Establishment of a system in which type VII collagen and laminin 5 or their genes are continuously delivered from the dermal side to the basement membrane zone
Establishment of a system in which type VII collagen and laminin 5 or their genes are continuously delivered from the dermal side to the basement membrane zone
批准号:
15390337
负责人:
SAWAMURA Daisuke
金额:
$9.41万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004
中文摘要
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英文摘要
Epidermolysis bullosa is caused by mutations in the genes encoding structural proteins of basement membrane zone. Especially, the subtypes resulting from type VII collagen and laminin 5 genes showed severe phenotype and low quality of life. These structural proteins are thought to be produced by epidermal keratinocytes. Many dermatological investigators intend to introduce the causative genes to keratinocytes and to supply those gene products to basement membrane. The aim of this study was to establish a system in which type VII collagen and laminin 5 or their genes were continuously delivered from the dermal side to the basement membrane zone. We succeeded in purification of a large amount of recombinant type VII collagen last year. The injection of the protein induced deposition of type VII collagen in the basement membrane zone. Also injection of gene-transferred fibroblasts enabled type VII collagen to go into the basement membrane. Furthermore, implantation of these fibroblasts in scaffold increased the amount of type VII collagen in the basement membrane zone. Thus, we think that we can achieve establishment of the system in which type VII collagen and laminin 5 or their genes are continuously delivered from the dermal side to the basement membrane zone.
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Keratotic lesions in epidermolysis bullosa simplex with mottled pigmentation.
单纯性大疱性表皮松解症的角化病变伴有斑驳色素沉着。
DOI:
--
发表时间:
2005
期刊:
J Dermatol Sci 52
影响因子:
--
作者:
[Toki T, Katsuoka F, Ito E et al., J.Sasaki, Nakamura H, T.Wada, Yasukawa K]
通讯作者:
Yasukawa K
Keratinocyte-specific modulation of type VII collagen gene expression by pro-inflammatory cytokines (tumor necrosis factor- and interleukin-1).
促炎细胞因子(肿瘤坏死因子和白细胞介素 1)对 VII 型胶原蛋白基因表达的角质形成细胞特异性调节。
DOI:
--
发表时间:
期刊:
Exp Dermatol (in press)
影响因子:
--
作者:
[Takeda H, et al.]
通讯作者:
et al.
Sawamura D, et al.: "Identification of COL7A1 alternative splicing inserting 9 amino acid residues into the fibronectin type III linker domain."J Invest Dermatol. 120. 942-948 (2003)
Sawamura D 等人:“鉴定将 9 个氨基酸残基插入纤连蛋白 III 型接头结构域的 COL7A1 选择性剪接。”J Invest Dermatol。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
Sasaki H, et al.: "A novel Sp 1-family-related cis-acting element for transcription of type VII collagen gene (COL7A1)"J Dermaol Sci. 32. 239-242 (2003)
Sasaki H 等人:“用于 VII 型胶原蛋白基因 (COL7A1) 转录的新型 Sp 1 家族相关顺式作用元件”J Dermaol Sci。
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[]
通讯作者:
DOI:
10.1038/sj.gt.3302472
发表时间:
2005-05-01
期刊:
GENE THERAPY
影响因子:
5.1
作者:
[Sawamura, D, Goto, M, Shimizu, H]
通讯作者:
Shimizu, H
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