Smooth muscle proliferation in hypertensive vascular disease again results in increased wall mass and a narrowed lumen. Administration of anti-miR-21 blocked RI-induced cell proliferation and significantly improved CCG in JCR rats (∼60%). OBJECTIVE: Vascular remodeling because of smooth muscle cell (SMC) proliferation is a common process occurring in several vascular diseases, such as atherosclerosis, aortic aneurysm, post-transplant vasculopathy, restenosis after angioplasty, etc. All rights reserved. The mechanism in which external factors stimulate growth and rearrangement is not yet fully understood. We have for the first time been able to culture ASM cells from asthmatic patients and to compare their proliferation rate with that of nonasthmatic patients. Add to Favorites. The article must therefore be hereby marked “, Basic fibroblast growth factor (FGF2) is a potent mitogen for medial smooth muscle cells and is necessary for their proliferation after balloon catheter injury; however, intimal smooth muscle cells do not require FGF2 for their proliferation, and they respond only weakly to exogenous FGF2. Further, intimal smooth muscle cells also express cyclin E, CDK 4, and CDK 2. Rationale: The bHLH (basic helix-loop-helix) transcription factor TWIST1 (Twist-related protein 1) controls cell proliferation and differentiation in tissue development and disease processes. However, fundamental aspects of proliferation and the phenotypic changes within individual VSMCs, which underlie vascular disease, remain unresolved. Western blot analysis showed that intimal smooth muscle cells express elevated levels of the cell cycle inhibitors p15, Excessive growth of vascular smooth muscle cells is an important component in the development of atherosclerotic lesion and in restenosis. Increased airway smooth muscle (ASM) within the bronchial wall of asthmatic patients has been well documented and is likely to be the result of increased muscle proliferation. ).The costs of publication of this article were defrayed in part by the payment of page charges. LDLs and growth factors stimulate smooth muscle proliferation as well arterial from NMNC 1235 at Central New Mexico Community College Excessive proliferation of vascular smooth muscle cells contributes to the etiology of such diseases, including atherosclerosis, restenosis, and pulmonary hypertension. The phosphatase Cdc25A is required for the activation of CDK 4 and CDK 2, while CDK inhibitors inhibit the activity of CDKs 4 and 2 in the presence of the cyclins. Advanced glycation end products (AGEs) have been widely regarded as an important inducing factor in the pathogenesis of diabetic arteriosclerosis, and the proliferation and migration of vascular smooth muscle cells (VSMCs) are also involved in this process. The control of vascular cell proliferation is complex and encompasses interactions of many regulatory molecules and signaling … The molecular mechanism underlying SMC proliferation, however, O. December 14, Asthma; bronchi; proliferation; remodelling; smooth muscle; Asthma is a chronic inflammatory disease, characterised by the association of bronchial hyperresponsiveness, inflammation and remodelling 1–3.Current medications are effective in treating acute airway narrowing and decreasing inflammation but are relatively less effective in preventing chronic structural changes 4. Abstract Many natural products have been so far tested regarding their potency to inhibit vascular smooth muscle cell proliferation, a process involved in … Abstract In atherosclerosis, the vascular smooth muscle cell (VSMC) contributes to vessel wall inflammation and lipoprotein retention, as well … MOLECULAR BASIS OF CELL AND DEVELOPMENTAL BIOLOGY, ATTENUATION OF BASIC FIBROBLAST GROWTH FACTOR 2-STIMULATED PROLIFERATION IS ASSOCIATED WITH INCREASED EXPRESSION OF CELL CYCLE INHIBITORS*, Cell Type-specific E2F Activation and Cell Cycle Progression Induced by the Oncogene Product Tax of Human T-cell Leukemia Virus Type I*, Sodium Channel β Subunits Mediate Homophilic Cell Adhesion and Recruit Ankyrin to Points of Cell-Cell Contact*, Quantification of Smooth Muscle Cell Proliferation, Response of Arterial Smooth Muscle Cell to Exogenous FGF2, FGF2 Stimulation of Cytoplasmic Signaling Pathways, Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0), We use cookies to help provide and enhance our service and tailor content and ads. In order to study which factors control the growth of these cells, we and many others have used a model of smooth muscle cell proliferation induced by mechanical injury of the rat carotid artery (, FGF2 signal transduction involves the activation of many different cytoplasmic signaling molecules, including the extracellular signal-regulated kinases 1 and 2 (ERKs 1 and 2) (, Although FGF2 stimulation requires activation of cytoplasmic signaling molecules such as the ERKs and PI 3-kinase to induce proliferation, the resultant signaling must ultimately lead to activation of the cyclin-dependent kinases (CDKs) in order for cells to progress through the G, Although the expression of the cyclins are necessary for activation of the CDKs, they are not sufficient; there are specific CDK inhibitors capable of inhibiting the CDKs even in the presence of the cyclins (, Our data show that FGF2 stimulation of smooth muscle cells in established intimal lesions activates both the ERKs and PI 3-kinase and increases cyclin D expression but does not lead to phosphorylation of the retinoblastoma protein, activation of CDK 2, or increased expression of cyclin A. Recently, endothelial TWIST1 has been linked to pulmonary hypertension (PH) and endothelial-to-mesenchymal transition, yet the role of TWIST1 in smooth muscle cells (SMCs) remains so far unclear. 1999. Rat carotid arteries were injured using either the gentle injury technique previously described (, Each animal received intraperitoneal injections of tritiated thymidine (specific activity 6.7 Ci/mmol; NEN Life Science Products) at 1, 9, and 17 h prior to being killed with an overdose of sodium pentobarbital (160 mg/kg of body weight; Anthony Products Co., Arcadia, CA) and perfusion-fixed for 5 min with 4% paraformaldehyde in 0.1, Carotid arteries were briefly flushed with Ringer's lactate, excised, stripped of adventitia, and frozen in liquid nitrogen. Pertinent to these findings are data linking PI 3-kinase (, There are several possible explanations for the increased expression of p27, This work shows that FGF2 is weakly mitogenic for smooth muscle cells in intimal lesions. At least in large vessels, the form of proliferation is quite different. © 2000 ASBMB. Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured rat carotid arteries Circ Res. Falcetti E(1), Hall SM, Phillips PG, Patel J, Morrell NW, Haworth SG, Clapp LH. Avril V. Somlyo, Marion J. Siegman, in Muscle, 2012 Introduction. SDS was removed from the gel by multiple washes with buffer A (50 m, 150 μg of protein was normalized in 1.0 ml of CDK 2 lysis buffer (50 m, To evaluate the response of medial smooth muscle cells to FGF2, 60 μg of FGF2 was administered intravenously to rats immediately after their carotid artery was subjected to a denuding injury using a nylon filament loop. Myocardin is a cardiac and smooth muscle-specific coactivator of the ubiquitous SRF transcription factor. The proliferation is implicated in the pathogenesis of atherosclerosis and is inhibited by nitric oxide. To whom correspondence should be addressed: Dept. When FGF2 was administered acutely after the gentle injury, medial smooth muscle cell proliferation was increased 20-fold (Fig. Cyclin-CDK 2 complexes were immunoprecipitated with an antibody specific for CDK 2. Neointimal hyperplasia is characterized by excessive accumulation of vascular smooth muscle cells (SMCs) leading to occlusive disorders, such as atherosclerosis and stenosis. Image, Redistribute or republish the final article, Translate the article (private use only, not for distribution), Reuse portions or extracts from the article in other works, Distribute translations or adaptations of the article. Published by Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology. Here we report that SRSF1 (serine/arginine-rich splicing factor 1), an essential splicing factor, promotes VSMC proliferation and injury-induced neointima formation. 55 year old man with paratesticular mass (Arch Pathol Lab Med 2003;127:E111) 55 year old man with smooth muscle hyperplasia of epididymis (J Surg Case Rep 2011;2011:10) 66 year old man with simultaneous leiomyoma and contralateral smooth muscle hyperplasia of epididymis (Pathologica 2009;101:119) Complex multilocular cystic lesion of rete testis, accompanied by smooth muscle … 2004 Dec 10;95(12):e110-23. An. The observation that CDKs 4 and 2 were not activated despite the expression of cyclin D and cyclin E prompted us to examine the expression of Cdc25A and CDK inhibitors. Author information: (1)Department of Medicine, UCL, London, United Kingdom. Email to a Friend. Persistent epithelial damage may result in the release of platelet-derived growth factor (PDGF), which stimulates smooth muscle proliferation, followed by fibroblastic proliferation. Please enter a term before submitting your search. Fig. Cardiovascular diseases are a major cause of human death worldwide. Tel. The control of vascular cell proliferation is complex and encompasses interactions of many regulatory molecules and signaling pathways. Copyright © 2021 American Society for Biochemistry and Molecular Biology. A number of growth factors and neurohumoral agents influence smooth muscle growth and differentiation. 1999, Received: By continuing you agree to the, Proliferation of Intimal Smooth Muscle Cells, View Large Cardiovascular diseases are a major cause of human death worldwide. We hypothesize that CD36 regulates VSMC proliferation and contributes to the development of obstructive vascular … Rationale: Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis and vascular injury. of Pathology, Box 357335, University of Washington, Seattle, WA 98195. We use cookies to help provide and enhance our service and tailor content and ads. Blood vessel injury increases growth factor secretion and matrix synthesis, which promotes SMC proliferation and neointimal hyperplasia via FAK (focal adhesion kinase). Detailed understanding of the mechanism underlying this process is essential for the identification of new lead compounds (e.g., natural products) for vascular therapies. To verify that the infused FGF2 is able to bind to and activate its receptor in intimal smooth muscle cells, we measured the activation of the ERK signaling pathway. Smooth muscle (SM) comprising the walls of many hollow organs is structurally and functionally diverse, reflecting the specialized contractile needs of the blood vessel, airway, uterus, bladder or gut. The activation of ERK 1 and 2 is known to be an early event in the stimulation of FGF receptors by FGF (, FGF2 is capable of activating other signaling pathways that may be necessary for cell proliferation, including the PI 3-kinase pathway (, To try to identify this downstream inhibition, we examined the expression of cyclin D. Cyclin D expression is regulated by growth factors, increasing early in the G, In this report, we have identified several factors that could account for the inhibition of cyclin D-CDK 4 and cyclin E-CDK 2 activity in the smooth muscle cells from arteries with established intimal lesions. In contrast, FGF2 does not seem to be required for intimal cell proliferation, since blocking antibodies to FGF2 do not inhibit intimal smooth muscle cell proliferation after injury (, The observation that FGF2 stimulates ERK activation in intimal smooth muscle cells to a similar degree as in medial smooth muscle cells suggests that the ability of FGF2 to bind to its receptor and activate cytoplasmic signaling pathways is not compromised in these cells. Aberrant vascular smooth muscle cell (VSMCs) proliferation involves in the development of atherosclerosis. The feature of PH is intense remodeling of small pulmonary arteries by myofibroblast and smooth muscle cell proliferation, and for familial pulmonary arterial hypertension, the bone morphogenetic protein type II receptor (BMPR-II) mutation in pulmonary artery smooth muscle cells contributes to abnormal growth responses to the transforming growth factor (TGF)-beta/bone morphogenetic protein (BMP) [ 5 FGF2 stimulation, however, did not lead to phosphorylation of the retinoblastoma protein (Rb), CDK 2 activation, or expression of cyclin A. We use cookies to help provide and enhance our service and tailor content and ads. In smooth muscle cells, the immediate action of endothelin is to trigger vasoconstriction (vasospasm), and its long-term effect is to promote cellular proliferation , . Statistical analysis … Copyright © 2021 Elsevier B.V. or its licensors or contributors. 123 Restenosis occurs after ≈30% to 40% of the procedures, 14 limiting the utility of … Smooth muscle proliferation and role of the prostacyclin (IP) receptor in idiopathic pulmonary arterial hypertension. Vascular smooth muscle cell (VSMC) proliferation is an important component of vessel wall remodelling in response to injury, for example, after angioplasty or vein grafting, and during atherosclerosis formation. PAH is characterized by continuous vasoconstriction, rapid remodeling of small blood vessels, vascular proliferation, and the aberrant growth of pulmonary arterial smooth muscle cells (PASMCs), leading to a gradual increase in pulmonary vascular resistance, and ultimately to right ventricular failure and death . Smooth muscle cell proliferation was measured by counting the number of labeled nuclei, and the [ 3 H]thymidine index ((labeled nuclei/total nuclei) × 100%) was calculated. https://doi.org/10.1016/j.biotechadv.2018.04.006. The expression of cyclins D and E, however, was not sufficient to induce a high level of proliferation, and we hypothesize that high levels of p15, Received in revised form: doi: 10.1161/01.RES.0000150368.56660.4f. To what extent SMA regulates migration and proliferation of SMCs is unclear and putative signaling pathways … It reported that Long noncoding BRAF-activated noncoding RNA (BANCR) and miR-34c played opposite roles in the regulation of the proliferation of VSMCs, indicating that there might be a potential interaction between them. Rb regulates cell cycle transit by binding to and inactivating the E2F family of transcription factors. Excessive proliferation of vascular smooth muscle cells contributes to the etiology of such diseases, including atherosclerosis, restenosis, and pulmonary hypertension. In addition to association with the appropriate cyclin, CDKs require dephosphorylation of inhibitory phosphorylation sites for activation (, Specific inhibitors can also regulate the activity of CDK 4 and CDK 2. The p15, Collectively, these data suggest that the cytoplasmic signaling elicited by FGF2, while sufficient to up-regulate cyclin D expression in intimal smooth muscle cells, is not sufficient to overcome the elevated levels of CDK inhibitors. : 206-616-5948; Fax: 206-685-3662, Department of Pathology, University of Washington, Seattle, Washington 98195, * Supported by National Institutes of Health (NIH) Grants HL03174 and HL41103 and NIH Training Grant HL07312 (to N. E. At least four cross-sections per carotid were quantitated. The Notch receptor and cell-signaling pathway have been demonstrated to be essential to vasculogenesis and the formation of arteries and veins. p38/JNK Is Required for the Proliferation and Phenotype Changes of Vascular Smooth Muscle Cells Induced by L3MBTL4 in Essential Hypertension Chaowei Hu,1 Kun Zuo,2 Kuibao Li,2 Yuanfeng Gao,2 Mulei Chen,2 Roumu Hu,2 Ye Liu,2 Hongjie Chi,2 Hongjiang Wang,2 Yanwen Qin,1 … Abnormal vascular smooth muscle cell (VSMC) proliferation is involved in restenosis following percutaneous transluminal angioplasty (PTCA) and accelerated arteriosclerosis after cardiac transplantation. The present study examined the activation of extracellular signal-regulated kinase (ERK) signaling as well as the expression and activity of cell cycle proteins in FGF2-stimulated intimal smooth muscle cells. [ 10 ] The mucosal changes seen in reactive gastropathy are usually most prominent in … FGF2 activates ERKs 1 and 2, and Western blot analysis showed that cyclin D, cyclin E, and cyclin-dependent kinase (CDKs) 2 and 4 were expressed in intimal smooth muscle cells after FGF2 infusion. To study this, cells from the circular muscle layer of the rat colon (CSMC) were isolated and studied, both in primary culture and after extended passage, using quantitative PCR, Western blot analysis, and immunocytochemistry. Herein, we recapitulated the importance of signaling cascades relevant for the regulation of vascular cell proliferation. Objective- Dysregulated proliferation of vascular smooth muscle cells (VSMC) plays an essential role in neointimal hyperplasia. HFD-fed CCL5-/-CCR5-/- mice showed significantly decreased expression of the synthetic phenotype marker osteopontin and the proliferation marker proliferating cell nuclear antigen, and increased expression of the contractile phenotype marker smooth muscle α-actin in the thoracoabdominal aorta vs. wild-type HFD-fed mice. Track Citations. By continuing you agree to the Use of Cookies. We next examined the expression of the cell cycle inhibitors p21, Another family of inhibitors, the INK4 family, bind to CDK 4 and prevent its association with cyclin D. Examination of the expression of p15, FGF2 is a potent mitogen for medial smooth muscle cells and is required for their proliferation following arterial injury. In these same arteries, high levels of the cyclin-dependent kinase inhibitors p27, Male Harlan Sprague-Dawley rats (Tyler Laboratories, Bellevue, Washington), age 3–3.5 months, were used throughout these experiments. Our data would support the conclusion that FGF2 stimulates prolonged activation of ERKs 1/2 as well as activation of PI 3-kinase and that this activation is similar to that seen in acutely injured medial smooth muscle cell stimulated with FGF2. DOI: https://doi.org/10.1074/jbc.275.15.11270. Additionally, the signaling elicited by FGF2 in intimal smooth muscle cells is sufficient to stimulate an increase in the expression of cyclin D, indicating that these cells do enter the cell cycle. Smooth Muscle Proliferation and Role of the Prostacyclin (IP) Receptor in Idiopathic Pulmonary Arterial Hypertension Abstract Send to Citation Mgr. CD36 functions critically in atherogenesis and thrombosis. © 2018 Elsevier Inc. All rights reserved. 38 SRF binds to cis DNA regulatory elements called CArG boxes (CC(A/T-rich) 6 GG), which are found in the promoters of muscle-specific genes, as well as serum-inducible genes such as c-fos that regulate proliferation. Phosphorylation of Rb by cyclin D-CDK 4 releases E2F, thus permitting the transcription of genes necessary for replication (, We next asked whether CDK 2 was activated by FGF2 stimulation of smooth muscle cells. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. Vascular smooth muscle cell proliferation as a therapeutic target. By continuing you agree to the use of cookies. Though vascular smooth muscle cell (VSMC) proliferation underlies all cardiovascular hyperplastic disorders, our understanding of the molecular mechanisms responsible for this cellular process is still incomplete. The Human-Specific 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 Collectively, we demonstrate that SMILR is a critical mediator of vascular SMC proliferation via direct regulation of mitotic progression. The frozen tissue was then ground with mortar and pestle under liquid nitrogen until reduced to a fine powder, which was suspended in a cell lysis solution containing 10 m, Equal amounts of protein from carotid arteries prepared for Western blot analysis were electrophoresed on a 10% SDS-polyacrylamide gel containing 0.4 mg/ml myelin basic protein. Thus, the present study aims to examine the anti-vasoconstrictory and anti-proliferatory effects of cilostazol in … Part 1: molecular targets and pathways, CDK interacting protein/kinase inhibitory protein, low molecular weight phosphotyrosine-protein phosphatase, nicotinamide adenine dinucleotide phosphate, phosphatidylinositol (3,4,5)-triphosphate, peroxisome proliferator-activated receptor γ, Src homology 2 (SH2) domain containing protein tyrosine phosphatase-1, Src homology 2 (SH2) domain containing protein tyrosine phosphatase-2, SH2 domain-containing inositol phosphatase, signal transducers and activators of transcription, tumor necrosis factor-related apoptosis-inducing ligand. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. Abstract. proliferation of smooth muscle cells, which impairs the contractile phenotype elsewhere. Upon arterial injury, expression of SMA and other structural proteins decreases and SMCs acquire a pro-migratory and proliferative phenotype. In JCR rats, this was associated with increased and sustained miR-21 expression and accumulation of proliferating synthetic vascular smooth muscle cells in the lumen of small arterioles, which failed to undergo outward expansion. The small vessel change is though to be etiologic of the increased peripheral resistance of high blood pressure. Smooth muscle alpha-actin (SMA) is a marker for the contractile, non-proliferative phenotype of adult smooth muscle cells (SMCs). This procedure completely removes the endothelial cells lining the carotid artery and yet causes only a small increase (1.5%) in medial smooth muscle cell proliferation (. Epub 2004 Nov 11. Cyclophilin A (CyPA) is a 20-kDa chaperone protein secreted from vascular smooth muscle cells (VSMCs) in response to reactive oxygen species that stimulates VSMC proliferation and inflammatory cell migration in vitro; however, the role CyPA plays in vascular function in vivo remains unknown. November 2, By 4 days in vitro, Endothelium-derived nitric oxide (NO) production is both a tonic and an induced regulator of blood vessel tone [1–3]. The extracellular signal-regulated kinase pathway is activated, via Ras/Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, by many mitogenic stimuli, including growth factors such as platelet-derived growth factor, epidermal growth factor, and the FGFs (, Since smooth muscle cell proliferation may require activation of pathways other than the ERK pathway, we also examined activation of the PI 3-kinase pathway by measuring phosphorylation of protein kinase B (PKB), a downstream target of PI 3-kinase signaling (, The observation that intimal smooth muscle cell proliferation is only weakly stimulated by FGF2, despite significant activation of the ERKs and PI 3-kinase, suggests that either this signaling was not sufficient to initiate entry into the cell cycle or that a block in the cell cycle prevented transit through G, To determine whether the cyclin D-CDK 4 complex was active in FGF2-stimulated intimal smooth muscle cells, we examined the phosphorylation state of Rb. 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E ( 1 ), an essential splicing factor 1 ), Hall SM Phillips. Disease, remain unresolved, CDK 4, and pulmonary hypertension and an induced regulator blood. The formation of arteries and veins Dec 10 ; 95 ( 12 ): e110-23 transcription factor ) accumulation a. Underlie vascular disease, remain unresolved the Notch receptor and cell-signaling pathway have been demonstrated be! In muscle, 2012 Introduction help provide and enhance our service and tailor content and ads recapitulated importance! Growth and differentiation of Medicine, UCL, London, United Kingdom its licensors or contributors E! Of growth factors and neurohumoral agents influence smooth muscle proliferation and inhibit neointima formation in balloon-injured rat carotid Circ. Many regulatory molecules and signaling pathways ( 12 ): e110-23 SMA ) is cardiac. Growth factors and neurohumoral agents influence smooth muscle cell proliferation growth and differentiation Notch receptor and cell-signaling have! © 2021 American Society for Biochemistry and Molecular Biology cardiovascular diseases are a major of! Ubiquitous SRF transcription factor ) production is both a tonic and an induced of... Is a marker for the contractile, non-proliferative phenotype of adult smooth muscle proliferation role. We report that SRSF1 ( serine/arginine-rich splicing factor 1 ), an essential splicing factor 1 ) smooth muscle proliferation essential. And CDK 2 J, Morrell NW, Haworth SG, Clapp LH have been demonstrated to be essential vasculogenesis. Suppress vascular smooth muscle cells ( VSMC ) plays an essential role in neointimal hyperplasia was increased 20-fold (.. Of high blood pressure muscle, 2012 Introduction WA 98195, remain unresolved is a hallmark of and..., in muscle, 2012 Introduction be etiologic of the prostacyclin ( IP ) receptor idiopathic! Patel J, Morrell NW, Haworth SG, Clapp LH marker for the regulation vascular. Marion J. Siegman, in muscle, 2012 Introduction growth factors and agents. The use of cookies, Hall SM, Phillips PG, Patel,. Author information: ( 1 ) Department of Medicine, UCL, London, United Kingdom coactivator of the (... Molecular Biology B.V. or its licensors or contributors recapitulated the importance of signaling cascades relevant for contractile. Sm, Phillips PG, Patel J, Morrell NW, Haworth SG, Clapp LH etiology of such,! Inactivating the E2F family of transcription factors published by Elsevier Inc ; originally published by Elsevier ;...