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[瘢痕疙瘩增殖与上皮细胞凋亡及皮肤附属器结构和功能破坏之间的关系]

[Relationship between keloid proliferation and apoptosis of epithelial cell with destruction of structure and function of skin appendages].

作者信息

Jiang Duyin, Fu Xiaobing, Chen Wei, Sun Tongzhu, Sheng Zhiyong

机构信息

Key Laboratory of Wound Repair of PLA, 304th Clinical Department, General Hospital of PLA, Beijing, 100037, P R China.

出版信息

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2005 Jan;19(1):15-9.

Abstract

OBJECTIVE

To investigate the relationship between keloid proliferation and destruction of skin appendages (SAs).

METHODS

Pathological biopsies of keloids were derived from 17 patients who underwent scar resection. All samples were divided into 4 groups: infiltrating growth locus of keloids (K-I, n = 9), proliferative keloids (K-P, n = 17), atrophic keloids (K-A, n = 10), and edging normal skin (K-N, n = 6). Normal skin derived from thorax of patients was used as control (NS, n = 6). The density of SAs and the expressive characteristics of pan-cytokeratin (CKp), cytokeratin 19 (CK19), secretory component of glandular epithelium (SC), proliferating cell nuclear antigen (PCNA), and apoptosis related proteins (Bcl-2 and Bax) were observed with immunohistochemical method.

RESULTS

Compared with K-N and NS, the density of SAs expressing CKP and SC in keloids was apparently decreased, and remnant of CKp protein was observed after the disappearance of SAs structures. Protein expression of Bax was increased in epithelial cells of most SAs. SAs containing positive immunostaining signals of Bcl-2, PCNA and CK19 exhibited squamous epithelization and abnormal structure. The structure of SAs underwent 3 morphological stages: infiltrating, proliferating, and maturing. In correspondence to each stage, SAs underwent proliferation, structural destruction, and fibrosis which were caused by cellular migration, inflammatory reaction, and vascular occlusion respectively.

CONCLUSION

Abnormal proliferation of epithelial cells and their structural destruction of SAs may be associated with tissue fibrosis in keloid lesion.

摘要

目的

探讨瘢痕疙瘩增殖与皮肤附属器(SAs)破坏之间的关系。

方法

对17例行瘢痕切除患者的瘢痕疙瘩进行病理活检。所有样本分为4组:瘢痕疙瘩浸润性生长部位(K-I,n = 9)、增殖性瘢痕疙瘩(K-P,n = 17)、萎缩性瘢痕疙瘩(K-A,n = 10)和边缘正常皮肤(K-N,n = 6)。取患者胸部正常皮肤作为对照(NS,n = 6)。采用免疫组织化学方法观察SAs密度及全细胞角蛋白(CKp)、细胞角蛋白19(CK19)、腺上皮分泌成分(SC)、增殖细胞核抗原(PCNA)和凋亡相关蛋白(Bcl-2和Bax)的表达特征。

结果

与K-N和NS相比,瘢痕疙瘩中表达CKP和SC的SAs密度明显降低,SAs结构消失后仍观察到CKp蛋白残留。大多数SAs上皮细胞中Bax蛋白表达增加。含有Bcl-2、PCNA和CK19阳性免疫染色信号的SAs表现为鳞状上皮化生和结构异常。SAs结构经历3个形态学阶段:浸润、增殖和成熟。对应于每个阶段,SAs分别经历由细胞迁移、炎症反应和血管闭塞引起的增殖、结构破坏和纤维化。

结论

上皮细胞异常增殖及其对SAs的结构破坏可能与瘢痕疙瘩病变中的组织纤维化有关。

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