• Türkçe
    • English
  • English 
    • Türkçe
    • English
  • Login
View Item 
  •   DSpace@İSÜ
  • Araştırma Çıktıları | TR-Dizin | WoS | Scopus | PubMed | DergiPark
  • PubMed İndeksli Yayınlar Koleksiyonu
  • View Item
  •   DSpace@İSÜ
  • Araştırma Çıktıları | TR-Dizin | WoS | Scopus | PubMed | DergiPark
  • PubMed İndeksli Yayınlar Koleksiyonu
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLC gamma dependent autophagy pathways in human umbilical vein endothelial cells

Thumbnail

View/Open

Tam Metin / Full Text (973.2Kb)

Date

2021

Author

Aydinlik, Seyma
Uvez, Ayca
Kiyan, Hulya Tuba
Gurel-Gurevin, Ebru
Yilmaz, Veysel Turan
Ulukaya, Engin

Metadata

Show full item record

Citation

Aydinlik, S., Uvez, A., Kiyan, H. T., Gurel-Gurevin, E., Yilmaz, V. T., Ulukaya, E., & Armutak, E. I. (2021). Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLCγ dependent autophagy pathways in human umbilical vein endothelial cells. Microvascular research, 104229. Advance online publication. https://doi.org/10.1016/j.mvr.2021.104229

Abstract

The current study assessed the effects of the thalidomide and palladium (II) saccharinate complex of terpyridine on the suppression of angiogenesis-mediated cell proliferation. The viability was assessed after treatment with palladium (II) complex (1.56–100 μM) and thalidomide (0.1-400 µM) alone by using ATP assay for 48h. Palladium (II) complex was found to inhibit growth statistically significant in a dose-dependent manner in HUVECs and promoted PARP-1 cleavage through the production of ROS. On the other hand, thalidomide did not cause any significant change in cell viability. Moreover, cell death was observed to be manifested as late apoptosis due to Annexin V/SYTOX staining after palladium (II) complex treatment however, thalidomide did not demonstrate similar results. Thalidomide and palladium (II) complex also suppressed HUVEC migration and capillary-like structure tube formation in vitro in a time-dependent manner. Palladium (II) complex (5 mg/ml) treatment showed a strong antiangiogenic effect similar to positive control thalidomide (5mg/ml) and successfully disrupted the vasculature and reduced the thickness of the vessels compared to control (agar). Furthermore, suppression of autophagy enhanced the cell death and antiangiogenic effect of thalidomide and palladium (II) complex. We also showed that being treated with thalidomide and palladium (II) complex inhibited phosphorylation of the signaling regulators downstream of the VEGFR2. These results provide evidence for the regulation of endothelial cell functions that are relevant to angiogenesis through the suppression of the FAK/Src/Akt/ERK1/2 signaling pathway. Our results also indicate that PLC-γ1 phosphorylation leads to activation of p-Akt and p-Erk1/2 which cause stimulation on cell proliferation at lower doses. Hence, we demonstrated that palladium (II) and thalidomide can induce cell death via the Erk/Akt/PLCγ signaling pathway and that this pathway might be a novel mechanism.

Source

Journal Pre-proof

URI

https://doi.org/10.1016/j.mvr.2021.104229
https://hdl.handle.net/20.500.12713/1980

Collections

  • Makale Koleksiyonu [225]
  • PubMed İndeksli Yayınlar Koleksiyonu [987]
  • Scopus İndeksli Yayınlar Koleksiyonu [1541]
  • WoS İndeksli Yayınlar Koleksiyonu [1616]



DSpace software copyright © 2002-2015  DuraSpace
Contact Us | Send Feedback
Theme by 
@mire NV
 

 




| Instruction | Guide | Contact |

DSpace@İSÜ

by OpenAIRE
Advanced Search

sherpa/romeo

Browse

All of DSpaceCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsTypeLanguageDepartmentCategoryPublisherAccess TypeInstitution AuthorThis CollectionBy Issue DateAuthorsTitlesSubjectsTypeLanguageDepartmentCategoryPublisherAccess TypeInstitution Author

My Account

LoginRegister

Statistics

View Google Analytics Statistics

DSpace software copyright © 2002-2015  DuraSpace
Contact Us | Send Feedback
Theme by 
@mire NV
 

 


|| Guide|| Instruction || Library || İstinye University || OAI-PMH ||

İstinye University, İstanbul, Turkey
If you find any errors in content, please contact:

Creative Commons License
İstinye University Institutional Repository is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 Unported License..

DSpace@İSÜ:


DSpace 6.2

tarafından İdeal DSpace hizmetleri çerçevesinde özelleştirilerek kurulmuştur.