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W4245796012 abstract "HomeCirculation ResearchVol. 115, No. 12Circulation Research “In This Issue” Anthology Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBCirculation Research “In This Issue” Anthology Ruth Williams and The Editors Ruth WilliamsRuth Williams Search for more papers by this author and The Editors Search for more papers by this author Originally published5 Dec 2014https://doi.org/10.1161/RES.0000000000000042Circulation Research. 2014;115:e40–e70Circulation Research, vol 112, 2013Abcg2 and Division of Cardiac Stem Cells (p 27)1Sereti et al identify cell-surface protein Abcg2 as a promoter of both proliferation and symmetric cell division in cardiac progenitors.Download figureDownload PowerPointIt is currently believed that to maintain homeostasis, cardiac progenitor cells divide asymmetrically, giving rise to one cell that differentiates and another that replaces the progenitor. After an injury, however, it is thought that the progenitor cell population is depleted as these cells differentiate into cardiac myocytes, and that replenishment of the pro genitors occurs by symmetrical division. Understanding the molecular mechanisms that drive cardiac progenitor cell division might therefore be useful in developing potential cell-based therapies for heart repair. The cell surface protein Abcg2, which is expressed on cardiac progenitors, was previously found to regulate proliferation in these cells. Now Sereti et al have discovered that this protein not only promotes cell-cycle progression, but also symmetric division. Progenitor cells that lacked Abcg2 tended to arrest before DNA replication—at G0 and G1 stages of the cell cycles—while those that did divide tended to do so asymmetrically. Thus, the authors suggest that regulating Abcg2 levels after injury could maximize the regenerative potential of the heart.S100A1 in Angiogenesis (p 66)2Lack of calcium-binding protein S100A1 in ischemic tissue prevents the production, and thus protective effects, of nitric oxide, say Most et al.Download figureDownload PowerPointIt is well known that nitric oxide (NO) protects blood vessels during ischemia. And it has also been reported that the calcium-binding protein S100A1, expressed in endothelial cells, increases NO synthesis via eNOS. Furthermore, S100A1 has been found to be crucial for endothelial function. Most et al now bring these separate pieces of evidence together and show that ischemic tissue samples taken from both patients with chronic critical limb ischemia and mice with induced limb ischemia display a near-complete loss of S100A1 expression, which is associated with a decrease in NO. The team created S100A1 knockout (SKO) mice and showed that these animals have impaired reperfusion and neovascularization after ischemia. However NO injections restored the angiogenic potential in these mice. The team also showed that S100A1 directly binds and activates eNOS and also indirectly activates the enzyme by suppressing the activity of an eNOS inhibitor. Altogether, these results show that S100A1 is a critical regulator of eNOS and that it could be a therapeutically important protein for the treatment of ischemic vascular disease.Stem Cells in Dilated Cardiomyopathy (p 165)3Bone marrow stem cell transplants lead to long-term improvements in heart function for cardiomyopathy patients, report Vrtovec et al.Download figureDownload PowerPointVrtovec et al report the results of a 5-year follow-up study of dilated cardiomyopathy (DCM) showing that patients who received intracoronary bone marrow transplants have better exercise capacity, heart function and better chance of survival compared with patients that did not receive the treatment. The 55 randomly selected DCM patients who received the bone marrow generally had higher left ventricle ejection fraction, could walk further, had lower levels of NT-proBNP—a protein marker of heart failure—in their blood, and fewer of them died. Interestingly, symptomatic improvement correlated with the extent to which the bone marrow cells integrated into the myocardium—which was assessed by radioactive tracing on the day of the transplantation. The improvements generally tended to be most significant within the first few years of the procedure. Ejection fraction, for example, showed a dramatic difference between test subjects and controls after one year, which persisted for a further two years, but then started to decline. This suggests that repeating the treatment regimen every few years, might further improve outcomes in DCM patients, say the authors.Sarcolemmal Invaginations and Nuclear Ca2+ (p 236)4Ibarra et al reveal how calcium signals get to cardiac myocyte nuclei without interference from the cytoplasm.Download figureDownload PowerPointCalcium signaling in the nucleus regulates several cell functions including, chromatin condensation, nuclear transport and the activation of transcription factors. However, in cardiac myocytes, where the calcium signals in the cytosol are in constant flux, it is unclear how nuclear calcium signals are separated from the cytosolic noise. Stimulation of the cell surface receptor, insulin-like growth factor 1 receptor (IGF-1R), has been known to activate nuclear calcium signaling in cardiac myocytes, but how this signal is transmitted has remained a mystery. Now Ibarra et al show that IGF-1R is localized to invaginations of the plasma membrane or T-tubules that reach right up to the nucleus. They found that components of the signaling cascade, downstream of IGF-1R, including an associated G-protein, inositol 1,4,5 triphosphate, and phospholipase C, are also localized to the nuclear region. Furthermore, IGF-1R adopted a similar location and function in embryonic and neonatal cardiac myocytes, where T-tubules are thought to be underdeveloped. The authors suggest that the newly discovered nuclear signaling function of T-tubules might be of clinical relevance as dysfunctional T-tubules are associated with heart disease and myocardial ischemic injury.miRNA-15a/-16 in Critical Limb Ischemia (p 335)5Spinetti et al discover two microRNAs that impair function and survival of proangiogenic cells in critical limb ischemia.Download figureDownload PowerPointCritical limb is chemia (CLI) is an advanced form of peripheral artery disease that can cause extensive tissue injury and cell death. In severe cases, amputation is the only option. To prevent the need for such drastic treatments, researchers are investigating the use of autologous bone-marrow pro-angiogenic cells (PACs) for therapy. PAC function is impaired in CLI patients, however, so Spinetti et al wanted to know why. They found that 2 microRNAs, miR-15a and miR-16, were over-expressed in PACs and were associated with impaired survival and migration of these cells. Over-expressing miR-15a and miR-16 in healthy PACs increased their rate of apoptosis and decreased migration, while suppressing expression of the miRs in patient PACs, improved cell migration. Furthermore, PACs in which miR-15a and -16 expression was repressed, improved post-ischemic blood flow and vessel density when injected into mice with limb ischemia. The authors suggest that not only could the miRs serve as biomarkers of the disease, but that repression of miR-15a and -16 might improve PAC-based therapies in patients with CLI.Endothelin Axis in RVH (p 347)6Drugs for lowering pulmonary artery blood pressure could have detrimental effects on the heart, say Nagendran et al.Download figureDownload PowerPointChronic pulmonary arterial hypertension (PAH) is not, as the name might suggest, a problem restricted to the arteries of the lungs. It is also associated with decreased functioning of the right ventricle of the heart, which can ultimately lead to heart failure and death. Endothelin receptor antagonists are currently used for the treatment of PAH, but Nagendran et al suggest that despite their favorable profile, these drugs might have detrimental effects. The drugs lower blood pressure by blocking the activity of a vasoconstrictor called Endothelin-1, which is upregulated in the pulmonary arteries of patients with PAH. However, the authors show that both Endothelin-1 and the Endothelin receptor are also upregulated in the right ventricle of these patients, and in rats with PAH. In the heart, Endothelin-1 might be part of an important compensatory response to maintain contractility, the authors suggest. Indeed, ex vivo treatment of PAH model rat hearts with an Endothelin receptor antagonist reduced contractility. On the basis of these observations, they caution that direct cardiac effects of endothelin receptor antagonists should be taken into account when considering the use of these drugs to treat PAH patients.β-Adrenergic Signaling and CPC Function (p 476)7β-Adrenergic stimulation of cardiac progenitor cells is a double-edged sword, say Khan et al.Download figureDownload PowerPointDuring heart failure, β-adrenergic stimulation of the heart is increased to aid in contraction, providing temporary relief to weakened heart muscles. In the long-term however, this stimulation causes cardiac myocytes to die. To prevent this damage β-adrenergic blockers are often used to treat heart failure patients. When cardiac myocytes die, they are replaced, albeit slowly, by cardiac progenitor cells. However, it is unclear how exactly these progenitors are affected by β-blockers, or indeed, by β-adrenergic stimulation. Now, Khan et al report that β-adrenergic stimulation induces mouse cardiac progenitor cells to proliferate. But, just like adult cardiac myocytes, the progenitor cells underwent apoptosis as soon as they were induced to differentiate. The investigators found that progenitor cells expressed only one type of β-adrenergic receptor, β1-AR, but upon differentiation, they started to express a second, β2-AR—also found in mature cardiac myocytes. And because these 2 receptors convey separate effects, the authors suggest that a bipartite approach, involving β1-AR activation and β2-AR blockade, could be more effective in treating heart failure.Pro- and Anti-Apoptotic Signaling of cAMP (p 498)8Zhang et al suggest replacing β-blockers with a PKA inhibitor to treat heart failure.Download figureDownload PowerPointMuch like Khan and colleagues, Zhang et al were interested in the effects of β-adrenergic stimulation and β-blockers on the heart. They knew that long-term β-adrenergic stimulationduring heart failure causes heart cells to die. They also knew that β-blockers prevent this cell death. However, the molecular details of these processes were unclear. β-Adrenergic–induced cell death is thought to be mediated by the stimulation of protein kinase A (PKA), but the effects of β-adrenergic stimulation could also be PKA-independent. To differentiate between PKA and non-PKA effects, the team created transgenic mice expressing a PKA inhibitor. They found that β-adrenergic stimulation in these mice prevented cardiac myocyte death and that the level of protection offered by PKA inhibition was similar to that provided by β-blockers. There was one important distinction, however. The hearts of the transgenic mice when stimulated also exhibited marked ERK activation, which offered further protection to cardiac myocytes. Following myocardial infarction, these PKA-inhibited mice also showed greater improvement in cardiac function than wild-type mice treated with β-blockers. The authors suggest that for treating heart failure patients, PKA-inhibitors may be more effective than β-blockers.Remodeling of Diabetic Bone Marrow (p 510)9Vascular problems beget more vascular problems in the bone marrow of patients with diabetes, report Spinetti et al.Download figureDownload PowerPointCardiovascular complications, such as atherosclerosis and capillary damage are common in diabetes and can have far reaching clinical consequences. In mouse models such capillary damage can affect even the bone marrow. Worse still, in the bone marrow, the failing microvasculature, which feeds the stem cell niche, could reduce the production of progenitors, including pro-angiogenic cells. While it has been shown that circulating progenitor cell levels are suppressed in people with diabetes it is unclear whether, like mice, human bone marrow microvasculature is also affected. Spinetti et al show that bone specimens from diabetes patients do indeed exhibit decreased capillary densities and also contain fewer progenitor cells. The team found that while impaired blood supply did contribute to the reduction in progenitor cell populations, high glucose itself also caused these cells to upregulate a pro-apoptosis pathway. This involved inactivation of microRNA miR-155, and the upregulation of its target - the transcription factor, FOXO3a. Taken together, the data suggest that specific treatments designed to preserve the integrity of capillaries of the bone marrow and the function of progenitor cells could prove important for managing diabetes.AKT2 Protects Against AAD (p 618)10The protein kinase AKT2 is protective against aortic aneurysm, report Shen et al.Download figureDownload PowerPointProgressive degeneration and weakening of the aortic walls can lead to dilation (aneurysm), tearing (dissection), and even rupturing of the aorta. Although aortic aneurysms are associated with a loss of smooth muscle cells and destruction of the extracellular matrix in the artery wall, little else is known about the pathology of this potentially deadly condition. The protein kinase AKT2 is known to promote the proliferation and migration of smooth muscle cells in vessel walls. While this activity can be harmful in conditions such as atherosclerosis—where it may cause vessel narrowing—Shen and colleagues wondered if it could protect against the weakening of the aortic wall. They found that mice lacking AKT2 had thinner aortic walls and when treated with angiotensin II were more prone to aortic aneurysm, dissection, and rupture. Furthermore, aortic tissues taken from patients with aneurysms and dissections exhibited lower levels of AKT2 than control tissues. Rather than promoting smooth muscle cell proliferation, as initially thought, however, AKT2 appears to protect aortic walls by not only inhibiting production of MMP-9, an enzyme that breaks down extracellular matrices, but also by promoting the production of TIMP-1, an inhibitor of MMP-9. Thus both AKT2 and these downstream factors could be targets for the development of novel aneurysm therapies.Dihydropyridines Activate Ca2+-sensing Receptors (p 640)11Drugs commonly used to treat pulmonary arterial hypertension could actually be exacerbating the condition, say Yamamura et al.Download figureDownload PowerPointWhile dihydropyridine calcium channel blockers, such as nifedipine and nicardipine, are often prescribed for pulmonary arterial hypertension (PAH), they are effective in only 15–20% of patients, who are referred to as vasoreactive responders. These drugs work by blocking calcium channels in vascular smooth muscle cells, which lowers cytosolic calcium levels and prevents contraction. Yamamura et al have discovered that these drugs also activate a second type of calcium protein in smooth muscle cells called the calcium sensing receptor (CaSR). And they show that activation of this receptor actually increases cytosolic calcium. In normal vascular smooth muscle cells the expression level of CaSR proteins is too low for this counteraction to be problematic, which explains why such drugs are successful vasodilators for many other conditions. In PAH patient smooth muscle cells, however, CaSR proteins tend to be upregulated. The findings not only offer an explanation as to why so few PAH patients respond to dihydropyridine channel blockers, but they also suggest that by raising smooth muscle cell calcium levels, these drugs could actually worsen PAH. Alternative options, such as non-dihydropyridine calcium channel blockers and CaSR blockers could prove to be more effective for the treatment of PAH, say the authors.Titin Phosphoryla+2tion by CaMKII (p 664)12CaMKII kinase regulates elasticity of the cardiomyocyte protein titin, show Hamdani et al.Download figureDownload PowerPointTitin is a large elastic protein found in cardiomyocytes that controls the stiffness of these cells, and as a result the myocardium as a whole. The protein is phosphorylated by many different kinases, and Hamdani and colleagues now add the Ca2+/calmodulin-dependent protein kinase-II (CaMKII) to that list. By performing mass spectrometry of heart tissue from wild type mice and CaMKII-null and overexpressing mice, the team identified several different CaMKII phosphorylation sites in the spring elements of titin. They also showed that phosphorylation of titin by CaMKII reduced the passive force, or stiffness, of cardiomyocytes, which would be expected to facilitate heart filling during diastole. But the authors warn that excessive phosphorylation of these sites might be harmful. Indeed, they found that heart tissue from patients with end-stage heart failure exhibited significantly increased phosphorylation at 4 of the 5 CaMKII sites. CaMKII expression and activity were also increased in failing human hearts, consistent with previous reports linking CaMKII upregulation with heart failure. The authors therefore suggest that manipulating phosphorylation of titin at CaMKII sites could help alter myocardial stiffness and improve overall cardiac function in heart failure patients.Macrophage Targeted PET/MRI (p 755)13Majmudar et al devise a macrophage imaging technique that could help identify unstable atherosclerotic plaques.Download figureDownload PowerPointMacrophage abundance in atherosclerotic plaques is strongly associated with the risk of plaque rupture, which can cause thrombus formation and even myocardial infarction or stroke. Therefore, it is important to image and quantify macrophages in human plaques to identify high-risk patients and to inform therapeutic interventions. However, existing imaging techniques lack sufficient sensitivity. Therefore, Majmudar and colleagues set out to develop a viable alternative. They generated radioactive dextran nanoparticles that could be efficiently taken up by macrophages. They injected these nanoparticles into the tail veins of mice and, after allowing time for phagocytosis, they tracked their vascular distribution using a combination of positron emission tomography (PET)—to detect the radioactive signal—and MRI—to determine anatomical location. They found that compared with wild-type mice, mice that were prone to atherosclerosis exhibited considerably higher nanoparticle PET signals from their aortas. The team also found that preventing the recruitment of macrophages to inflammation sites lowered these aortic PET signals. Because nanoparticles used in the study were biodegradable, this technique could perhaps be used to monitor atherosclerotic plaques in humans, say the authors.Cathelicidins and Monocyte Adhesion (p 792)14Wantha et al show how neutrophils recruit monocytes to sites of inflammation.Download figureDownload PowerPointIt is currently believed that during early stages of acute inflammation, soluble granule proteins released from neutrophils are required for subsequent recruitment of monocytes to the inflammation site. However, the underlying mechanisms remain unclear. Wantha and colleagues investigated the monocyte-attracting ability of cathelicidin and cathepsin - two neutrophil granule proteins conserved between mice and humans. They found that deletion of cathelicidin in mice reduced the recruitment of classical monocytes to inflammation sites. Mice lacking cathepsin, on the other hand, showed no such defect. In vitro experiments using cathelicidin treated human vascular endothelial cells confirmed that the protein is indeed able to recruit classical monocytes. By blocking different receptor proteins on the surface of monocytes, the team discovered that one specific receptor was responsible for mediating cathelicidin-dependent recruitment. Interaction between cathelicidin and this receptor, FRP2, induced the activation of integrins that enable monocytes to adhere to sites of inflammation. This interaction could thus be targeted to treat for a variety of inflammatory disorders, say the authors.SDF-1 in Heart Failure (p 816)15Penn et al report the outcome of a Phase I gene therapy trial for the treatment of ischemic heart failure.Download figureDownload PowerPointThe tissue damage that occurs after a myocardial infarction can lead to progressive heart failure and, if left untreated, to death. Mending damaged cardiac tissue with the help of stem cells is the goal of several current therapeutic investigations. One such approach, adopted by Penn and colleagues, is to recruit the body’s own stem cells to the heart. Stromal cell-derived factor 1 (SDF-1) is a naturally occurring cytokine that attracts stem cells and is upregulated in injured tissues. In the infarcted heart tissue, however, SDF-1 action lasts less than a week, after which stem cell recruitment diminishes. Artificially maintaining SDF-1 expression in damaged myocardium has been shown to improve cardiac function in a number of pre-clinical studies. Penn et al now provide preliminary evidence that the same approach works in patients too. They injected a non-viral DNA vector encoding the SDF-1 gene into the peri-infarcted myocardia of 17 heart failure patients. Four months later, these patients exhibited improvements in quality of life, 6 minute walking distance, and in the overall clinical classification of their condition. And 12 months later, these improvements persisted. Although this was a relatively small Phase I trial, the results indicate that a larger, randomized trial is warranted.Scrib in Endothelial Cell Migration (p 924)16Polarity protein Scrib tells vascular endothelial cells which way to go, report Michaelis et al.Download figureDownload PowerPointAs new blood vessels form, endothelial cells must not only migrate into their appropriate positions, but also arrange themselves so that their apical surfaces face the vessel lumen. In other cell types, migration and orientation are controlled by factors called polarity proteins, but surprisingly few studies have examined the role of these factors in endothelial cells. Michaelis and colleagues have now discovered that silencing the polarity protein, Scrib, in cultured vascular endothelial cells disrupts cell orientation, directed migration, and vessel formation. Their immunoprecipitation studies reveal that Scrib interacts with integrin α5, a transmembrane protein responsible for binding the extracellular matrix and regulating cell migration. Scrib not only promoted the cell surface expression of integrin 5, but also prevented its lysosomal degradation. In addition, the team showed that either the knock-out of Scrib in mouse embryos or the knock-down of Scrib in zebrafish embryos caused both the delay and disruption of blood vessel development. This newly identified role in angiogenesis could make Scrib a promising target for both pro- and anti-angiogenic treatments, say the authors.Living Without Creatine (p 945)17Contrary to popular belief, creatine may not be essential for high-energy performance, say Lygate et al.Download figureDownload PowerPointCreatine, a molecule abundant in heart and skeletal muscle cells, is dramatically reduced in the failing heart. And because creatine converts readily to and from phosphocreatine, it is thought to be a major transporter and source of phosphate for ATP production. In addition, mice lacking creatine have stunted maximal heart muscle activity and recover poorly if at all from myocardial infarction. Such observations have led to the conclusion that even though creatine may not be necessary for basal muscle activity, it is necessary for high-energy expenditure, particularly under conditions of stress. However, Lygate and colleagues now challenge that view. They say the method for eliminating creatine in previous studies might have caused off-target effects. To address this issue, the team engineered mice that lacked an essential creatine production enzyme. Surprisingly, these mice, although 100 percent creatine-free, could run just as far and just as fast as wild type mice. They also exhibited the same capacity for exercise on a treadmill and showed equivalent recovery and survival after myocardial infarction. These findings raise the question, if creatine is not required for high energy performance, why is it present in high-energy cells? The authors suggest creatine may play, an as yet undetermined role, in longer-term energy production.Mutation in VEGFC and Primary Lymphedema (p 956)18Gordon et al discover a novel mutation that causes Milroy disease-like primary lymphedema.Download figureDownload PowerPointMilroy disease is an inherited condition in which congenital abnormalities in the lymphatic vessels prevent the proper drainage of tissue fluid, causing characteristic swelling in the legs and feet. Although the most common cause of Milroy disease is a mutation in the vascular endothelial growth factor receptor 3 (VEGFR3), nearly 30 percent of patients do not carry such a mutation. To search for alternative causes, Gordon and colleagues performed whole exome sequencing on five Milroy disease patients that were free of mutations in VEGFR3. One of these patients showed a mutation in a VEGFC, a ligand of VEGFR3. This mutation caused a translational frameshift that generated a truncated protein. Three members of this patient’s family also displayed Milroy-like lymphedema, while carrying the very same VEGFC mutation. Functional studies in zebrafish showed that while wild type VEGFC protein induced the sprouting of both blood and lymph vessels, the mutant truncated form of the protein did not. In light of these results, the authors suggest that patients who present with Milroy disease symptoms without a VEGFR3 mutation should be screened for mutations in VEGFC.Myeloid FoxO in Atherosclerosis (p 992)19Atherosclerosis worsens when macrophages lack FoxO proteins, report Tsuchiya et al.Download figureDownload PowerPointAtherosclerosis is a leading cause of death in patients with type 2 diabetes. But exactly how high blood sugar and insulin resistance are linked to the development of atherosclerosis is unclear. It is known that insulin signaling in myeloid cells, such as macrophages, is mediated by a family of transcription factors called FoxO. Given that macrophages are a principle cell type in atherosclerotic plaques, Tsuchiya and colleagues removed FoxO factors from these cells and examined the effect on atherogenesis. They found that atherosclerosis-prone mice lacking FoxO factors in their myeloid cells had larger plaques that contained increased numbers of macrophages. The cause of this amplified lesion formation appeared to be bipartite: First, increased proliferation and decreased apoptosis contributed to the overabundance of myeloid cells in the lesion. And second reactive oxygen species, which are known to accelerate atherogenesis, were more abundant in the FoxO-lacking cells. Importantly, Tsuchiya et al showed that treating these mice with an antioxidant decreased myeloid cell numbers and lesion formation. Further studies on FoxO could aid in the design of effective anti-atherosclerosis treatments for diabetic patients.LTC4, Orai3, and Neointimal Hyperplasia (p 1013)20Gonzalez-Cobos et al identify a potential new target to stop neointima formation.Download figureDownload PowerPointUnlike cardiac and skeletal muscle cells, vascular smooth muscle cells (VSMCs) are not terminally differentiated. Instead, they retain the ability to proliferate and migrate when necessary, such as when blood vessels require regrowth after an injury. However, VSMC proliferation and migration can sometimes lead to an overgrowth of the cells, which may contribute to neointima formation, atherosclerosis or other vascular problems. This switch from a resting to a proliferative and migratory phenotype has been associated with the upregulation of calcium channel component Orai1, and inhibiting Orai1 upregulation has been shown to prevent neointima formation in mice. The bad news, however, is that Orai1 functions in multiple cell types, making it a non-specific target for potential therapies. Gonzales-Cobos and colleagues thus investigated Orai 3, a lesser-known homologue of Orai1. They found that, like Orai1, Orai3 was upregulated in proliferative and migratory VSMCs, but, it created an alternative form of calcium channel. Even though the channels differed, the effect of suppressing Orai3 expression in mice was the same, that is, neointima formation was prevented. Thus, for neointima-directed therapies, Orai3 may prove to be a better target than the ubiquitous Orai1.VSMC Phenotype Modulation and Arterial Stiffness (p 1035)21To avoid age-related cardiovascular problems, vascular smooth muscle cells need to stay relaxed say Galmiche et al.Download figureDownload PowerPointAs we age our arteries tend to stiffen, which can accelerate the process of cardiovascular degeneration. This vessel stiffening has been largely attributed to changes in the extracellular matrix of the arterial wall. But recent observations suggest that vascular smooth muscle cells (VSMC) surrounding the blood vessels also stiffen with age. To study the effect of changes in VSMC stiffness in living mice Galmiche and colleagues increased and decreased the expression of serum response factor (SRF) in these cells. SRF is a transcription factor that is expressed in many cell types. In VSMCs, however, it controls the expression of cytoskeletal and contractile proteins. The team fou" @default.
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