• Original article (Clinical research) • Previous Articles     Next Articles

Increased glycated basic fibroblast growth factor in diabetic skin reduces the cell viability and angiogenesis of human dermal microvascular endothelial cells

CAO Xiao-zan1,2, XIE Ting3, SUN Xiao-fang3, WANG Qi2, LU Shu-liang2, GU Ming-min1   

  1. 1.Department of Medical Genetics, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; 2.Department of Burns Institute, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; 3.Department of Wound Healing, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
  • Online:2016-05-28 Published:2016-05-26
  • Supported by:

    National Natural Science Foundation of China (81071568, 81272111); National Science and Technology Support Plan (2012BAI11B00)

Abstract:

Objective To explore the glycation of basic fibroblast growth factor (bFGF) in diabetic skin. Methods The abdominal full-thickness skin tissues from 58 patients (29 diabetic and 29 non-diabetic) aged 40 to 69 years and granulation tissues from 15 patients (8 diabetic and 7 non-diabetic) aged 50 to 59 were analyzed. The proportion of advanced glycation end products (AGEs)-bFGF in total bFGF was measured with co-immunoprecipitation and the histological characteristics of wound skin were detected with hematoxylin and eosin staining. The cell viability, apoptosis, and angiogenesis of human dermal microvascular endothelial cells (HDMECs) after exposure to AGEs-bFGF or bFGF were measured with cell counting kit-8, flow cytometry, and tube formation assay, respectively. Results The proportion of AGEs-bFGF in total bFGF showed age-dependent increase both in diabetic and non-diabetic skin. As compared with non-diabetic skin, the constituent ratio in diabetic skin increased significantly in the equal age-group, and the same result could be obtained in granulation tissues from patients aged 50 to 59. The proportion of AGEs-bFGF in diabetic granulation was lower than that in diabetic skin from patients aged 50 to 59. Histological analysis showed fewer vessels in diabetic skin wound. In vitro, the viability and vascularization of HDMECs were promoted by bFGF and inhibited after exposure to AGEs-bFGF for 7 d. Conclusion The present study indicates that one cause for impaired wound healing in diabetic skin could be the glycated bFGF and its changed angiogenic function.

Key words: advanced glycation end products, basic fibroblast growth factor, wound healing, diabetes