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The role of SWI/SNF in regulating smooth muscle differentiationZhang, Min. January 2009 (has links)
Thesis (Ph.D.)--Indiana University, 2009. / Title from screen (viewed on December 1, 2009). Department of Cellular and Integrative Physiology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): B. Paul Herring, Anthony B. Firulli, Frederick M. Pavalko, Simon J. Rhodes. Includes vitae. Includes bibliographical references (leaves 138-149).
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Cellular trafficking properties and physiological functions of the [alpha]1-adrenoceptor subtypesChalothorn, Dan. January 2003 (has links) (PDF)
Thesis (Ph. D.)--University of Kentucky, 2003. / Title from document title page. Document formatted into pages; contains x, 192p. : ill. Includes abstract. Includes bibliographical references (p. 165-189).
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Adaptation at a shortened length in rabbit femoral arteryBednarek, Melissa L., January 1900 (has links)
Thesis (Ph.D.)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Physiology. Title from title-page of electronic thesis. Bibliography: leaves 94-110.
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Effects of isoflavonoids on vascular smooth muscle cell proliferationWong, Wai-ming, 黃慧明 January 2006 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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Functional properties of aortic smooth muscle in bicuspid aortic valvediseaseHo, Ka-lai, Cally., 何嘉麗. January 2011 (has links)
published_or_final_version / Physiology / Master / Master of Medical Sciences
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Role of mitogen-activated protein kinases in vascular relaxation in porcine coronary arteriesChiu, Tsz-ling, 趙芷菱 January 2014 (has links)
Background: Regulation of vascular tone is complex. Various complementary signaling pathways causing contraction and relaxation of vascular smooth muscle take place to ensure proper blood flow within the vasculature. Mitogen activated protein kinase (MAPK) signaling cascade is observed to be one of the many signaling pathways that regulate vascular tone.
Aim: This study examines the role of the following MAPK: mitogen-activated extracellular-regulated protein kinase kinase (MEK), extracellular signal-regulated kinase (ERK), and p38 MAPK in the regulation of relaxation in the endothelium and smooth muscle.
Method: Isometric tension of isolated porcine coronary artery rings were measured with organ chamber setup. The effects of MEK inhibitor, PD98059 (30 μM), ERK inhibitor, U0126 (10 μM) and p38 MAPK inhibitor, SB203580 (10 μM), on relaxations induced by bradykinin (a vasodilating peptide), SKA-31 [an activator of small and intermediate conductance calcium-activated potassium channels (SKCa and IKCa,, respectively)], Deta NONOate (a nitric oxide donor) and forskolin (an adenylate cyclase activator) were examined in arteries with and without endothelium, contracted with an thromboxane A2 analog, U46619 (300 nM – 1 μM). In some experiments, rings were also incubated with the following pharmacological inhibitors, indomethacin (cyclooxygenase inhibitor, 10 μM), L-NAME (nitric oxide synthase inhibitor, 300 μM), TRAM34 (IKCa blocker, 1 μM), and UCL1684 (SKCa blocker, 1 μM), alone or in combination.
Results:
1. Bradykinin-induced relaxation was potentiated by MEK and ERK inhibition but not by p38 MAPK inhibition.
2. SKA-31-induced relaxation was potentiated by MEK and p38 MAPK inhibition but not by ERK inhibition.
3. Deta NONOate-induced relaxation was potentiated by MEK, p38 MAPK inhibition, but not by ERK inhibition except in the presence of indomethacin, TRAM-34 plus UCL1684.
4. Forskolin-induced relaxation was potentiated by MEK and p38 MAPK inhibition, but not by ERK inhibition.
Discussion: MAPK plays a role in regulating the vascular tone in both the endothelium and smooth muscle of porcine coronary arteries. MEK appears to have an inhibitory action on relaxation that is downstream of the generation of endothelium-derived nitric oxide, activation of IKCa and SKCa and activation of adenylate cyclase. ERK are unlikely to be the downstream target of MEK for inhibiting relaxation, in view of the lack of effects of its inhibitor on endothelium-derived hyperpolarizing factor (EDHF)-mediated and endothelium-independent relaxations. The involvement of ERK in relaxation pathways in the endothelium appears to be complicated, since U0126 caused opposing effects (inhibition and potentiation) on bradykinin-induced relaxation in the presence of indomethacin without and with L-NAME or TRAM-34 plus UCL1684. As inhibition of p38 MAPK results in potentiation of relaxations to all relaxing agents tested except bradykinin, this MAPK may have opposing action in the endothelium and smooth muscle; endothelial p38 MAPK may facilitate relaxation while smooth muscle p38 MAPK attenuates it. In conclusion, this study provided additional information on the influences of MEK, ERK and p38 MAPK on relaxation; this knowledge may contribute to the understanding of the mechanisms underlying the development of vascular disorders. / published_or_final_version / Pharmacology and Pharmacy / Master / Master of Medical Sciences
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Regulation of vascular smooth muscle cell survival by the Akt pathwayTucka, Joanna Barbara January 2012 (has links)
No description available.
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Oxygen Regulation of Vascular Smooth Muscle Cell Proliferation and SurvivalBasu Ray, Julie 03 March 2010 (has links)
Arterial smooth muscle cells (SMCs) from the systemic and pulmonary circulations experience a broad range of oxygen concentrations under physiological conditions. The hypoxic response, however, has been inconsistent, with both enhanced proliferation and growth arrest being reported. This variability precludes a definitive conclusion regarding the role of oxygen tension in arterial disease. In the first part of this study, we determined if hypoxia elicits different proliferative and apoptotic responses in human aortic SMCs (HASMCs) incubated under conditions which do or do not result in cellular ATP depletion and whether these effects are relevant to vascular remodeling in vivo. Gene expression profiling was used to identify potential regulatory pathways. In HASMCs incubated at 3% O2, proliferation and progression through G1/S interphase are enhanced. Incubation at 1% O2 reduced proliferation, delayed G1/S transition, increased apoptosis and cellular ATP levels were reduced. In aorta and mesenteric artery from hypoxia exposed rats, both proliferation and apoptosis are increased after 48hrs. p53 and p21expression is differentially affected in HASMCs incubated at 1% and 3% O2. Hypoxia induces a state of enhanced cell turnover, conferring the ability to remodel the vasculature in response to changing tissue metabolic needs while avoiding the accumulation of mutations that may lead to malignant transformation or abnormal vascular structure formation. A unifying hypothesis in which events at the G1/S transition and apoptosis activation are coordinated by effects on p53, p21, their downstream effector genes and regulatory factors is proposed. Differences in the contractile responses of systemic and pulmonary arterial smooth muscle cells to hypoxia are well studied. Differences in proliferation and survival are anticipated because of differences in embryonal cell origin, oxygen concentrations within their respective microenvironments and in cellular energetics but these responses have not been directly compared. In the second part of the study, human pulmonary arterial SMCs (HPASMCs) proliferated at oxygen concentrations which inhibited cell growth in HASMCs. HPASMCs survived and maintained their intracellular ATP levels at levels of hypoxia sufficient to deplete ATP and induce apoptosis in HASMCs. In vivo studies in rats show proliferation and apoptosis in main or branch PASMCs only after 7 days of hypoxia. VSMCs are able to proliferate under hypoxic conditions as long as cellular ATP levels are maintained. HPASMCs have an enhanced capacity to maintain cellular energy status compared to HASMCs and hence their viability is preserved and the proliferative response predominates at lower oxygen concentrations.
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Role of IgE in modulating the expression and function of smMLCK in human airway smooth muscle cellsBalhara, Jyoti 04 April 2012 (has links)
Aberrant phenotypes of airway smooth muscle cells are central to the pathophysiology of asthma. The hypercontractile nature of these cells and hypertrophy are the key reasons for the excessive narrowing of the airways observed in allergic asthma. Although previous studies have indicated a role of enhanced content of smMLCK in modulating the contractile reactivity, as well as an indication of hypertrophy of HASM cells in asthmatic conditions, the effect of IgE on the expression of smMLCK in HASM cells is not fully understood. In this study, we demonstrate that IgE augments the expression of smMLCK at the mRNA and protein level. Inhibition of IgE binding with anti-FcεRI blocking antibody, Syk silencing, pharmacological inhibitors to MAPK (ERK1/2, p38, and JNK) and PI3K significantly diminished the IgE-mediated smMLCK expression in HASM cells. Finally, we found that IgE, similar to metacholine induces the contraction of HASM cells grown on collagen gel matrix. Our data suggest that IgE stimulates the phosphorylation of ERK, P38, STAT3 and induces the dephosphorylation of smMLCK to phosphorylate myosin regulatory light chain in HASM cells. Taken together, our data suggest a modulatory role of IgE in regulating the contractile machinery and hypertrophic phenotype of HASM cells.
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Oxygen Regulation of Vascular Smooth Muscle Cell Proliferation and SurvivalBasu Ray, Julie 03 March 2010 (has links)
Arterial smooth muscle cells (SMCs) from the systemic and pulmonary circulations experience a broad range of oxygen concentrations under physiological conditions. The hypoxic response, however, has been inconsistent, with both enhanced proliferation and growth arrest being reported. This variability precludes a definitive conclusion regarding the role of oxygen tension in arterial disease. In the first part of this study, we determined if hypoxia elicits different proliferative and apoptotic responses in human aortic SMCs (HASMCs) incubated under conditions which do or do not result in cellular ATP depletion and whether these effects are relevant to vascular remodeling in vivo. Gene expression profiling was used to identify potential regulatory pathways. In HASMCs incubated at 3% O2, proliferation and progression through G1/S interphase are enhanced. Incubation at 1% O2 reduced proliferation, delayed G1/S transition, increased apoptosis and cellular ATP levels were reduced. In aorta and mesenteric artery from hypoxia exposed rats, both proliferation and apoptosis are increased after 48hrs. p53 and p21expression is differentially affected in HASMCs incubated at 1% and 3% O2. Hypoxia induces a state of enhanced cell turnover, conferring the ability to remodel the vasculature in response to changing tissue metabolic needs while avoiding the accumulation of mutations that may lead to malignant transformation or abnormal vascular structure formation. A unifying hypothesis in which events at the G1/S transition and apoptosis activation are coordinated by effects on p53, p21, their downstream effector genes and regulatory factors is proposed. Differences in the contractile responses of systemic and pulmonary arterial smooth muscle cells to hypoxia are well studied. Differences in proliferation and survival are anticipated because of differences in embryonal cell origin, oxygen concentrations within their respective microenvironments and in cellular energetics but these responses have not been directly compared. In the second part of the study, human pulmonary arterial SMCs (HPASMCs) proliferated at oxygen concentrations which inhibited cell growth in HASMCs. HPASMCs survived and maintained their intracellular ATP levels at levels of hypoxia sufficient to deplete ATP and induce apoptosis in HASMCs. In vivo studies in rats show proliferation and apoptosis in main or branch PASMCs only after 7 days of hypoxia. VSMCs are able to proliferate under hypoxic conditions as long as cellular ATP levels are maintained. HPASMCs have an enhanced capacity to maintain cellular energy status compared to HASMCs and hence their viability is preserved and the proliferative response predominates at lower oxygen concentrations.
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