ABSTRACT
Podoplanin (PDPN), being mucin-like transmembrane sialoglycoprotein, is expressed on lymphatic endothelial cells, with its significant role in the development of inflammation, separation of blood and lymphatic circulation, platelet aggregation, integrity of the renal filtration barrier and alveolar. In recent years, many researches have demonstrated that PDPN is overexpressed on the surface of some tumor cells. The interaction between PDPN and CLEC-2 plays an important role in the development of tumor growth, migration and transfer, therefore, anti-PDPN antibody offers a new direction for the treatment of tumor patients. This paper aims at reviewing the progress and application prospect of PDPN.
ABSTRACT
Objective To evaluate the role of C-type lectin domain family 2,member B (CLEC2B) gene in the pathogenesis of vitiligo.Methods Real time fluorescence-based PCR was performed to detect the expression of CLEC2B mRNA in the peripheral blood and lesional skin of 37 patients with vitiligo as well as in the peripheral blood and normal skin of 40 healthy controls.Data were statistically analyzed by t test and chisquare test.Results Among the 37 patients,23 had progressive vitiligo,14 stable vitiligo,31 vitiligo vulgaris,6 segmental vitiligo.The expression level of CLEC2B mRNA was significantly higher in vitiligo lesions than in the control skin (1.21 ± 0.03 vs.1.00,t =4.432,P ＜ 0.05),but was of no significant difference in peripheral blood between the patients and healthy controls (1.02 ± 0.05 vs.1.00,t =1.435,P ＞ 0.05).Increased expression of CLEC2B mRNA was noted in lesions of vulgaris vitiligo compared with those of segmental vitiligo (1.21 ± 0.03 vs.1.02 ± 0.01,t =5.330,P ＜ 0.05),as well as in lesions of progressive vitiligo compared with those of stable vitiligo (1.25 ± 0.05 vs.1.08 ± 0.03,t =3.046,P ＜ 0.05).No significant difference was observed in the expression of CLEC2B mRNA among lesions of vitiligo with different courses (P ＞ 0.05).Conclusion The differential expression of CLEC2B mRNA may take part in the pathogenesis of vitiligo.