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ORIGINAL RESEARCH

EDIL3 and VEGF Synergistically Affect Angiogenesis in Endothelial Cells

, , , , , & ORCID Icon show all
Pages 1269-1277 | Received 06 Mar 2023, Accepted 12 May 2023, Published online: 18 May 2023
 

Abstract

Background

Angiogenesis is one of the histologically predominant characteristics of psoriasis. Vascular endothelial growth factor (VEGF) and epidermal growth factor-like repeats and discoidin I-like domains 3 (EDIL3) have critical effects on angiogenesis. Both these proteins are vital proangiogenic factors in tumor occurrence and progression; however, the relationship between EDIL3 and VEGF with psoriasis remains unclear.

Objective

We aimed to elucidate the role of EDIL3 and VEGF and the involved mechanisms in psoriasis-associated angiogenesis.

Methods

EDIL3 and VEGF expression in cutaneous tissue was determined by immunohistochemical assay. The effects of EDIL3 on VEGF, VEGFR2, and the growth, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) were analyzed by Western blotting assay, cell counting kit-8 assay, Transwell assay, and Matrigel tube formation assay.

Results

EDIL3 and VEGF levels in psoriatic lesions significantly increased as compared to those in normal individuals and showed a positive relationship with the Psoriasis Area and Severity Index. The downregulation of EDIL3 decreased VEGF and VEGFR2 expression in HUVECs. Moreover, the decreased expression of EDIL3 and VEGF reduced the growth, invasion, and tube formation abilities of HUVECs, while EDIL3 resistance to VEGF and VEGFR2 was restored by using the EDIL3 recombinant protein.

Conclusion

These results suggest that psoriasis is also characterized by EDIL3 and VEGF-mediated angiogenesis. Thus, EDIL3 and VEGF could serve as novel targets for treating psoriasis.

Data Sharing Statement

The data utilized in this work can be found in the article.

Ethical Statement

This work gained approval from the institutional ethics committee of Taiyuan City Central Hospital and carried out following the Declaration of Helsinki.

Acknowledgments

Our thanks should go to the National Natural Science Foundation of China and every volunteer for their efforts in the present work.

Disclosure

The authors declare no competing interest.

Additional information

Funding

The present work was funded by grants from the National Natural Science Foundation of the People’s Republic of China (No. 81803146).