| Autor: |
Rajashree Rana, Thomas A. Natoli, Puneet Khandelwal, Pavlos Pissios, Abdul Bari Muhammad, Vaja Chipashvili, Krista P. Farrington, Wen Zhou, Gang Zheng, Nikolay O. Bukanov, Alessandro Pocai, Maria Chiara Magnone |
| Jazyk: |
angličtina |
| Rok vydání: |
2024 |
| Předmět: |
|
| Zdroj: |
Physiological Reports, Vol 12, Iss 18, Pp n/a-n/a (2024) |
| Druh dokumentu: |
article |
| ISSN: |
2051-817X |
| DOI: |
10.14814/phy2.70058 |
| Popis: |
Abstract Diabetic kidney disease (DKD) is the leading cause of end‐stage kidney disease. DKD is a heterogeneous disease with complex pathophysiology where early endothelial dysfunction is associated with disease progression. The Tie2 receptor and Angiopoietin 1 and 2 ligands are critical for maintaining endothelial cell permeability and integrity. Tie2 signaling is negatively regulated by the endothelial specific transmembrane receptor Vascular Endothelial Protein Tyrosine Phosphatase (VEPTP). Genetic deletion of VEPTP protects from hypertension and diabetes induced renal injury in a mouse model of DKD. Here, we show that VEPTP inhibition with an extracellular domain targeting VEPTP antibody induced Tie2 phosphorylation and improved VEGF‐A induced vascular permeability both in vitro and in vivo. Treatment with the VEPTP blocking antibody decreased the renal expression of endothelial activation markers (Angpt2, Edn1, and Icam1) but failed to improve kidney function in db/db uninephrectomized ReninAAV DKD mice. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
|
|
Nepřihlášeným uživatelům se plný text nezobrazuje |
K zobrazení výsledku je třeba se přihlásit.
|
