Gene expression
Hair
Immune privilege
Immunoregulation
Keratinocytes
Lymphocytes B
Lymphocytes T
p53
p53 Protein
Polymerase chain reaction
Scalp
Survivin
Transcription
Tumor suppressor genes
Tumors
Title Expression of survivin and p53 genes in patients with alopecia areata: A case–control study
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fajd.13433
https://www.ncbi.nlm.nih.gov/pubmed/32951213
https://www.proquest.com/docview/2489135378
https://www.proquest.com/docview/2444607482
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