NDLI: Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction

Please wait, while we are loading the content...

Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction

Content Provider	Scilit
Author	Meloni, Marco Caporali, Andrea Graiani, Gallia Lagrasta, Costanza Katare, Rajesh Linthout, Sophie Van Spillmann, Frank Campesi, Ilaria Madeddu, Paolo Quaini, Federico Emanueli, Costanza
Copyright Year	2010
Description	Journal: Circulation Research Rationale : Nerve growth factor (NGF) promotes angiogenesis and cardiomyocyte survival, which are both desirable for postinfarction myocardial healing. Nonetheless, the NGF potential for cardiac repair has never been investigated. Objective : To define expression and localization of NGF and its high-affinity receptor TrkA (tropomyosin-related receptor A) in the human infarcted heart and to investigate the cardiac roles of both endogenous and engineered NGF using a mouse model of myocardial infarction (MI). Methods and Results : Immunostaining for NGF and TrkA was performed on heart samples from humans deceased of MI or unrelated pathologies. To study the post-MI functions of endogenous NGF, a NGF-neutralizing antibody (Ab-NGF) or nonimmune IgG (control) was given to MI mice. To investigate the NGF therapeutic potential, human NGF gene or control (empty vector) was delivered to the murine periinfarct myocardium. Results indicate that NGF is present in the infarcted human heart. Both cardiomyocytes and endothelial cells (ECs) possess TrkA, which suggests NGF cardiovascular actions in humans. In MI mice, Ab-NGF abrogated native reparative angiogenesis, increased EC and cardiomyocyte apoptosis and worsened cardiac function. Conversely, NGF gene transfer ameliorated EC and cardiomyocyte survival, promoted neovascularization and improved myocardial blood flow and cardiac function. The prosurvival/proangiogenic Akt/Foxo pathway mediated the therapeutic benefits of NGF transfer. Moreover, NGF overexpression increased stem cell factor (the c-kit receptor ligand) expression, which translated in higher myocardial abundance of c-kit$ ^{pos}$ progenitor cells in NGF -engineered hearts. Conclusions : NGF elicits pleiotropic beneficial actions in the post-MI heart. NGF should be considered as a candidate for therapeutic cardiac regeneration.
Related Links	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881000/pdf https://www.ahajournals.org/doi/pdf/10.1161/CIRCRESAHA.109.210088
Ending Page	1284
Page Count	10
Starting Page	1275
ISSN	00097330
e-ISSN	15244571
DOI	10.1161/circresaha.109.210088
Journal	Circulation Research
Issue Number	7
Volume Number	106
Language	English
Publisher	Ovid Technologies (Wolters Kluwer Health)
Publisher Date	2010-04-16
Access Restriction	Open
Subject Keyword	Journal: Circulation Research Peripheral Vascular Disease Myocardial Infarction
Content Type	Text
Resource Type	Article
Subject	Physiology Cardiology and Cardiovascular Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

The Biological Basis for Cardiac Repair After Myocardial Infarction

Stem Cell Factor Gene Transfer Promotes Cardiac Repair After Myocardial Infarction via In Situ Recruitment and Expansion of c-kit$ ^{+}$ Cells

Notch1 in Bone Marrow–Derived Cells Mediates Cardiac Repair After Myocardial Infarction

Integrative Physiology Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction

Embryonic Stem Cell–Derived Exosomes Promote Endogenous Repair Mechanisms and Enhance Cardiac Function Following Myocardial Infarction

Role of the Autonomic Nervous System in Atrial Fibrillation

Overexpression of Tbx20 in Adult Cardiomyocytes Promotes Proliferation and Improves Cardiac Function After Myocardial Infarction

Regulation of the Inflammatory Response in Cardiac Repair

FoxO4 Promotes Early Inflammatory Response Upon Myocardial Infarction via Endothelial Arg1

Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction

Similar Documents

The Biological Basis for Cardiac Repair After Myocardial Infarction

Stem Cell Factor Gene Transfer Promotes Cardiac Repair After Myocardial Infarction via In Situ Recruitment and Expansion of c-kit$ ^{+}$ Cells

Notch1 in Bone Marrow–Derived Cells Mediates Cardiac Repair After Myocardial Infarction

Integrative Physiology Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction

Embryonic Stem Cell–Derived Exosomes Promote Endogenous Repair Mechanisms and Enhance Cardiac Function Following Myocardial Infarction

Role of the Autonomic Nervous System in Atrial Fibrillation

Overexpression of Tbx20 in Adult Cardiomyocytes Promotes Proliferation and Improves Cardiac Function After Myocardial Infarction

Regulation of the Inflammatory Response in Cardiac Repair

FoxO4 Promotes Early Inflammatory Response Upon Myocardial Infarction via Endothelial Arg1

Nerve Growth Factor Promotes Cardiac Repair following Myocardial Infarction