Amyloidosis cutis dyschromica. DNA repair reduction in the cellular response to UV light

Moriwaki, Shinichi

doi:10.1001/archderm.128.7.966

Cited by 31 publications

(46 citation statements)

References 13 publications

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“…10 Qiao et al in his series has convincingly shown 100% positivity to immunohistochemical staining for keratin, CK34 E12 and CK5/6, that the amyloid is thought to be of epidermal origin. 6 This finding seems to agree with the work of Moriwaki et al 9 that points at a disturbance of keratinocyte repairs after irradiation with ultraviolet. At the third month, some improvement was obtained in our patient as the mottled pigmentation became lightened.…”

Section: Discussionsupporting

confidence: 90%

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Familial amyloidosis cutis dyschromica in three siblings: report from Indonesia

2014

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Amyloidosis cutis dyschromica (ACD) is an extremely rare type of primary cutaneous amyloidosis. To date there are fewer than 40 published cases worldwide; some were reported affecting several family members. Its resemblance to other common pigmentation disorders makes it rarely recognized at first sight. Our patient, the 12-year-old firstborn son of non-consanguineous parents presented with generalized mottled pigmentation starting from lower extremities. His siblings suffered from similar condition. The clue for diagnosis is the amyloid deposition in the papillary dermis. The etiology of ACD is still unknown, but genetic factors and ultraviolet radiation are implicated. It is proposed that disturbance of keratinocyte repair following ultraviolet radiation results in amyloid deposition. The treatment remains a challenge. Oral acitretin treatment, thought to repair keratinization defect, gave a slight improvement in our case. Our is the first case of ACD reported in Indonesia.

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Section: Discussionsupporting

confidence: 90%

“…There is a possibility of DNA repair defects caused by sensitivity to UV radiation. 9 The lesions in our patient were more pronounced on exposed parts of body, that we thought sun exposure might be an important cause. Many therapeutic modalities have been proposed with variable success.…”

Section: Discussionsupporting

confidence: 45%

Familial amyloidosis cutis dyschromica in three siblings: report from Indonesia

2014

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“…DNA repair studies were performed with one cell strain previously established from the fibroblast of the 3-y-old donor (Moriwaki et al, 1992) and 12 cells strains newly established from the fibroblasts of the other donors with their written informed consent. Experiments using normal human skin fibroblasts were approved by the Institutional Review Board of the Hamamatsu University School of Medicine and conducted according to the Declaration of Helsinki Guidelines.…”

Section: Methodsmentioning

confidence: 99%

Decreased Gene Expression Responsible for Post-Ultraviolet DNA Repair Synthesis in Aging: A Possible Mechanism of Age-Related Reduction in DNA Repair Capacity

Takahashi

Moriwaki

Sugiyama³

et al. 2005

Journal of Investigative Dermatology

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A reduction in the post-ultraviolet (UV) DNA repair capacity is associated with aging. To clarify the mechanism of this change, we examined the DNA repair capacity of skin fibroblasts from healthy donors of different ages by the two methods: host cell reactivation (HCR) assay and ELISA of cyclobutane pyrimidine dimers and pyrimidine-pyrimidone (6-4) photoproducts. In HCR assay, cells from elderly donors exhibited significant declines in the ability to restore transfected reporter DNA damaged by UV light. In contrast, the ability to remove DNA damage declined little with age in ELISA. These results imply that the age-sensitive step took place after the damage excision in nucleotide excision repair (NER). The mRNA expression of DNA repair synthesis-related genes (DNA polymerase delta, replication factor C, and proliferating cell nuclear antigen) were markedly decreased in the cells from multiple elderly subjects compared with those from young subjects. Further, the protein level of DNA polymerase delta1, a catalytic subunit of the pivotal factor in repair synthesis, correlated with the mRNA level. These findings suggest that the reduced post-UV DNA repair capacity in aging results from an impairment in the latter step of NER by the decreased expression of factors in repair synthesis.

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“…235 It is suggested that this latter form might be related to amyloidosis cutis dyschromic, which is another familial type of amyloidosis characterized by reticulate hyperpigmentation and hypopigmentation of the trunk and limbs. [236][237][238] CONCLUSIONS Amyloidosis is a disease due to the deposit of amyloid, a complex substance mainly (but not only) made of proteins. The latter can be immunostained in many cases in the biopsies of the involved organs, so a closely approached diagnosis can be obtained.…”

Section: Some Variations In Plcamentioning

confidence: 99%

Cutaneous Amyloidosis: A Concept Review

Fernández-Flores

2012

The American Journal of Dermatopathology

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Concepts and semantics are crucial for good communication between clinicians and pathologists. Amyloidosis was described more than 150 years ago. Therefore, the terminology related to it is abundant, varied, and sometimes complex. In this report, we intend to discuss several terms related to the disease, with special emphasis on cutaneous amyloidosis. We present a review, from Virchow to present, of the concepts related to amyloidosis: its nature, the classification of cutaneous forms of the disease, and the techniques used in its diagnosis.

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Amyloidosis cutis dyschromica. DNA repair reduction in the cellular response to UV light

Cited by 31 publications

References 13 publications

Familial amyloidosis cutis dyschromica in three siblings: report from Indonesia

Familial amyloidosis cutis dyschromica in three siblings: report from Indonesia

Decreased Gene Expression Responsible for Post-Ultraviolet DNA Repair Synthesis in Aging: A Possible Mechanism of Age-Related Reduction in DNA Repair Capacity

Cutaneous Amyloidosis: A Concept Review

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