PubMed Journals Articles About "Thymine Glycosylase Regulator CaMKII Expression Vascular Smooth Muscle" RSS

19:26 EST 26th January 2020 | BioPortfolio

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Showing "Thymine Glycosylase Regulator CaMKII Expression Vascular Smooth Muscle" PubMed Articles 1–25 of 22,000+

Thymine DNA Glycosylase (TDG) is a Key Regulator of CaMKIIγ Expression and Vascular Smooth Muscle Phenotype.

Multifunctional Ca/calmodulin-dependent protein kinase II (CaMKII) is a multi-gene family with isoform-specific regulation of vascular smooth muscle (VSM) functions. In previous studies we found that vascular injury resulted in VSM de-differentiation and reduced expression of the CaMKIIg isoform in medial wall VSM. Smooth muscle knockout of CaMKIIg enhanced injury-induced VSM neointimal hyperplasia whereas CaMKIIg over-expression inhibited VSM proliferation and neointimal formation. In this study, we evalua...

The long non-coding RNA metastasis-associated lung adenocarcinoma transcript-1 regulates CCDC80 expression by targeting miR-141-3p/miR-200a-3p in vascular smooth muscle cells.

Our previous study showed that Coiled-Coil Domain Containing 80 (CCDC80) accelerates the development of atherosclerosis by decreasing lipoprotein lipase (LPL) expression and activity in apoE knockout mice. However, the regulatory mechanism for CCDC80 expression is unclear. This study was designed to evaluate whether non-coding RNAs involved the regulation of CCDC80 expression in vascular smooth muscle cells (VSMCs).

Up-regulation of cullin7 promotes proliferation and migration of pulmonary artery smooth muscle cells in hypoxia-induced pulmonary hypertension.

It has well been demonstrated that E3 ubiquitin ligase cullin7 plays important roles in cancer cell growth control via down-regulating p53 expression. The noncanonical function or the pathogenic role of p53 has more recently been implicated in pulmonary vascular remodeling. Therefore, whether cullin7 participates in hypoxia-induced pulmonary vascular remodeling deserves to be elucidated. The present study found that hypoxia up-regulated the expression of cullin7 mRNA and protein in pulmonary arteries and pu...

Blocking PERK resuces vascular smooth muscle cells from homocysteine-induced ER stress and apoptosis.

Hyperhomocysteinemia induces stress response in endoplasmic reticulum (ERS). Here, we tested whether blockage of homocysteine (Hcy) induced ERS and subsequent apoptosis in vascular smooth muscle cells can be inhibited by  blockage of PERK/eIF2α/ATF4/CHOP signaling. Short-term exposure of vascular smooth muscle cells to Hcy led to the phosphorylation of PERK (pPERK), which in turn, phosphorylated eIF2 alpha (peIF2a) and inhibited the unfolded protein response. Long-term Hcy exposure, however, increased the...

Anti-high mobility group box-1 antibody attenuated vascular smooth muscle cell phenotypic switching and vascular remodelling after subarachnoid haemorrhage in rats.

Although cerebral vascular smooth muscle cell (VSMC) phenotypic switching is involved in the vascular dysfunction after subarachnoid haemorrhage (SAH), the precise mechanisms are still unclear. High mobility group box-1 (HMGB1) has been identified as a modulator in VSMC proliferation. The purpose of this study was to investigate the potential role of HMGB1 in the VSMC phenotypic switching following SAH. An endovascular perforation SAH model was used in our experiments. The expression levels of HMGB1, α-smo...

RhoGDI stability is regulated by SUMOylation and ubiquitination via the AT1 receptor and participates in Ang II-induced smooth muscle proliferation and vascular remodeling.

The physiological role of Rho-specific guanine nucleotide dissociation inhibitor (RhoGDI) in vascular remodeling remains unknown. We investigated the function of RhoGDI in angiotensin II (Ang II)-induced vascular remodeling in cultured human aortic vascular smooth muscle cells (HA-VSMCs) and in an Ang II-infusion vascular remodeling mouse model.

The role of vascular smooth muscle cell membrane-bound thrombomodulin in neointima formation.

Thrombomodulin (TM) is an endothelial cell membrane-bound anticoagulant protein expressed in normal arteries. After vascular injury, medial and neointimal smooth muscle cells (SMCs) exhibit large amounts of TM. The purpose of this study was to investigate the physiological significance of vascular SMC-bound TM.

Inhibition of vascular smooth muscle cell calcification by vasorin through interference with TGFβ1 signaling.

Elevated transforming growth factor β1 (TGFβ1) levels are frequently observed in chronic kidney disease (CKD) patients. TGFβ1 contributes to development of medial vascular calcification during hyperphosphatemia, a pathological process promoted by osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Vasorin is a transmembrane glycoprotein highly expressed in VSMCs, which is able to bind TGFβ to inhibit TGFβ signaling. Thus, the present study explored the effects of vasorin o...

Exosomal Notch3 from high glucose-stimulated endothelial cells regulates vascular smooth muscle cell calcification/aging.

Vascular calcification/aging can cause different kind of serious diabetic vascular complications. High glucose could induce vascular smooth muscle cells (VSMCs) calcification/aging and then lead to diabetes-related vascular calcification/aging. In this study, we investigated how information in the blood is transmitted to VSMCs and the mechanisms of VSMC calcification/aging under hyperglycaemic conditions.

Reticulocalbin 2 enhances osteogenic differentiation of human vascular smooth muscle cells in diabetic conditions.

Diabetes accelerates pro-atherogenic and pro-osteogenic phenotypes of vascular smooth muscle cells (VSMCs), an important process for vascular calcification. Reticulocalbin 2 (RCN2) is a candidate gene for atherosclerosis and involved in vascular remodeling in hypertension. However, the role of RCN2 in VSMCs calcification under diabetic conditions is unclear.

Potassium Channels in Vascular Smooth Muscle: A Pathophysiological and Pharmacological Perspective.

Potassium (K ) ion channels are the main determinant of vascular tone by regulating cell resting membrane potential (Em). Systemic arterial tone as well as pulmonary arterial tone is mainly controlled by the Em of systemic vascular smooth muscle cells (SVSMC) or pulmonary arterial smooth muscle cells (PASMC), and via endothelial cell (EC) functions. Resting membrane potential is dependent of membrane permeability to cations and anions. This article is protected by copyright. All rights reserved.

Lamin A/C negatively regulated by miR-124-3p modulates apoptosis of vascular smooth muscle cells during cyclic stretch application in rats.

Apoptosis of vascular smooth muscle cells (VSMCs) influenced by abnormal cyclic stretch is crucial for vascular remodeling during hypertension. Lamin A/C, a nuclear envelope protein, is mechano-responsive, but the role of lamin A/C in VSMC apoptosis is still unclear.

The Human- and Smooth Muscle Cell-Enriched lncRNA SMILR Promotes Proliferation by Regulating Mitotic CENPF mRNA and Drives Cell-Cycle Progression Which Can Be Targeted to Limit Vascular Remodeling.

In response to blood vessel wall injury, aberrant proliferation of vascular smooth muscle cells causes pathologic remodeling. However, the controlling mechanisms are not completely understood.

Adenosine Attenuates Aortic Smooth Muscle Cell Calcification through A Adenosine Receptor.

Vascular calcification is a typical feature of atherosclerosis and is associated with adverse cardiovascular events such as myocardial infarction and stroke. Several studies have suggested that adenosine, an ATP metabolite may function as an endogenous regulator of arterial calcification. However, its effects on vascular smooth muscle cell calcification have not been clarified. In this study, we investigated the inhibitory effects of adenosine on vascular calcification in vitro by utilizing the culture of h...

LncRNA MALAT1 regulates proliferation and apoptosis of vascular smooth muscle cells by targeting miRNA-124-3p/PPARα axis.

To uncover the involvement of long non-coding RNA (lncRNA) MALAT1 in the proliferation and apoptosis of vascular smooth muscle cells (VSMCs), and the underlying mechanism.

Fibroblast growth factor 23 expression in human calcified vascular tissues.

Vascular calcification is a major risk for cardiovascular disease and implies the transformation of smooth muscle cells to an osteoblastic phenotype as a consequence of dysregulation of calcium and phosphate metabolism. Fibroblast growth factor (FGF) 23 is the most potent phosphate regulator. Observational studies suggest that high levels of FGF23 are related to cardiovascular morbidity and mortality. In this work, we determined the levels of both the intact and the carboxi-terminal fragments of circulating...

Impact of C-reactive protein on osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells.

Medial vascular calcification occurs during the aging process and is strongly accelerated by chronic kidney disease (CKD). Elevated C-reactive protein (CRP) levels are associated with vascular calcification, cardiovascular events and mortality in CKD patients. CRP is an important promoter of vascular inflammation. Inflammatory processes are critically involved in initiation and progression of vascular calcification. Thus, the present study explored a possible impact of CRP on vascular calcification. We foun...

Smooth muscle-specific TMEM16A expression protects against angiotensin II-induced cerebrovascular remodeling via suppressing extracellular matrix deposition.

Cerebrovascular remodeling is the leading factor for stroke and characterized by increased extracellular matrix deposition, migration and proliferation of vascular smooth muscle cells, and inhibition of their apoptosis. TMEM16A is an important component of Ca-activated Cl channels. Previously, we showed that downregulation of TMEM16A in the basilar artery was negatively correlated with cerebrovascular remodeling during hypertension. However, it is unclear whether TMEM16A participates in angiotensin II (Ang ...

Role of polypyrimidine tract-binding protein 1/yin yang 2 signaling in regulating vascular smooth muscle cell proliferation and neointima hyperplasia.

Abnormal proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of vascular restenosis. We investigated whether polypyrimidine tract-binding protein 1 (PTBP1), a novel regulator of cell proliferation and differentiation, is implicated in VSMC proliferation and neointima hyperplasia responding to injury. C57BL/6 J mice of 10-12 weeks old were randomly divided into sham and carotid artery injury group. Primary VSMCs obtained from thoracic aortas of 10- to 12-week-old mice were treated with ph...

Klotho deficiency induces arteriolar hyalinosis in a trade-off with vascular calcification.

Hyalinosis is a vascular lesion affecting the renal vasculature and contributing to ageing-related renal function decline. We assessed whether arteriolar hyalinosis is caused by Klotho deficiency - a state known to induce both renal and vascular phenotypes associated with ageing. Histochemistry was used to assess hyalinosis in Klotho kidneys, compared to Klotho and wild-type littermates. Immunohistochemistry was used to investigate vascular lesion composition and the different layers of the vascular wall. F...

CAIII expression in skeletal muscle is regulated by Ca-CaMKII-MEF2C signaling.

Carbonic anhydrase III (CAIII) is selectively expressed in slow-twitch myofibers in skeletal muscle. The fast-twitch to slow-twitch transformation of myofibers following denervation is accompanied by increased CAIII expression, suggesting that the effects of nerve impulses on skeletal-muscle remodeling influence CAIII expression. Here, we determined the molecular mechanisms underlying the effects of nerve conduction on CAIII expression. The results indicated that changes in skeletal-muscle [Ca] altered CAII...

Lipopolysaccharide exposure modulates the contractile and migratory phenotypes of vascular smooth muscle cells.

Sepsis survivors are at higher risk for cardiovascular events. Lipopolysaccharide (LPS) activates Toll-like receptor 4 (TLR4) in sepsis. Activation of TLR4 modulates vascular smooth muscle cells (VSMCs) phenotype and contributes to cardiovascular changes after sepsis.

Smooth muscle in cardiac chambers is common in turtles and extensive in the emydid turtle, Trachemys scripta.

A prominent layer of smooth muscle lining the luminal side of the atria of freshwater turtles (Emydidae) was described more than a century ago. We recently demonstrated that this smooth muscle provides a previously unrecognized mechanism to change cardiac output in the emydid red-eared slider (Trachemys scripta) that possibly contributes to their tremendous diving capacity. The purpose of the present immunohistochemical study was firstly to screen major groups of vertebrates for the presence of cardiac smoo...

Sauchinone inhibits angiotensin II-induced proliferation and migration of vascular smooth muscle cells.

Hypertension is a common type of cardiovascular disease that remains a major cause of death in the world. Vascular remodeling is an important complication of hypertension, and vascular smooth muscle cells (VSMCs) play a major role in vascular remodeling. Sauchinone is one of the active lignin, which has been found to possess vascular protective effect. However, the functional role of sauchinone in hypertension has not been investigated. The aim of this study was to evaluate the role of sauchinone in the ang...

Expression of Long Noncoding RNA LIPCAR Promotes Cell Proliferation, Cell Migration, and Change in Phenotype of Vascular Smooth Muscle Cells.

BACKGROUND The long noncoding RNA LIPCAR is a type of transcription product (>200 nucleotides long). Recent studies demonstrated that LIPCAR is a potential biomarker in cardiovascular disease and can predict survival in patients with cardiovascular disease. Therefore, the present study explored the role of LIPCAR in the regulation of proliferation, migration, and change in phenotype of vascular smooth muscle cells. MATERIAL AND METHODS Human vascular smooth muscle cells (VSMCs) were treated with 20 g/mL oxi...

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