Indian Journal of Dermatology
  Publication of IADVL, WB
  Official organ of AADV
Indexed with Science Citation Index (E) , Web of Science and PubMed
 
Users online: 2426  
Home About  Editorial Board  Current Issue Archives Online Early Coming Soon Guidelines Subscriptions  e-Alerts    Login  
    Small font sizeDefault font sizeIncrease font size Print this page Email this page
BASIC RESEARCH
Year : 2013  |  Volume : 58  |  Issue : 2  |  Page : 101-106

The role of EGFR/ERK/ELK-1 MAP kinase pathway in the underlying damage to diabetic rat skin


1 Department of Dermatological, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China
2 Center of Laboratory Medicine, Yinchuan, Ningxia Hui Autonomous Region, China
3 Ningxia Medical University, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China

Correspondence Address:
Jianzhong Zhang
General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004
China
Login to access the Email id

Source of Support: This work was supported by Grant.in.Aid for National Natural Science Foundation of China (No.81060181) and Natural Science Foundation of Ningxia of China (NZ1222), Conflict of Interest: None


DOI: 10.4103/0019-5154.108035

Rights and Permissions

Background: Diabetes mellitus (DM) is a highly prevalent disease. Atrophy and spontaneous ulcers are the most common cutaneous manifestation of diabetic dermopathy (DD). Before spontaneous ulcers, we believe there is an underlying damage stage although the mechanism is unknown. Aims: To explore the expression of extracellular signal-regulated kinase1/2 (ERK1/2), its correlated upstream protein epidermal growth factor receptor (EGFR) and its downstream transcription factor E twenty-six (ETS)-like 1(ELK-1)in the damage of the diabetic rat skin, and to explore the role of ERK1/2 on the recessive damage to diabetic rat skin. Materials and Methods: Eighty Sprague-Dawley (SD) rats weighing 260-300 g were randomly divided into control and streptozotocin (STZ)-induced diabetes groups. After 0.5, 2, 4, and 8 weeks, the shaved skin specimens from the back of rats in both groups were collected to observe the histological characteristics of the skin, to measure the thickness of the epidermis and the dermis, and to observe the ultrastructure. Immunohistochemistry (IHC) and Western blot techniques were used to detect the expression and activation of ERK1/2, EGFR, ELK-1 in the skin of the rats. Results: There are ultrastructural changes in the DM skin. With the continuance of the diabetes course, the thicknesses of the epidermis and dermis decreased, and the expression of phospho-ERK1/2 (P-ERK1/2), EGFR, and ELK-1 was decreased gradually in the back skin of the diabetes rats. It was significantly lower in 4 and 8 week DM than that of the normal control ( P < 0.05). The expression of P-EGFR and P-ERK1/2 in the back skin of the diabetes rats was positively correlated ( r = 0.572 P < 0.05), and the positive correlation was also obtained between P-ERK1/2 and P-ELK-1 ( r = 0.715, P < 0.05). Conclusion: The phenomenon of recessive damage exists in the skin of diabetes rats, which probably may relate to the weakness of the signal transduction: P-EGFR → ERK1/2 → ELK-1.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed2794    
    Printed58    
    Emailed0    
    PDF Downloaded53    
    Comments [Add]    

Recommend this journal