| 1992 — 1999 |
Tallant, Elisabeth Ann |
R01Activity Code Description:
To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Cellular Mechanisms For Angiotensin Responses in Brain
The central renin-angiotensin system participates in the regulation of arterial pressure and fluid balance. Since neuronal, glial and vascular elements within the central nervous system (CNS) all express high affinity angiotensin (Ang) receptors, it is not clear how these components interact to bring about this regulation. However, we have evidence suggesting that astrocytes may be responsible for many of the central effects of the renin- angiotensin system. We have shown that cultured human astrocytes produce and secrete angiotensinogen (Aogen). Furthermore, we have recently demonstrated that Aogen secretion can be regulated by Ang II in a region- specific manner. In addition, we have detected the presence of multiple Ang receptor subtypes on astrocytes that are distinguishable by the cellular signals they elicit, their selectivity for Ang peptides, and their inhibition by subtype selective receptor antagonists. For example, Ang II and Ang-(2-8) mobilize intracellular Ca2+ by activation of a phosphoinositide-specific phospholipase C while Ang II and Ang-(1-7) release prostaglandins via a Ca2+-independent pathway. Since prostaglandins display many of the same cardiovascular effects as Ang II and have recently been suggested as the mechanism by which Ang II causes vasopressin release, we hypothesize that many of the known actions of angiotensin peptides in the CNS are mediated by effects of astrocyte functions. Because transformed astrocytes were used to generate the above information, we must now clearly demonstrate that non-transformed astrocytes express Ang peptide receptor subtypes and produce distinct cellular signals. We will therefore identify Ang peptide binding sites, their activation of specific signal transduction mechanisms and their role in expression of Aogen mRNA in primary cultures of astrocytes from rat brain. Furthermore, to determine whether Ang peptide receptors on astrocytes are involved in the central control of blood pressure and cardiovascular function, we will isolate astrocytes from brain areas which are known to participate in the regulation of blood pressure and study expression of Ang peptide receptors and their cellular responses in cultured astrocytes from these specific regions. We will then be able to relate our findings to the known location of brain areas involved in blood pressure regulation and design physiological studies to elucidate the potential involvement of Ang peptide receptors on astrocytes in cardiovascular function.
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| 1994 — 1998 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Neural-Vascular Angiotensins--Alterations in Signal Transduction
The focus of this project is to determine whether tissue-specific increases in angiotensin (Ang) peptides alter Ang peptide receptors or their mechanisms of signal transduction. A genetic model of high blood pressure will be used--the transgenic (TG) rat which contains the mouse Ren-2 gene. In this model, plasma renin is not elevated, suggesting that the hypertension is to due to activation of the circulating renin- angiotensin system (RAS). However, the elevated blood pressures in TG rats can be reduced by angiotensin converting enzyme (ACE) inhibitors or the AT1 receptor antagonist losartan, implicating the participation of the RAS in the hypertensive process. Although circulating levels of Ang peptides were not elevated in TG rats compared to controls rats, the brains of TG rats contained higher levels of Ang I, Ang II and Ang-(1-7). Furthermore, treatment of TG rats or SHRs with ACE inhibitors elevates Ang-(1-7) levels and decreases the density of Ang receptors in the brain, in agreement with alterations in Ang receptors following ICV infusions of Ang peptides. In addition, our previous results have shown that Ang- (1-7) can be generated by tissue specific processing pathways and that Ang-(1-7) activates distinct signalling pathways. Our hypothesis is that the tissue-specific expression of the Ren-2 transgene results in elevated local production of Ang peptides which alter expression of Ang peptide receptors or their activation of select signalling pathways. The proposed studies focused on the cellular components of two tissue RAS-- the central RAS present in brain areas which participate in control of cardiovascular function as compared to the vascular RAS contained within the wall of the blood vessel, since previous studies have shown that Ang II receptors and their signal transduction mechanisms are altered in both the brain and vasculature of the SHR. To determine whether Ang peptide levels are elevated by the expression of the transgene, renin mRNA, renin activity, Ang peptide levels and Ang processing enzymes will be measured in cells from T G rats versus their negative littermates. Ang peptides receptors and their activation of specific signalling pathways in cells from TG rats will be compared to cells from their normotensive littemates. Finally, the effects of chronic elevated levels of Ang peptides as may occur endogenously in the rat, and of various peptidase inhibitors or receptor antagonists which interfere with the RAS, on Ang peptide receptors and signalling pathways will be studied in vitro, in isolated cells.
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| 1999 — 2002 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Angiotensin-(1-7) and Regulation of Vascular Growth
Vascular smooth muscle cell (VSMC) growth is regulated by a balance between proliferative and anti-proliferative factors. Angiotensin-(1-7) [Ang-(1-7)] inhibits VSMC growth and reduces neointimal formation following vascular injury. The reduction in vascular growth in response to treatment of VSMC with Ang-(1-7) was prevented by the sarcosine antagonists of Angiotensin II (Ang II) but not by AT1 or AT2 receptor antagonists. This suggests that the anti-proliferative effects of Ang- (1-7) are mediated by a novel non-AT1, non-AT2 receptor, the AT(1-7) receptor. We hypothesize that Ang-(1-7) inhibits vascular growth by the production of prostacyclin, an increased in cAMP production and the activation of cAMP-mediated cellular responses. Further, the anti- proliferative effects of Ang-(1-7) are mediated by the AT(1-7) receptor. Thus, the goals of this project of this project are to determine the mechanisms by which Ang-(1-7) inhibits VSMC growth and define the receptor mediating the effects of Ang-(1-7) in the vasculature. In Specific Aim 1, the contribution of prostacyclin to the regulation of VSMC growth by Ang-(1-7) in the vasculature. In Specific Aim 1, the contribution of prostacyclin to the regulation of VSMC growth by Ang-(1- 7) will be examined and the role of distinct metabolites of arachidonic acid in the counter-regulatory effects of Ang II and Ang-(1-7) on vascular growth will be evaluated. In Specific Aim 2, the participation of cAMP and cAMP-mediated responses in vascular growth inhibition by Ang-(1-7) will be determined. In Specific Aim 3, the receptor activated by Ang-(1-7) in VSMC will be pharmacologically characterized and its cDNA will be identified by expression cloning. RT-PCR analyses will be used to determine whether the AT(1-7) receptor is altered in vascular tissues from hypertensive rats (both spontaneous hypertensive rats or (mRen2)27 transgenic rats) or in rats fed a low salt diet, in parallel to studies described in Projects 1, 2 and 3. The results of these studies will identify the receptor and the signaling pathway(s) activated by Ang-(1-7) to counter-regulate the proliferative effects of Ang II and evaluate the contribution of the AT(1-7) receptor to the regulation of arterial pressure in hypertensive animals and during activation of the renin-angiotensin system by low salt.
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| 2003 — 2004 |
Tallant, Elisabeth Ann |
R03Activity Code Description:
To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
Prevention of Lung Cancer Growth by Angiotensin-(1-7) @ Wake Forest University Health Sciences
DESCRIPTION (provided by applicant): Lung cancer is a leading cause of death in both men and women, accounting for approximately 160,000 deaths annually in the United States with over 1,000,000 new cases of lung cancer worldwide. Despite a number of clinical trials testing various compounds as chemopreventive agents, none were effective in reducing the risk of lung cancer. However, treatment of hypertensive patients with angiotensin converting enzyme (ACE) inhibitors reduced the risk of cancer, especially lung cancer. Inhibition of ACE activity decreases angiotensin II (Ang II) and increases the levels of both bradykinin and angiotensin-(1-7) [Ang-(1-7)]. We showed that Ang-(1-7) reduces vascular growth in vitro and prevents neointimal formation in vivo. More importantly, our preliminary studies showed that Ang-(1-7) markedly inhibits the growth of human lung cancer cells and reduces tumor growth in vivo. Thus, we propose that the antiproliferative response to Ang-(1-7) extends beyond its effects on vascular cells and that Ang-(1-7) inhibits the growth of cancer cells. The studies outlined in this application are designed to determine whether Ang-(1-7) inhibits the proliferation of human lung cancer cells and identify the molecular mechanisms involved in this regulation. Established cell lines of human lung carcinomas will be examined for growth inhibition following treatment with various doses of Ang-(1-7). Attenuation of cell growth will be assessed by 3H-thymidine incorporation into proliferating cells, reductions in cell number using the modified MTT assay, and cell cycle analysis by flow cytometry. The specificity of the antiproliferative response to Ang-(1-7) will be determined using other angiotensin peptides and receptor antagonists. The attenuation of lung cancer cell growth by Ang-(1-7) will be examined in mice with chemically-induced lung tumors, to demonstrate that Ang-(1-7) prevents or reduces lung tumor formation in vivo. Gene array analysis identified candidate genes regulated by Ang-(1-7) following mitogen stimulation of human lung cancer cells, including up-regulation of genes encoding tumor suppressors and cell death signals and downregulation of genes encoding signaling pathways stimulating cell growth. Regulation of specific genes and proteins by Ang-(1-7) will be assessed by reverse transcriptase-polymerase chain reaction (RT-PCR) assays and Western blot hybridization, to determine their role in Ang-(1-7)-mediated lung cancer cell growth inhibition. The results of these studies will determine whether Ang-(1-7) effectively attenuates the proliferation of human lung cancer cells and identify the cellular pathways involved in the inhibitory response. The ultimate goal of this work is to determine whether administration of Ang-(1-7) or agents, which increase circulating Ang-(1-7) is an effective chemopreventive treatment for lung cancers.
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| 2004 — 2006 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Cardiac Growth and Angiolensin- (1-7) @ Wake Forest University Health Sciences
The heptapeptide angiotensin-(1-7) [Ang-(1-7)] opposes the pressor and proliferative effects of angiotensin (Ang) II and contributes to the anti-hypertensive and anti-proliferative actions of ACE inhibitors and AT1 receptor antagonists. We were the first to show that Ang-(1-7) inhibits vascular smooth muscle cell (VSMC) growth and neointimal formation following vascular injury, through activation of a novel AT(1-7) receptor. In preliminary studies, we demonstrate that antisense oligonucleotide blockade of mas, a proposed Ang-(1-7) receptor, reverses Ang-(1-7)-mediated inhibition of enzymatic pathways leading to VSMC proliferation, suggesting that mas is the AT(1-7) receptor coupled to the anti-proliferative response. In exciting new studies, we now report that Ang-(1-7) reduces myocyte hypertrophy as well as cardiac fibroblast hyperplasia and collagen production, in agreement with published studies showing a reduction in myocyte hypertrophy and attenuated ventricular dysfunction and remodeling following Ang-(1-7) infusion in rats post myocardial infarction (MI). A novel member of the renin-angiotensin system, angiotensin converting enzyme 2 (ACE2), which forms Ang-(1-7) from Ang II, was identified in the heart and was up-regulated when AT1 receptors were blocked in rats following a MI. Thus, we propose that Ang-(1-7) activates mas to counter-regulate the effects of Ang II to prevent myocardial hypertrophy and reduce fibroblast proliferation and collagen production. In Specific Aim 1, we will investigate the role of ACE2 and other Ang-(1-7)-forming enzymes in cardiac myocytes and cardiac fibroblasts. In Specific Aims 2 and 3, we will identify the molecular mechanisms by which Ang-(1-7) reduces myocyte hypertrophy and cardiac fibroblast proliferation and collagen synthesis. In Specific Aim 4, we will determine whether mas mediates the anti-hypertrophic response to Ang-(1-7) in cardiac myocytes and the anti-proliferative response to Ang-(1-7) in cardiac fibroblasts. An understanding of the role of Ang-(1-7) in regulating myocyte hypertrophy and cardiac fibroblast proliferation and collagen synthesis will provide insight into the pathophysiological consequences of cardiac hypertrophy and fibrosis that contribute to reduced ventricular function leading to heart failure.
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| 2007 — 2008 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Cardiac Growth and Angiotensin-(1-7) @ Wake Forest University Health Sciences
The heptapeptide angiotensin-(1-7) [Ang-(1-7)] opposes the pressor and proliferative effects of angiotensin (Ang) II and contributes to the anti-hypertensive and anti-proliferative actions of ACE inhibitors and AT1 receptor antagonists. We were the first to show that Ang-(1-7) inhibits vascular smooth muscle cell (VSMC) growth and neointimal formation following vascular injury, through activation of a novel AT(1-7) receptor. In preliminary studies, we demonstrate that antisense oligonucleotide blockade of mas, a proposed Ang-(1-7) receptor, reverses Ang-(1-7)-mediated inhibition of enzymatic pathways leading to VSMC proliferation, suggesting that mas is the AT(1-7) receptor coupled to the anti-proliferative response. In exciting new studies, we now report that Ang-(1-7) reduces myocyte hypertrophy as well as cardiac fibroblast hyperplasia and collagen production, in agreement with published studies showing a reduction in myocyte hypertrophy and attenuated ventricular dysfunction and remodeling following Ang-(1-7) infusion in rats post myocardial infarction (MI). A novel member of the renin-angiotensin system, angiotensin converting enzyme 2 (ACE2), which forms Ang-(1-7) from Ang II, was identified in the heart and was up-regulated when AT1 receptors were blocked in rats following a MI. Thus, we propose that Ang-(1-7) activates mas to counter-regulate the effects of Ang II to prevent myocardial hypertrophy and reduce fibroblast proliferation and collagen production. In Specific Aim 1, we will investigate the role of ACE2 and other Ang-(1-7)-forming enzymes in cardiac myocytes and cardiac fibroblasts. In Specific Aims 2 and 3, we will identify the molecular mechanisms by which Ang-(1-7) reduces myocyte hypertrophy and cardiac fibroblast proliferation and collagen synthesis. In Specific Aim 4, we will determine whether mas mediates the anti-hypertrophic response to Ang-(1-7) in cardiac myocytes and the anti-proliferative response to Ang-(1-7) in cardiac fibroblasts. An understanding of the role of Ang-(1-7) in regulating myocyte hypertrophy and cardiac fibroblast proliferation and collagen synthesis will provide insight into the pathophysiological consequences of cardiac hypertrophy and fibrosis that contribute to reduced ventricular function leading to heart failure.
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| 2008 — 2011 |
Diz, Debra I. [⬀]
Tallant, Elisabeth Ann |
R25Activity Code Description:
For support to develop and/or implement a program as it relates to a category in one or more of the areas of education, information, training, technical assistance, coordination, or evaluation. |
Excellence in Cardiovascular Sciences Summer Research @ Wake Forest University Health Sciences
[unreadable] DESCRIPTION (provided by applicant): [unreadable] [unreadable] This program will continue to provide short-term training for minority undergraduate, graduate and health professional students. The focus is on research training related to the cardiovascular system with an emphasis on teams of investigators involved in translational research, taking advantage of the broad, multidisciplinary cardiovascular research ongoing at Wake Forest University School of Medicine (WFUSM). Faculty from the Hypertension & Vascular Research Center, Department of Physiology & Pharmacology, Molecular Genetics Program, Molecular Medicine Program, Molecular & Cellular Pathology, Neuroscience Program, Divisions of Medicine and Surgery participate; many have participated in the program for 10-15 years. New faculty were recruited for the renewal in keeping with the program directors desire to develop mentoring skills in newly appointed or young investigators. The trainees will be minority students wishing to pursue a research project with one or more of the mentors. The overall objectives remain to 1) introduce students to biomedical research via hands-on participation in a research project; 2) introduce students to critical scientific evaluation by presenting a journal club paper; 3) provide experience in scientific writing and speaking via presentation of the research project as a poster; 4) provide exposure to research faculty, both basic science and clinical; and 5) foster a long-term commitment to pursue a career in the medical and behavioral sciences through an experience that exemplifies the excitement and challenges of clinically relevant investigation. Three new objectives include: 6) providing a focus on clinical and translational research with an emphasis on research teams; 7) promoting awareness of global issues in biomedical sciences relating to health disparities and limited diversity in biomedical research and graduate education through interactions with exchange students from Brazil; and 8) establishing an email newsletter to emphasize success of prior participants and help maintain contacts. The program is evaluated annually by trainees prior to their departure as well as biennially by all previous participants by survey. Approximately 35% of former participants attend graduate school (half in PhD and half in Master's programs), 25% enter a professional school (46% of these wish to include research as part of their career) and 15% enter technical or post-bac research programs; thus, 75% of those not currently still attending undergraduate school are in graduate, medical, or technical positions and 16% chose to continue study or work at WFUSM. Moroever, students overwhelmingly regard the experience as a positive influence on career choices. This program will continue to provide short-term training for minority undergraduate, graduate and health professional students. The focus is on research training related to the cardiovascular system with an emphasis on teams of investigators involved in translational research, taking advantage of the broad, multidisciplinary cardiovascular research ongoing at Wake Forest University School of Medicine (WFUSM). (End of Abstract) [unreadable] [unreadable] [unreadable]
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| 2009 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Angiotensin-(1-7) Inhibition of Hypertrophy/ Fibrosis @ Wake Forest University Health Sciences
Age; aged; Aging; angiotensin I (1-7); Angiotensin II; Angiotensins; Anti-inflammatory; Anti-Inflammatory Agents; Attenuated; base; Biochemical; Blood Pressure; Blood Vessels; Cardiac; cell growth; Cell Proliferation; Cells; Chronic; Collagen; congenic; Congenic Strain; Coronary artery; cyclooxygenase 2; Development; Dinoprostone; DUSP1 gene; Endothelin; Endothelin-1; Enzymes; Fibroblasts; Fibrosis; Funding; G-Protein-Coupled Receptors; Goals; Growth; Heart; Heart Diseases; Heart failure; hemodynamics; Hormones; Hypertension; Hypertrophy; improved; In Vitro; in vivo; indexing; Inflammation; Inflammatory Response; interstitial; Lentivirus Vector; Ligation; MAPK1 gene; MAPK3 gene; Measures; Mediating; Mitogen-Activated Protein Kinases; Mitogens; Modeling; Molecular; Molecular Biology; Muscle Cells; Muscle, Smooth, Vascular; Myocardial; Myocardial Infarction; normotensive; Pathology; Pathway interactions; Peptides; Perivascular Fibrosis; Phosphoric Monoester Hydrolases; Phosphorylation Inhibition; Phosphotransferases; Physiological; Platelet-Derived Growth Factor; preclinical study; pressure; prevent; Prevention; Principal Investigator; Production; prostaglandin E synthase; Prostaglandin-Endoperoxide Synthase; Prostaglandins; Protein phosphatase; Proteins; Rat Strains; Rattus; Regulation; Reperfusion Injury; response; response to injury; Role; Signal Pathway; small hairpin RNA; Structure; Subfamily lentivirinae; Techniques; Therapeutic; Therapeutic Agents; tissue/cell culture; Tissues; Transforming Growth Factor beta; Up-Regulation (Physiology)
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| 2010 — 2011 |
Tallant, Elisabeth Ann |
P01Activity Code Description:
For the support of a broadly based, multidisciplinary, often long-term research program which has a specific major objective or a basic theme. A program project generally involves the organized efforts of relatively large groups, members of which are conducting research projects designed to elucidate the various aspects or components of this objective. Each research project is usually under the leadership of an established investigator. The grant can provide support for certain basic resources used by these groups in the program, including clinical components, the sharing of which facilitates the total research effort. A program project is directed toward a range of problems having a central research focus, in contrast to the usually narrower thrust of the traditional research project. Each project supported through this mechanism should contribute or be directly related to the common theme of the total research effort. These scientifically meritorious projects should demonstrate an essential element of unity and interdependence, i.e., a system of research activities and projects directed toward a well-defined research program goal. |
Angiotensin-(1-7) Inhibition of Hypertrophy &Fibrosis @ Wake Forest University Health Sciences
aged; Aging; angiotensin I (1-7); Angiotensin II; Angiotensins; Attenuated; base; Biochemical; Blood Pressure; Blood Vessels; Cardiac; Cardiac Myocytes; cell growth; Cell Proliferation; Cells; Chronic; Collagen; Congenic Strain; Coronary artery; cyclooxygenase 2; Down-Regulation; DUSP1 gene; Endothelin; Enzymes; Fibroblasts; Fibrosis; Funding; G-Protein-Coupled Receptors; Goals; Growth; Heart; Heart Diseases; Heart failure; hemodynamics; Hormones; human TGFB1 protein; Hypertension; Hypertrophy; In Vitro; in vivo; indexing; Inflammation; Inflammatory Response; interstitial; Lentivirus Vector; MAPK1 gene; MAPK3 gene; Measures; Mediating; Mitogen-Activated Protein Kinases; Mitogens; Modeling; Molecular; Molecular Biology; Muscle Cells; Myocardial; Myocardial Infarction; normotensive; Pathology; Peptides; Perivascular Fibrosis; Phosphoric Monoester Hydrolases; Phosphorylation Inhibition; Physiological; Platelet-Derived Growth Factor; preclinical study; pressure; prostaglandin E synthase; Prostaglandin-Endoperoxide Synthase; Prostaglandins; Protein phosphatase; Rattus; Reperfusion Injury; response; response to injury; Role; small hairpin RNA; Smooth Muscle Myocytes; Structure; Subfamily lentivirinae; Techniques; Therapeutic; Therapeutic Agents; tissue/cell culture; Up-Regulation (Physiology)
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