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results)</h2></header><div class="c-sortpagination"><div class="c-sort"><div class="o-input__droplist1"><label for="c-sort1">Sort By:</label><select name="sort" id="c-sort1" form="facetForm"><option selected="" value="rel">Relevance</option><option value="a-title">A-Z By Title</option><option value="z-title">Z-A By Title</option><option value="a-author">A-Z By Author</option><option value="z-author">Z-A By Author</option><option value="asc">Date Ascending</option><option value="desc">Date Descending</option></select></div><div class="o-input__droplist1 c-sort__page-input"><label for="c-sort2">Show:</label><select name="rows" id="c-sort2" form="facetForm"><option selected="" value="10">10</option><option value="20">20</option><option value="30">30</option></select></div></div><input type="hidden" name="start" form="facetForm" value="0"/><nav class="c-pagination"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li></ul></nav></div><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/7kf1s24r"><div class="c-clientmarkup">Cell–cell interaction in the heart via Wnt/β-catenin pathway after cardiac injury</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">The adult mammalian heart predominantly comprises myocytes, fibroblasts, endothelial cells, smooth muscle cells, and epicardial cells arranged in a precise three-dimensional framework. Following cardiac injury, the spatial arrangement of cells is disrupted as different populations of cells are recruited to the heart in a temporally regulated manner. The alteration of the cellular composition of the heart after cardiac injury thus enables different phenotypes of cells to interact with each other in a spatio-temporal-dependent manner. It can be argued that the integrated study of such cellular interactions rather than the examination of single populations of cells can provide more insights into the biology of cardiac repair especially at an organ-wide level. Many signalling systems undoubtedly mediate such cross talk between cells after cardiac injury. The Wnt/β-catenin system plays an important role during cardiac development and disease. Here, we describe how cell populations in the heart after cardiac injury mediate their interactions via the Wnt/β-catenin pathway, determine how such interactions can affect a cardiac repair response and finally suggest an integrated approach to study cardiac cellular interactions.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/7kf1s24r"><img src="/cms-assets/700281c2950a3a6e92d33830d0800c32e87eb7eb031304e82b69e51fe113be46" alt="Cover page: Cell–cell interaction in the heart via Wnt/β-catenin pathway after cardiac injury"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/6v51q6r4"><div class="c-clientmarkup">Cardiac fibroblast in development and wound healing</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AUbil%2C%20Eric">Ubil, Eric</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Cardiac fibroblasts are the most abundant cell type in the mammalian heart and comprise approximately two-thirds of the total number of cardiac cell types. During development, epicardial cells undergo epithelial-mesenchymal-transition to generate cardiac fibroblasts that subsequently migrate into the developing myocardium to become resident cardiac fibroblasts. Fibroblasts form a structural scaffold for the attachment of cardiac cell types during development, express growth factors and cytokines and regulate proliferation of embryonic cardiomyocytes. In post natal life, cardiac fibroblasts play a critical role in orchestrating an injury response. Fibroblast activation and proliferation early after cardiac injury are critical for maintaining cardiac integrity and function, while the persistence of fibroblasts long after injury leads to chronic scarring and adverse ventricular remodeling. In this review, we discuss the physiologic function of the fibroblast during cardiac development and wound healing, molecular mediators of activation that could be possible targets for drug development for fibrosis and finally the use of reprogramming technologies for reversing scar. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium."</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/6v51q6r4"><img src="/cms-assets/0b4fdbfb7439ba29fe527570600b9423c868ad94312b69572a14c7dc46719b02" alt="Cover page: Cardiac fibroblast in development and wound healing"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/0kg0v7m1"><div class="c-clientmarkup">Hypertrophic Preconditioning</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AWang%2C%20Yibin">Wang, Yibin</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2015)</div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/0kg0v7m1"><img src="/cms-assets/b390f6f77be3843b2542b22db87ebdf9a6a1391bf14c5f926234d7b4d2996653" alt="Cover page: Hypertrophic Preconditioning"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8868v4qn"><div class="c-clientmarkup">DDR2, a discoidin domain receptor, is a marker of periosteal osteoblast and osteoblast progenitors</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AYang%2C%20Haili">Yang, Haili</a>; </li><li><a href="/search/?q=author%3ASun%2C%20Lei">Sun, Lei</a>; </li><li><a href="/search/?q=author%3ACai%2C%20Wenqian">Cai, Wenqian</a>; </li><li><a href="/search/?q=author%3AGu%2C%20Jingkai">Gu, Jingkai</a>; </li><li><a href="/search/?q=author%3AXu%2C%20Dacai">Xu, Dacai</a>; </li><li><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ADuan%2C%20Jinzhu">Duan, Jinzhu</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2020)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Introduction</h3>The periosteum has a bilayered structure that surrounds cortical bone. The outer layer is rich in connective tissue and fibroblasts, while the inner layer in contact with the cortical surface of the bone predominantly consists of osteoblasts and osteoblast progenitors. The identification of cell-specific surface markers of the bilayered structure of the periosteum is important for the purpose of tissue regeneration.<h3>Materials and methods</h3>We investigated the expression of the discoidin domain tyrosine kinase receptor DDR2, fibroblast specific protein-1 (FSP-1) and alkaline phosphatase (ALP) in the periosteum of cortical bone by immunohistochemistry. Osteogenic differentiation was compared between DDR2- and FSP-1-expressing cells flow-sorted from the periosteum.<h3>Results</h3>We showed that DDR2 predominantly labeled osteogenic cells residing in the inner layer of the periosteum and that Pearson's coefficient of colocalization indicated a significant correlation with the expression of ALP. The mineralization of DDR2-expressing osteogenic cells isolated from the periosteum was significantly induced. In contrast, FSP-1 predominantly labeled the outer layer of periosteal fibroblasts, and Pearson's coefficient of colocalization indicated that FSP-1 was poorly correlated with the expression of DDR2 and ALP. FSP-1-expressing periosteal fibroblasts did not exhibit osteogenic differentiation for the induction of bone mineralization.<h3>Conclusion</h3>DDR2 is a novel potential cell surface marker for identifying and isolating osteoblasts and osteoblast progenitors within the periosteum that can be used for musculoskeletal regenerative therapies.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8868v4qn"><img src="/cms-assets/c9833fcc11ee2b84a3078435674e9b4d24af100312724fa3b4a0fbb427215317" alt="Cover page: DDR2, a discoidin domain receptor, is a marker of periosteal osteoblast and osteoblast progenitors"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/9f22h25j"><div class="c-clientmarkup">Cardiac fibroblast proliferation rates and collagen expression mature early and are unaltered with advancing age</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AWu%2C%20Rimao">Wu, Rimao</a>; </li><li><a href="/search/?q=author%3AMa%2C%20Feiyang">Ma, Feiyang</a>; </li><li><a href="/search/?q=author%3ATosevska%2C%20Anela">Tosevska, Anela</a>; </li><li><a href="/search/?q=author%3AFarrell%2C%20Colin">Farrell, Colin</a>; </li><li><a href="/search/?q=author%3APellegrini%2C%20Matteo">Pellegrini, Matteo</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2020)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Cardiac fibrosis is a pathophysiologic hallmark of the aging heart, but little is known about how fibroblast proliferation and transcriptional programs change throughout the life span of the organism. Using EdU pulse labeling, we demonstrated that more than 50% of cardiac fibroblasts were actively proliferating in the first day of postnatal life. However, by 4 weeks, only 10% of cardiac fibroblasts were proliferating. By early adulthood, the fraction of proliferating cardiac fibroblasts further decreased to approximately 2%, where it remained throughout the rest of the organism's life. We observed that maximal changes in cardiac fibroblast transcriptional programs and, in particular, collagen and ECM gene expression both in the heart and cardiac fibroblast were maximal in the newly born and juvenile animal and decreased with organismal aging. Examination of DNA methylation changes both in the heart and in cardiac fibroblasts did not demonstrate significant changes in differentially methylated regions between young and old mice. Our observations demonstrate that cardiac fibroblasts attain a stable proliferation rate and transcriptional program early in the life span of the organism and suggest that phenotypic changes in the aging heart are not directly attributable to changes in proliferation rate or altered collagen expression in cardiac fibroblasts.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/9f22h25j"><img src="/cms-assets/d1327122708f64a954e0073dd212d626381dfb55f58e0970482ef0b6fec040bd" alt="Cover page: Cardiac fibroblast proliferation rates and collagen expression mature early and are unaltered with advancing age"/></a><a href="https://creativecommons.org/licenses/by/4.0/" class="c-scholworks__license"><img class="c-lazyimage" data-src="/images/cc-by-small.svg" alt="Creative Commons 'BY' version 4.0 license"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/3x1202rf"><div class="c-clientmarkup">Prognostic Significance of Left Ventricular Fibrosis in Patients With Congenital Bicuspid Aortic Valve.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ALluri%2C%20Gentian">Lluri, Gentian</a>; </li><li><a href="/search/?q=author%3ARenella%2C%20Pierangelo">Renella, Pierangelo</a>; </li><li><a href="/search/?q=author%3AFinn%2C%20J%20Paul">Finn, J Paul</a>; </li><li><a href="/search/?q=author%3AVorobiof%2C%20Gabriel">Vorobiof, Gabriel</a>; </li><li><a href="/search/?q=author%3AAboulhosn%2C%20Jamil">Aboulhosn, Jamil</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2017)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">This study sought to evaluate the prognostic value of left ventricular (LV) fibrosis assessed by late gadolinium enhancement (LGE) of the myocardium during cardiac magnetic resonance (CMR) imaging in patients with bicuspid aortic valve (BAV), which is associated with early aortic valve fibrosis and calcification. To what degree the LV myocardial wall is affected by fibrosis and its prognostic value is currently unknown. This is a retrospective, single-center study evaluating all adult patients with BAV who had CMR and followed from March 2002 to March 2016. CMR and transthoracic echocardiogram images were reviewed. Clinical data were abstracted from the electronic medical record. A total of 29 patients were included in the study, of which 11 (38%) had CMR studies that demonstrated the presence of LGE. Patients with LGE had significantly higher aortic valve mean gradients by echocardiography when compared with LGE-negative patients (30.3 ± 7.2 mm Hg vs 14.7 ± 3.6 mm Hg, p = 0.049). They were also more likely to have LV hypertrophy. Patients with LGE were 10 times more likely to need aortic valve replacement within 1 year of the CMR study than did patients without LGE (55% vs 5.5%, p = 0.0028). In conclusion, evaluation of LGE by CMR as a marker of LV myocardial fibrosis can have additional prognostic value when evaluating patients with aortic stenosis secondary to BAV.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/3x1202rf"><img src="/cms-assets/f3ab0ff1759d4d931a9ea23a3fb532eafded2f8b1c49acc8d026c3cf362b80e1" alt="Cover page: Prognostic Significance of Left Ventricular Fibrosis in Patients With Congenital Bicuspid Aortic Valve."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/76j9p7s6"><div class="c-clientmarkup">COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AHilser%2C%20James%20R">Hilser, James R</a>; </li><li><a href="/search/?q=author%3ASpencer%2C%20Neal%20J">Spencer, Neal J</a>; </li><li><a href="/search/?q=author%3AAfshari%2C%20Kimia">Afshari, Kimia</a>; </li><li><a href="/search/?q=author%3AGilliland%2C%20Frank%20D">Gilliland, Frank D</a>; </li><li><a href="/search/?q=author%3AHu%2C%20Howard">Hu, Howard</a>; </li><li><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li><a href="/search/?q=author%3ALusis%2C%20Aldons%20J">Lusis, Aldons J</a>; </li><li><a href="/search/?q=author%3AWilson%20Tang%2C%20WH">Wilson Tang, WH</a>; </li><li><a href="/search/?q=author%3AHartiala%2C%20Jaana%20A">Hartiala, Jaana A</a>; </li><li><a href="/search/?q=author%3AHazen%2C%20Stanley%20L">Hazen, Stanley L</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AAllayee%2C%20Hooman">Allayee, Hooman</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2024)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post-COVID-19 are not known.<h3>Methods</h3>Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR<sup>+</sup>)-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based <i>International Classification of Diseases version-10 (ICD-10</i>) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score-matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components.<h3>Results</h3>The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94-2.25]; <i>P</i><0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51-4.24]; <i>P</i><0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08-1.37]; <i>P</i><0.005). A significant genetic interaction was observed between the <i>ABO</i> locus and hospitalization for COVID-19 (<i>P</i><sub>interaction</sub>=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29-2.09]; <i>P</i>=4.8×10<sup>-5</sup>) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66-1.39]; <i>P</i>=0.82).<h3>Conclusions</h3>Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post-acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/76j9p7s6"><img src="/cms-assets/479765340a9d4e11dae4fd634203a0bca69550478b4746ca0e5f17211d77fc9f" alt="Cover page: COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/99p1707r"><div class="c-clientmarkup">Skeletal and cardiac muscle pericytes: Functions and therapeutic potential</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMurray%2C%20Iain%20R">Murray, Iain R</a>; </li><li><a href="/search/?q=author%3ABaily%2C%20James%20E">Baily, James E</a>; </li><li><a href="/search/?q=author%3AChen%2C%20William%20CW">Chen, William CW</a>; </li><li><a href="/search/?q=author%3ADar%2C%20Ayelet">Dar, Ayelet</a>; </li><li><a href="/search/?q=author%3AGonzalez%2C%20Zaniah%20N">Gonzalez, Zaniah N</a>; </li><li><a href="/search/?q=author%3AJensen%2C%20Andrew%20R">Jensen, Andrew R</a>; </li><li><a href="/search/?q=author%3APetrigliano%2C%20Frank%20A">Petrigliano, Frank A</a>; </li><li><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AHenderson%2C%20Neil%20C">Henderson, Neil C</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2017)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Pericytes are periendothelial mesenchymal cells residing within the microvasculature. Skeletal muscle and cardiac pericytes are now recognized to fulfill an increasing number of functions in normal tissue homeostasis, including contributing to microvascular function by maintaining vessel stability and regulating capillary flow. In the setting of muscle injury, pericytes contribute to a regenerative microenvironment through release of trophic factors and by modulating local immune responses. In skeletal muscle, pericytes also directly enhance tissue healing by differentiating into myofibers. Conversely, pericytes have also been implicated in the development of disease states, including fibrosis, heterotopic ossication and calcification, atherosclerosis, and tumor angiogenesis. Despite increased recognition of pericyte heterogeneity, it is not yet clear whether specific subsets of pericytes are responsible for individual functions in skeletal and cardiac muscle homeostasis and disease.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/99p1707r"><img src="/cms-assets/c1db0579d59362f4583cb1c1e4d81655bad1cbe7bb233f9bd4e5e352007c3d8f" alt="Cover page: Skeletal and cardiac muscle pericytes: Functions and therapeutic potential"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/75893093"><div class="c-clientmarkup">A systems genetics approach identifies <i>Trp53inp2</i> as a link between cardiomyocyte glucose utilization and hypertrophic response.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ASeldin%2C%20Marcus%20M">Seldin, Marcus M</a>; </li><li><a href="/search/?q=author%3AKim%2C%20Eric%20D">Kim, Eric D</a>; </li><li><a href="/search/?q=author%3ARomay%2C%20Milagros%20C">Romay, Milagros C</a>; </li><li><a href="/search/?q=author%3ALi%2C%20Shen">Li, Shen</a>; </li><li><a href="/search/?q=author%3ARau%2C%20Christoph%20D">Rau, Christoph D</a>; </li><li><a href="/search/?q=author%3AWang%2C%20Jessica%20J">Wang, Jessica J</a>; </li><li><a href="/search/?q=author%3AKrishnan%2C%20Karthickeyan%20Chella">Krishnan, Karthickeyan Chella</a>; </li><li><a href="/search/?q=author%3AWang%2C%20Yibin">Wang, Yibin</a>; </li><li><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALusis%2C%20Aldons%20J">Lusis, Aldons J</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2017)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Cardiac failure has been widely associated with an increase in glucose utilization. The aim of our study was to identify factors that mechanistically bridge this link between hyperglycemia and heart failure. Here, we screened the Hybrid Mouse Diversity Panel (HMDP) for substrate-specific cardiomyocyte candidates based on heart transcriptional profile and circulating nutrients. Next, we utilized an in vitro model of rat cardiomyocytes to demonstrate that the gene expression changes were in direct response to substrate abundance. After overlaying candidates of interest with a separate HMDP study evaluating isoproterenol-induced heart failure, we chose to focus on the gene <i>Trp53inp2</i> as a cardiomyocyte glucose utilization-specific factor. <i>Trp53inp2</i> gene knockdown in rat cardiomyocytes reduced expression and protein abundance of key glycolytic enzymes. This resulted in reduction of both glucose uptake and glycogen content in cardiomyocytes stimulated with isoproterenol. Furthermore, this reduction effectively blunted the capacity of glucose and isoprotereonol to synergistically induce hypertrophic gene expression and cell size expansion. We conclude that <i>Trp53inp2</i> serves as regulator of cardiomyocyte glycolytic activity and can consequently regulate hypertrophic response in the context of elevated glucose content.<b>NEW & NOTEWORTHY</b> Here, we apply a novel method for screening transcripts based on a substrate-specific expression pattern to identify <i>Trp53inp2</i> as an induced cardiomyocyte glucose utilization factor. We further show that reducing expression of the gene could effectively blunt hypertrophic response in the context of elevated glucose content.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/75893093"><img src="/cms-assets/4e9edb17cbb9d3b73ca2ce11b9051aca965b1317a39fac406c40c51e64d3a1ea" alt="Cover page: A systems genetics approach identifies <i>Trp53inp2</i> as a link between cardiomyocyte glucose utilization and hypertrophic response."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/1jh2p26q"><div class="c-clientmarkup">Modulating the extracellular matrix to treat wound healing defects in Ehlers-Danlos syndrome</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AKelly-Scumpia%2C%20Kindra%20M">Kelly-Scumpia, Kindra M</a>; </li><li><a href="/search/?q=author%3AArchang%2C%20Maani%20M">Archang, Maani M</a>; </li><li><a href="/search/?q=author%3APurbey%2C%20Prabhat%20K">Purbey, Prabhat K</a>; </li><li><a href="/search/?q=author%3AYokota%2C%20Tomohiro">Yokota, Tomohiro</a>; </li><li><a href="/search/?q=author%3AWu%2C%20Rimao">Wu, Rimao</a>; </li><li><a href="/search/?q=author%3AMcCourt%2C%20Jackie">McCourt, Jackie</a>; </li><li><a href="/search/?q=author%3ALi%2C%20Shen">Li, Shen</a>; </li><li><a href="/search/?q=author%3ACrosbie%2C%20Rachelle%20H">Crosbie, Rachelle H</a>; </li><li><a href="/search/?q=author%3AScumpia%2C%20Philip%20O">Scumpia, Philip O</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ADeb%2C%20Arjun">Deb, Arjun</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2024)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Classic Ehlers-Danlos syndrome (cEDS) is a genetic disorder of the connective tissue that is characterized by mutations in genes coding type V collagen. Wound healing defects are characteristic of cEDS and no therapeutic strategies exist. Herein we describe a murine model of cEDS that phenocopies wound healing defects seen in humans. Our model features mice with conditional loss of <i>Col5a1</i> in <i>Col1a2</i> <sup>+</sup> fibroblasts (Col5a1CKO). This model shows that an abnormal extracellular matrix (ECM) characterized by fibrillar disarray, altered mechanical properties, and decreased collagen deposition contribute to the wound healing defect. The cEDS animals exhibit decreased expression of epidermal genes and increased inflammation. Finally, we demonstrate that inhibiting mechanosensitive integrin signaling or by injecting wild-type (WT) fibroblasts into cEDS animals enhances epidermal gene expression, decreases inflammation, and augments wound closure. These findings suggest that cell delivery and/or blocking integrin signaling are potentially therapeutic strategies to rescue wound healing defects in cEDS.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/1jh2p26q"><img src="/cms-assets/670fd569a153aebe038f19c81efc9bec03b343593f81f99cd3ec5d7a66a88d59" alt="Cover page: Modulating the extracellular matrix to treat wound healing defects in Ehlers-Danlos syndrome"/></a></div></section><nav class="c-pagination"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li></ul></nav></section></main></form></div><div><div class="c-toplink"><a href="javascript:window.scrollTo(0, 0)">Top</a></div><footer class="c-footer"><nav class="c-footer__nav"><ul><li><a href="/">Home</a></li><li><a href="/aboutEschol">About eScholarship</a></li><li><a href="/campuses">Campus Sites</a></li><li><a href="/ucoapolicies">UC Open Access Policy</a></li><li><a href="/publishing">eScholarship Publishing</a></li><li><a href="https://www.cdlib.org/about/accessibility.html">Accessibility</a></li><li><a href="/privacypolicy">Privacy Statement</a></li><li><a href="/policies">Site Policies</a></li><li><a href="/terms">Terms of Use</a></li><li><a href="/login"><strong>Admin Login</strong></a></li><li><a href="https://help.escholarship.org"><strong>Help</strong></a></li></ul></nav><div class="c-footer__logo"><a href="/"><img class="c-lazyimage" data-src="/images/logo_footer-eschol.svg" alt="eScholarship, University of California"/></a></div><div class="c-footer__copyright">Powered by the<br/><a href="http://www.cdlib.org">California Digital Library</a><br/>Copyright © 2017<br/>The Regents of the University of California</div></footer></div></div></div></div> <script src="/js/vendors~app-bundle-2aefc956e545366a5d4e.js"></script> <script src="/js/app-bundle-4477d7630fb8c6f70662.js"></script> </body> </html>