Результаты поиска

Growth restricted placentas show severely reduced volume of villous components with perivascular myofibroblasts.

INTRODUCTION: The restricted placental growth in IUGR is associated with a simultaneous weight and volume restriction for the placental vill … lacentas with quantitative microscopic techniques. Using immunohistochemical detection of placental myofibroblasts (γ-sm-actin) and foetoplacental endothelium (CD34), we distinguished between more centrally located villi showing the presence of myofibroblasts (contractile villi; C-villi) and more peripherally located villi showing the absence of myofibroblasts ( …

Optogenetic current in myofibroblasts acutely alters electrophysiology and conduction of co-cultured cardiomyocytes.

Interactions between cardiac myofibroblasts and myocytes may slow conduction and generate spontaneous beating in fibrosis, increasing the chance of life-threatening arrhythmia. While co-culture studies have shown that myofibroblasts can affect cardiomyocyte electrophysiology in vitro, the extent of myofibroblast-myocyte electrical conductance in a syncytium is unknown. In this neonatal rat study, cardiac myofibroblasts were transduced with Channelrhodopsin-2, which allowed acute and selective increase of myofibroblast current, and plated on top of cardiomyocytes. Optical mapping revealed signi…

Utility of nanomedicine targeting scar-forming myofibroblasts to attenuate corneal scarring and haze.

Corneal scarring refers to the loss of normal corneal tissue, replaced by fibrotic tissue (during wound repair) thereby affecting corneal transparency and vision quality. The corneal wound healing process involves a complex series of physiological events resulting in the transformation of transparent keratocytes into opaque myofibroblasts; the prominent cause of irregular extracellular matrix synthesis leading to the development of corneal opacity/hazy vision. Globally, corneal scarring/haze is one of the most prevalent causes of blindness. Ocular trauma (physical and chemical) and microbial i…

Stevia prevents experimental cirrhosis by reducing hepatic myofibroblasts and modulating molecular profibrotic pathways.

AIM: The aims of the present study were to investigate the capacity of stevia leaves to prevent experimental cirrhosis induced by chronic ad … noting that stevia downregulated several profibrogenic pathways, including the reduction of hepatic myofibroblasts and decreased matrix metalloproteinase (MMP)2 and MMP13 expression, thereby blocking the liberation of transforming growth factor-β from the extracellular matrix. Notably, stevia reduced the phosphorylation of pSmad3L, the most profibrogenic and mit …

Endostatin Stimulates Proliferation and Migration of Myofibroblasts Isolated from Myocardial Infarction Model Rats.

Myofibroblasts contribute to the healing of infarcted areas after myocardial infarction through proliferation, migration, and production of extracellular matrix (ECM). Expression of endostatin, a cleaved fragment of type XVIII collagen, increases in the heart tissue of an experimental myocardial infarction model. In the present study, we examined the effect of endostatin on the function of myofibroblasts derived from an infarcted area. The myocardial infarction model was created by ligating the left anterior descending artery in rats. Two weeks after the operation, α-smooth muscle actin (α-SMA…

Cytokine Interferon-γ suppresses the function of capsule myofibroblasts and induces cell apoptosis.

Myofibroblasts (MFs), a contractile subset of fibroblasts, play a pivotal role in physiological wound healing and in the development of many fibroconnective disorders. The complex cytokine network regulating the function of MFs in joint stiffness is still poorly understood. In this in vitro study, we investigated the effect of the cytokine Interferon-gamma (IFN-γ) on MFs isolated from human joint capsules. MFs were cultivated either in the presence of increasing concentrations of IFN-γ alone or in combination with IFN-γ neutralizing antibodies. Cell viability, cytotoxicity, apoptosis, and mRNA…

Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis.

Persistent myofibroblast activation distinguishes pathological fibrosis from physiological wound healing, suggesting that therapies selectively inducing myofibroblast apoptosis could prevent progression and potentially reverse established fibrosis in diseases such as scleroderma, a heterogeneous autoimmune disease characterized by multiorgan fibrosis. We demonstrate that fibroblast-to-myofibroblast differentiation driven by matrix stiffness increases the mitochondrial priming (proximity to the apoptotic threshold) of these activated cells. Mitochondria in activated myofibroblasts, but not quie…

Normal skin wound and hypertrophic scar myofibroblasts have differential responses to apoptotic inductors.

During wound healing, myofibroblasts play a central role in matrix formation and wound contraction. At the end of healing, there is evidence that myofibroblasts disappear via apoptotic pathways. Hypertrophic scars are a fibroproliferative disorder that leads to considerable morbidity. It has been postulated that a defect in myofibroblast apoptosis could be responsible for the pathological scar formation, but no evidence exists. We have isolated and cultured human normal wound (Wmyo) and hypertrophic scar (Hmyo) myofibroblasts and compared their basal apoptotic rates and their sensitivity to se…

Aldosterone and D-glucose stimulate the proliferation of human cardiac myofibroblasts in vitro.

The renin-angiotensin-aldosterone-system appears to be involved in the development of cardiac fibrosis in rodents, characterized by nonepith … ns (10(-8) and 10(-7) mol/L) significantly (P<0.01) increased the proliferation of cultured cardiac myofibroblasts. Comparable effects were observed after incubation of the cells with high D-glucose concentrations (15 and 25 mmol/L, P<0.01). No additive growth stimulation was evident when the cells were incubated in medium containing both aldosterone and D -gluc …

The monoclonal antibody GB 42--a useful marker for the differentiation of myofibroblasts.

The expression patterns of a variety of cytoskeletal antigens were studied in normal human tissues (placenta, umbilical cord, myometrium, co … is expressed in smooth muscle cells, myoepithelial cells and in later stages of differentiation of myofibroblasts, in all the tissues investigated. Throughout the development of smooth muscle cells and myofibroblasts, the appearance of the GB 42-antigen occurs after the expression of vimentin, desmin and alpha-smooth muscle actin, but prior to the expression of …

Myofibroblasts in cotton-induced granulation tissue and the bovine adrenal capsule: morphological aspects.

Ultrastructural studies of one week old cotton-induced granulation tissue revealed the presence of polymorphonuclear neutrophils (PMN), macrophages and mast cells, whilst the granulation tissue from two week old cotton implants contained fibroblasts, myofibroblasts and abundant collagen fibres. Similarly, the bovine adrenal capsule contained both fibroblasts and myofibroblasts. It is proposed that the bovine adrenal capsule and two week cotton-induced granulation tissue could be utilized as in-vitro models to study the mechanism(s) involved in myofibroblast contraction.

Aortic valve stenosis serum IGFBP2 mediates female-specific Evogliptin resistance in valve myofibroblasts.

Aortic valve stenosis (AVS) is a sexually dimorphic cardiovascular disease characterized by fibro-calcification of the aortic valve leaflet. Sex differences in AVS arise in part from sexually dimorphic serum composition that differentially regulates valvular interstitial cell (VIC) myofibroblast activation. However, how individual serum factors contribute to sex-specific drug responses remains unknown. Here, we integrate serum proteomic profiling with in vitro drug screening using hydrogel biomaterials to identify sex-specific regulators of antifibrotic drug efficacy. We found that serum insul

Alcohol-related hepatitis induces a specific fibrosis profile through YAP activation in myofibroblasts.

BACKGROUND & AIMS: Yes-associated protein (YAP) impairs hepatocyte regeneration in alcohol-related hepatitis (AH), but its impact on fibroge … PCR, and bulk and spatial proteomics. The impact of organoids generated from AH and Cirrh livers on myofibroblasts was also evaluated. Cirrh organoids were transduced with constitutively active YAP (to mimic AH organoids) and co-cultured with myofibroblasts in a 3D co-culture model. In a 2D model, myofibroblasts were treated with growth differentiation factor 15 …

MICAL2 regulates myofibroblasts differentiation in epidural fibrosis via SRF/MRTF-A signaling pathway.

AIM: To determine the role of MICAL2 in myofibroblasts differentiation and epidural fibrosis. BACKGROUND: Epidural fibrosis (EF) may develop following laminectomy and aberrant myofibroblasts differentiation and excessive extracellular matrix (ECM) accumulation play key roles in the formation of EF. Dense epidural fibrosis results to the poor surgical outcomes and failed back surgery syndrome (FBSS), and there is no effective treatment available. Molecule interacting with Casl2 (MICAL2) has been demonstrated to participate in multiple cellular processes by regulating actin cytoskeleton dynamic…

Sphingosylphosphorylcholine alleviates hypoxia-caused apoptosis in cardiac myofibroblasts via CaM/p38/STAT3 pathway.

Blockade of hypoxia-caused nonmyocytes apoptosis helps improve survival and mitigate ventricular remodeling and dysfunction during the chronic stage of myocardial infarction. But tools affecting nonmyocyte apoptosis are very rare. Sphingosylphosphorylcholine (SPC), a naturally occurring bioactive sphingolipid in plasma, was proved to protect cardiomyocyte against apoptosis in an ischemic model in our previous study. Here, we showed that SPC also inhibited hypoxia-induced apoptosis in myofibroblasts, an important type of nonmyocytes in the heart. Calmodulin (CaM) is an identified receptor of SP…

Genetic, epigenetic and transcriptional comparison of esophagus tumor‑associated and adjacent normal myofibroblasts.

Myofibroblasts (MFs) are present in healthy tissues and are also key components of the tumor microenvironment. In the present study a comparative analysis of MFs obtained from various gastrointestinal tumor tissues and from tumor‑adjacent normal tissues of cancer patients was performed, with the aim to evaluate differences in MF morphology, gene expression profile and function. The goal was to correlate the observed morphological and functional variations with the underlying genetic and epigenetic backgrounds. The mutation frequency of MFs was assessed by next generation sequencing. The transc…

Cyclosporine A inhibits TGF-β2-induced myofibroblasts of primary cultured human pterygium fibroblasts.

Cyclosporine A (CsA), an immunomodulatory drug, and is increasingly used to treat moderate dry eye syndrome and ocular surface inflammation. However, any inhibitory effect on differentiation of fibroblasts to myofibroblasts remains unclear. Here, we show that the inhibitory effect of CsA on transforming growth factor-beta2 (TGF-β2)-induced myofibroblasts in primary cultured human pterygium fibroblasts. CsA significantly decreased mRNA and protein expression of myofibroblast-related markers including α-SMA, laminin, and fibronectin. These findings were supported by the results from immunofluore…

Portal myofibroblasts promote vascular remodeling underlying cirrhosis formation through the release of microparticles.

UNLABELLED: Liver fibrosis expanding from portal tracts and vascular remodeling are determinant factors in the progression of liver diseases to cirrhosis. In the present study, we examined the potential contribution of portal myofibroblasts (PMFs) to the vascular changes leading to cirrhosis. The analyses of liver cells based on the transcriptome of rat PMFs, compared to hepatic stellate cell HSC-derived myofibroblasts in culture, identified collagen, type XV, alpha 1 (COL15A1) as a marker of PMFs. Normal liver contained rare COL15A1-immunoreactive cells adjacent to the bile ducts and canals o…

TGFβ1 регулирует выражение склеракии в первичных миофибробластах сердца при помощи независимого от Smad механизма.

В сердечных ранах, заживающих после инфаркта миокарда (MI), относительно неактивные сердечные фибробласты-кардиады феноконвертируются до гиперсинтетических/секретарских миофибробластов, которые производят большое количество внеклеточной матрицы (ECM) и фибриллярных коллагенных белков. Наша лаборатория и другие установили, что TGFβ1 является постоянным стимулом в хронической и неуместной фазе заживления ран, которая характеризуется гипертрофическим шрамом и, в конечном итоге, усилением всего миокарда, что в конечном счете приводит к патогенезу сердечной недостаточности после ИС. Ski — мощный не

Совпадение в аннотации оригинала
In cardiac wound healing following myocardial infarction (MI), relatively inactive resident cardiac fibroblasts phenoconvert to hypersynthetic/secretory myofibroblasts that produce large quantities of extracellular matrix (ECM) and fibrillar collagen proteins. Our laboratory and others have identified TGFβ1 as being a persistent stimulus in the chronic and i…