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J Invest Dermatol 2002 Dec;119(6):1237-43

Loss of cell adhesion in Dsg3bal-Pas mice with homozygous deletion mutation (2079del14) in the desmoglein 3 gene.


Pemphigus encompasses a group of autoimmune blistering diseases with circulating pathogenic autoantibodies recognizing several proteins, including the desmosomal cadherin, desmoglein 3. Targeted disruption of the Dsg3 gene by homologous recombination (Dsg3tm1stan) in mouse results in fragility of the skin and oral mucous membranes, analogous to the human disease. In addition, the Dsg3tm1stan mice develop phenotypic runting and hair loss, identical to that of the mouse mutant, Dsg3bal-2J. The Dsg3bal-2J mice are homozygous for a 1 bp insertion (2275insT) in the Dsg3 gene resulting in a nonfunctional Dsg3 mRNA. In this study, we characterized an allelic mutation, Dsg3bal-Pas, with clinical features similar to those in Dsg3bal-2J. We have identified a 14 bp deletion in exon 13 of the Dsg3 gene resulting in a frameshift and premature termination codon 7 bp downstream from the site of the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating virtually all of the intracellular domain. We demonstrate that, although a Dsg3 mRNA transcript was detectable in Dsg3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal epithelium of homozygous Dsg3bal-Pas compared with that of +/Dsg3bal-Pas mice. No significant changes in the expression of desmogleins 1 and 2 were detected. To elucidate a potential mechanism causing loss of cell adhesion in the Dsg3bal-Pas mice, we generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes. The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cytoplasm possibly due to increased proteolytic degradation. Cell surface staining was also detected but was jagged, not linear along the cell-cell border like that observed for the full-length desmoglein 3. The expression of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining of other desmosomal proteins, including desmoglein 1 and 2, plakophilin 2, and plakoglobin. In addition, the cells expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell morphology and exhibited striking extensive filopodia. Collectively, these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in disadhesion of keratinocytes manifested with blistering phenotype.


Dermatol Surg 2002 Sep;28(9):804-7

A random study of Asian male androgenetic alopecia in Bangkok, Thailand.


BACKGROUND: Androgenetic alopecia remains the most common cause of male pattern baldness (MPB) in all races. The prevalence of MPB in Caucasians is well documented. The prevalence of MPB in Asians is believed to be very low, only one-fourth to one-third on average compared to Caucasians. However, according to my previous study, there is a clear trend indicating that it is approaching that of Caucasians. OBJECTIVE: To assess the prevalence of MPB in the Asian population in Bangkok, Thailand; to compare this prevalence to previous studies conducted on Asians; and to compare the results to previous studies conducted on Caucasian. METHODS: This study was conducted by two physicians and assisted by two registered nurses. The questionnaire included age, sex, Norwood classification, diet, family history of baldness, income, and education. The physicians examined the scalp of each interviewee upon completion of each questionnaire. The ethnic focus group in this study was Thai and Chinese who reside in Bangkok, Thailand. The interviews were conducted in hospitals, nursing homes, classroom, medical meetings, temples, parks, and villages. RESULTS: A total of 1124 men were randomized in this study. The prevalence of cosmetically significant MPB (Norwood III-VII) was 38.52% and steadily increasing with age, approaching that of Caucasians. Variant MPB was found to be 0.67% and other types of androgenetic alopecia was 0.6%. From an ethnic point of view, the majority of the groups were of mixed blood and mostly of Chinese origin, thus we were unable to distinguish between Chinese and Thai. CONCLUSION: This study shows that the prevalence of MPB in Asians is not as low as previously thought. The cause of this increasing prevalence is uncertain. There are no past studies in Thailand for comparison, however, it can be extrapolated that the socioeconomic environment and westernized diet may contribute to this prevalence.


Oncology 2002;62(2):97-102

Effectiveness of the MSC cold cap system in the prevention of chemotherapy-induced alopecia.


OBJECTIVE: To study the effectiveness of the MSC cold cap system to prevent chemotherapy-induced alopecia. METHODS: The system was applied in 83 cancer patients (mean age 49.8 years) undergoing chemotherapy with alopecia-causing agents. Seven patients did not tolerate the system. Seventy-six patients were evaluable for assessment; 26 received anthracycline (group A), 33 taxane (group T), 5 anthracycline plus taxane (group AT), 7 intravenous etoposide (group E) and 5 ifosfamide with or without other alopecia-causing drugs (group I). In group A, 18 patients received conventional (subgroup Ac) and 8 high doses (subgroup Ah). In group T, 8 patients received docetaxel (subgroup D) and 25 paclitaxel (subgroup P). Alopecia grade 0-1 (Dean's system) was considered as treatment success. RESULTS: Grade 0-1 alopecia was achieved in 49/76 (64.5%) patients: group T 23/33 (69.6%), subgroup P 16/25 (64%) and subgroup D 7/8 (87.5%); group A 18/26 (69.2%), subgroup Ac 16/18 (88.8%) and subgroup Ah 2/8 (25%); group AT 1/5 (20%); group E 6/7 (85.7%), and group I 1/5 (20%). CONCLUSIONS: The MSC cold cap system is effective in preventing alopecia from anthracycline, etoposide or taxane but not from anthracycline-taxane combinations or ifosfamide-containing regimens.


Am J Pathol. 2003 Mar;162(3):803-14.

Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.


It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.


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Related Web resources:


  • What is hair?
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  • The phenomenon of hair loss.
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  • Alopecia info.
  • Alopecia treatment info.
  • Alopecia treatment info.
  • Hair care info.
  • Hair loss and alopecia research articles: abstracts and source links.



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