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You searched for +publisher:"Temple University" +contributor:("Recchia, Fabio"). Showing records 1 – 3 of 3 total matches.

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Temple University

1. Powers, Jeffery. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.

Degree: PhD, 2016, Temple University

Physiology

Historical emphasis on the left ventricle (LV) has left clinicians with a lack of efficacious right ventricle (RV)-specific therapies, and classical pharmacological interventions for LV failure are often not effective when re-appropriated as interventions for RV failure. Different and still largely unknown molecular mechanisms governing the two ventricles, perhaps related to the distinct embryological origins, might at least in part explain the limited understanding of RV pathophysiology. microRNAs (miRs) are major post-transcriptional regulators and their altered expression has been implicated in several cardiovascular pathologies. We hypothesized that altered miR expression specific to the failing RV may underlie the molecular pathophysiology of progressive mechanical RV dysfunction. We applied an “-omics” approach to a pre-clinical, large animal model of heart failure. Ten dogs were subjected to 4-week tachypacing to induce congestive heart failure (HF) and secondary pulmonary hypertension. Ten non-paced dogs were used as normal controls. Hemodynamic and echocardiographic assessment confirmed development of RV dysfunction and secondary pulmonary hypertension in tachypaced dogs. In HF vs control, RV end-diastolic pressure and mean pulmonary arterial pressure were significantly increased, while tricuspid annular plane systolic excursion, tricuspid annular systolic velocity, and RV fractional area change were significantly decreased. miR microarray and quantitative RT-PCR analyses both showed upregulation of several miRs in HF-RV vs HF-LV and control myocardium. We focused on miR-21, which increased in HF-RV vs control RV (with no change in HF-LV vs control LV) and is known to target phosphatase and tensin homolog (PTEN), a negative regulator of fibroblast proliferation. PTEN also inhibits the phosphorylation/activation of Akt, a positive regulator of fibroblast proliferation. Myocardial PTEN was indeed selectively downregulated in HF-RV and not in HF-LV, consistent with increased fibrosis in HF-RV vs HF-LV. Moreover, Akt phosphorylation was increased by in RV-HF and reduced in HF-LV vs control. Isolated fibroblasts and myocytes from each ventricle were subjected to cyclic stretch and/or aldosterone treatment to mimic mechanical and hormonal stimuli occurring during HF. In RV fibroblasts, miR-21 was increased by both cyclic stretch and by aldosterone, with no significant miR-21 increase in any other cell type. Furthermore, in stretched/treated RV fibroblasts there was a significant downregulation of miR-21 targets PTEN and sprouty homolog 1, as well as a significant upregulation of pro-fibrotic mediator transforming growth factor-β1. These findings suggest that miR-21 upregulation due to RV fibroblast responsiveness to mechanical and hormonal stimuli is a novel determinant of RV fibrosis and functional impairment. This study uncovered a novel, major biological difference between the RV and LV, specifically a peculiar molecular response of RV fibroblasts to mechanical and hormonal stress. It is my hope…

Advisors/Committee Members: Recchia, Fabio;, Recchia, Fabio, Houser, Steven R., Sabri, Abdelkarim, Dries, Daniel;.

Subjects/Keywords: Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Powers, J. (2016). microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,417461

Chicago Manual of Style (16th Edition):

Powers, Jeffery. “microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,417461.

MLA Handbook (7th Edition):

Powers, Jeffery. “microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.” 2016. Web. 02 Jul 2020.

Vancouver:

Powers J. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,417461.

Council of Science Editors:

Powers J. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,417461


Temple University

2. Troupes, Constantine. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.

Degree: PhD, 2016, Temple University

Biomedical Sciences

Increases in cardiac afterload caused by disease conditions results in remodeling of heart structure by hypertrophy and alterations in the molecular regulation of contractile performance. These adaptations can be regulated by various Ca2+-dependent signaling processes. STIM1 is an important regulator of Ca2+ signaling in different cell types by sensing endoplasmic reticular Ca2+ levels and coupling to plasma membrane Orai channels. The role of STIM1 in heart is not well understood, given the robust Ca2+ regulatory machinery present within cardiac myocytes. Previous reports indicate that STIM1 may play a role in regulation of cardiac hypertrophy. The goal of this work is to understand how STIM1 can affect contractile Ca2+ regulation in normal and diseased myocytes. We induced cardiac hypertrophy by slow progressive pressure overload in adult cats. Isolated adult feline ventricular myocytes (AFMs) exhibited increased STIM1 expression and activity, which correlated with altered Ca2+ handling. Use of BTP2 to block Orai channels resulted in a reduction of action potential (AP) duration and diastolic spark rate of hypertrophied myocytes, without affecting myocytes from sham-operated animals. Overexpressed STIM1 in cultured AFMs caused persistent Ca2+ influx that resulted in increased diastolic spark rates and prolonged APs, similar to myocytes from banded animals. STIM1 mediated Ca2+ influx could load the sarcoplasmic reticulum and activated CaMKII, which increased spark rates and lead to spontaneous APs. Importantly, STIM1 operated by associating with Orai channels because these effects could be blocked with either BTP2 or with a dominant negative Orai construct. Prolonged Ca2+ entry through this pathway eventually causes cell death. In conclusion, the work presented in this thesis establishes a role for STIM1-Orai in contractile Ca2+ regulation.

Temple University – Theses

Advisors/Committee Members: Houser, Steven R;, Chen, Xiongwen, Soboloff, Jonathan, Recchia, Fabio;.

Subjects/Keywords: Physiology;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Troupes, C. (2016). The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,403786

Chicago Manual of Style (16th Edition):

Troupes, Constantine. “The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,403786.

MLA Handbook (7th Edition):

Troupes, Constantine. “The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.” 2016. Web. 02 Jul 2020.

Vancouver:

Troupes C. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,403786.

Council of Science Editors:

Troupes C. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,403786


Temple University

3. Sharp III, Thomas E. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.

Degree: PhD, 2017, Temple University

Physiology

Remarkable advances have been made in the treatment of cardiovascular diseases (CVD), however, CVD still accounts for the most deaths in industrialized nations. Ischemic heart disease (IHD) can lead to acute coronary syndrome (ACS) (myocardial infarction [MI]). The standard of care is reperfusion therapy followed by pharmacological intervention to attenuate clinical symptoms related to the MI. While survival from MI has dramatically increased with the implementation of reperfusion therapy, these individuals will inevitably suffer progressive pathological remodeling leaving them predispose to develop heart failure (HF). HF is a clinical syndrome defined as the impairment of the heart to maintain organ perfusion at rest and/or during times of exertion (i.e. exercise intolerance). Clinically, this is accompanied by dyspnea, pulmonary or splanchnic congestion and peripheral edema. Physiologically, there is neurohormal activation through the classical β–adrenergic and PKA–dependent signalin

Temple University – Theses

Advisors/Committee Members: Houser, Steven R.;, Sabri, Abdelkarim, Lefer, David J., Recchia, Fabio, Koch, Walter J.;.

Subjects/Keywords: Physiology;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Sharp III, T. E. (2017). DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,445275

Chicago Manual of Style (16th Edition):

Sharp III, Thomas E. “DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.” 2017. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,445275.

MLA Handbook (7th Edition):

Sharp III, Thomas E. “DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.” 2017. Web. 02 Jul 2020.

Vancouver:

Sharp III TE. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,445275.

Council of Science Editors:

Sharp III TE. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,445275

.