Entity

Time filter

Source Type

Boston, MA, United States

Camci-Unal G.,Brigham and Womens Hospital | Camci-Unal G.,Harvard-MIT Division of Health Sciences and Technology | Annabi N.,Brigham and Womens Hospital | Annabi N.,Harvard-MIT Division of Health Sciences and Technology | And 9 more authors.
NPG Asia Materials | Year: 2014

Cardiac failure is a critical condition that results in life-threatening consequences. Due to a limited number of organ donors, tissue engineering has emerged to generate functional tissue constructs and provide an alternative mean to repair and regenerate damaged heart tissues. In this paper, we review the emerging directions associated with cardiac tissue engineering approaches. In particular, we discuss the use of hydrogels in repair and regeneration of damaged hearts. Because of their tissue-like biological, chemical and mechanical properties, hydrogels represent a potentially powerful material for directing cells into functional cardiac tissues. Herein, we will summarize both traditional and next-generation hydrogels with conductive, elastomeric and oxygen-releasing capabilities that can promote vascularization and stem cell differentiation to form properly functioning cardiac tissues. © 2014 Nature Publishing Group All rights reserved.


Oikonomopoulos A.,Cardiac Muscle Research Laboratory | Oikonomopoulos A.,University of Crete | Sereti K.-I.,Cardiac Muscle Research Laboratory | Sereti K.-I.,University of Crete | And 17 more authors.
Circulation Research | Year: 2011

Rationale: Recent work in animal models and humans has demonstrated the presence of organ-specific progenitor cells required for the regenerative capacity of the adult heart. In response to tissue injury, progenitor cells differentiate into specialized cells, while their numbers are maintained through mechanisms of self-renewal. The molecular cues that dictate the self-renewal of adult progenitor cells in the heart, however, remain unclear. Objective: We investigate the role of canonical Wnt signaling on adult cardiac side population (CSP) cells under physiological and disease conditions. Methods and Results: CSP cells isolated from C57BL/6J mice were used to study the effects of canonical Wnt signaling on their proliferative capacity. The proliferative capacity of CSP cells was also tested after injection of recombinant Wnt3a protein (r-Wnt3a) in the left ventricular free wall. Wnt signaling was found to decrease the proliferation of adult CSP cells, both in vitro and in vivo, through suppression of cell cycle progression. Wnt stimulation exerted its antiproliferative effects through a previously unappreciated activation of insulin-like growth factor binding protein 3 (IGFBP3), which requires intact IGF binding site for its action. Moreover, injection of r-Wnt3a after myocardial infarction in mice showed that Wnt signaling limits CSP cell renewal, blocks endogenous cardiac regeneration and impairs cardiac performance, highlighting the importance of progenitor cells in maintaining tissue function after injury. Conclusions: Our study identifies canonical Wnt signaling and the novel downstream mediator, IGFBP3, as key regulators of adult cardiac progenitor self-renewal in physiological and pathological states. © 2011 American Heart Association, Inc.


Guan J.,Cardiac Muscle Research Laboratory | Mishra S.,Cardiac Muscle Research Laboratory | Falk R.H.,Harvard University | Liao R.,Cardiac Muscle Research Laboratory | Liao R.,Harvard University
American Journal of Physiology - Heart and Circulatory Physiology | Year: 2012

Amyloidosis represents a group of diseases in which proteins undergo misfolding to form insoluble fibrils with subsequent tissue deposition. While almost all deposited amyloid fibers share a common nonbranched morphology, the affected end organs, clinical presentation, treatment strategies, and prognosis vary greatly among this group of diseases and are largely dependent on the specific amyloid precursor protein. To date, at least 27 precursor proteins have been identified to result in either local tissue or systemic amyloidosis, with nine of them manifesting in cardiac deposition and resulting in a syndrome termed "cardiac amyloidosis" or "amyloid cardiomyopathy." Although cardiac amyloidosis has been traditionally considered to be a rare disorder, as clinical appreciation and understanding continues to grow, so too has the prevalence, suggesting that this disease may be greatly underdiagnosed. The most common form of cardiac amyloidosis is associated with circulating amyloidogenic monoclonal immunoglobulin light chain proteins. Other major cardiac amyloidoses result from a misfolding of products of mutated or wild-type transthyretin protein. While the various cardiac amyloidoses share a common functional consequence, namely, an infiltrative cardiomyopathy with restrictive pathophysiology leading to progressive heart failure, the underlying pathophysiology and clinical syndrome varies with each precursor protein. Herein, we aim to provide an up-to-date overview of cardiac amyloidosis from nomenclature to molecular mechanisms and treatment options, with a particular focus on amyloidogenic immunoglobulin light chain protein cardiac amyloidosis. © 2012 by the American Physiological Society.

Discover hidden collaborations