Deficiency of filamin A in endothelial cells impairs left ventricular remodelling after myocardial infarction.

Item request has been placed!

Item request cannot be made.

Processing Request

اقرأ أكثر حفظ في قائمتي

المؤلفون: Bandaru S;Bandaru S; Grönros J; Grönros J; Redfors B; Redfors B; Çil Ç; Çil Ç; Pazooki D; Pazooki D; Salimi R; Salimi R; Larsson E; Larsson E; Zhou AX; Zhou AX; Ömerovic E; Ömerovic E; Akyürek LM; Akyürek LM
المصدر:
Cardiovascular research [Cardiovasc Res] 2015 Feb 01; Vol. 105 (2), pp. 151-9. Date of Electronic Publication: 2014 Oct 24.
نوع النشر :
Journal Article; Research Support, Non-U.S. Gov't
اللغة:
English

معلومة اضافية
- المصدر:
  Publisher: Oxford Journals Country of Publication: England NLM ID: 0077427 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1755-3245 (Electronic) Linking ISSN: 00086363 NLM ISO Abbreviation: Cardiovasc Res Subsets: MEDLINE
- بيانات النشر:
  Publication: 2008- : Oxford : Oxford Journals
  Original Publication: London, British Medical Assn.
- الموضوع:
  Endothelial Cells/*metabolism ; Filamins/*metabolism ; Heart Ventricles/*physiopathology ; Myocardial Infarction/*metabolism ; Ventricular Dysfunction, Left/*genetics ; Ventricular Remodeling/*genetics; Animals ; Filamins/deficiency ; Heart Failure/genetics ; Male ; Mice, Transgenic ; Myocardial Infarction/genetics
- نبذة مختصرة :
  Aims: Actin-binding protein filamin A (FLNA) regulates signal transduction important for cell locomotion, but the role of FLNA after myocardial infarction (MI) has not been explored. The main purpose of this study was to determine the impact of endothelial deletion of FLNA on post-MI remodelling of the left ventricle (LV).
  Methods and Results: We found that FLNA is expressed in human and mouse endothelial cells (ECs) during MI. To determine the biological significance of endothelial expression of FLNA, we used mice that are deficient for endothelial FLNA by cross-breeding adult mice expressing floxed Flna (Flna(o/fl)) with mice expressing Cre under the vascular endothelial-specific cadherin promoter (VECadCre+). Male Flna(o/fl) and Flna(o/fl)/VECadCre+ mice were subjected to permanent coronary artery ligation to induce MI. Flna(o/fl)/VECadCre+ mice that were deficient for endothelial FLNA exhibited larger and thinner LV with impaired cardiac function as well as elevated plasma levels of NT-proBNP and decreased secretion of VEGF-A. The number of capillary structures within the infarcted areas was reduced in Flna(o/fl)/VECadCre+ hearts. ECs silenced for Flna mRNA expression exhibited impaired tubular formation and migration, secreted less VEGF-A, and produced lower levels of phosphorylated AKT and ERK1/2 as well as active RAC1.
  Conclusion: Deletion of FLNA in ECs aggravated MI-induced LV dysfunction and cardiac failure as a result of defective endothelial response and increased scar formation by impaired endothelial function and signalling.
  (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: journals.permissions@oup.com.)
- Contributed Indexing:
  Keywords: Actin-binding protein; Angiogenesis; Cell migration; Heart
- الرقم المعرف:
  0 (Filamins)
  0 (FlnA protein, mouse)
- الموضوع:
  Date Created: 20141026 Date Completed: 20150928 Latest Revision: 20150117
- الموضوع:
  20240628
- الرقم المعرف:
  10.1093/cvr/cvu226
- الرقم المعرف:
  25344364

تعليقات

No Comments.