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Actin Expression (actin + expression)

Distribution by Scientific Domains
Medical Sciences53%
Life Sciences38%

Kinds of Actin Expression

  • muscle actin expression
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  • smooth muscle actin expression
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    Selected Abstracts

    Alpha-smooth muscle actin expression enhances cell traction force

    CYTOSKELETON, Issue 4 2007
    Jianxin Chen
    Abstract Using an established corneal stromal cell differentiation model, we manipulated ,-smooth muscle actin (,-SMA) protein expression levels in fibroblasts by treating them with TGF-,1, bFGF, TGF-, type I receptor inhibitor (SB-431542), and siRNA against ,-SMA. The corresponding cell traction forces (CTFs) were determined by cell traction force microscopy. With all these treatments, we found that ,-SMA is not required for CTF induction, but its expression upregulates CTF. This upregulation involves the modification of stress fibers but does not appear to relate to non-muscle myosin II expression or ,-actin expression. Moreover, there exists a linear relationship between ,-SMA protein expression level and CTF magnitude. Finally, CTFs were found to vary among a population of myofibroblasts, suggesting that ,-SMA protein expression levels of individual cells also vary. Cell Motil. Cytoskeleton 2007. © 2006 Wiley-Liss, Inc. [source]

    Comparison of the antilipolytic effects of an A1 adenosine receptor partial agonist in normal and diabetic rats

    DIABETES OBESITY & METABOLISM, Issue 2 2009
    A. K. Dhalla
    Introduction and Aims:, Elevated plasma free fatty acid (FFA) concentrations play a role in the pathogenesis of type 2 diabetes (2DM). Antilipolytic agents that reduce FFA concentrations may be potentially useful in the treatment of 2DM. Our previous observation that CVT-3619 lowered plasma FFA and triglyceride concentrations in rats and enhanced insulin sensitivity in rodents with dietary-induced forms of insulin resistance suggested that it might be of use in the treatment of patients with 2DM. The present study was undertaken to compare the antilipolytic effects of CVT-3619 in normal (Sprague Dawley, SD) and Zucker diabetic fatty (ZDF) rats. Results:, ZDF rats had significantly higher fat pad weight, glucose, insulin and FFA concentrations than those of SD rats. EC50 values for forskolin-stimulated FFA release from isolated adipocytes from SD and ZDF rats were 750 and 53 nM, respectively (p < 0.05). Maximal forskolin stimulation of FFA release was significantly (p < 0.01) less in ZDF rats (133 ± 60 ,M) compared with SD rats (332 ± 38 ,M). EC50 values for isoproterenol to increase lipolysis in adipocytes from SD and ZDF rats were 2 and 7 nM respectively. Maximal isoproterenol-stimulated lipolysis was significantly (p < 0.01) lower in adipocytes from ZDF rats (179 ± 23 ,M) compared with SD rats (343 ± 27 ,M). Insulin inhibited lipolysis in adipocytes from SD rats with an IC50 value of 30 pM, whereas adipocytes from ZDF rats were resistant to the antilipolytic actions of insulin. In contrast, IC50 values for CVT-3619 to inhibit the release of FFA from SD and ZDF adipocytes were essentially the same (63 and 123 nM respectively). CVT-3619 inhibited lipolysis more than insulin in both SD (86 vs. 46%, p < 0.001) and ZDF (80 vs. 13%, p < 0.001) adipocytes. In in vivo experiments, CVT-3619 (5 mg/kg, PO) lowered FFA to a similar extent in both groups. Plasma concentrations of CVT-3619 were not different in SD and ZDF rats. There was no significant difference in the messenger RNA expression of the A1 receptors relative to ,-actin expression in adipocytes from SD (0.98 ± 0.2) and ZDF rats (0.99 ± 0.3). Conclusion:, The antilipolytic effects of CVT-3619 appear to be independent of insulin resistance and animal model. [source]

    Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats

    EXPERIMENTAL PHYSIOLOGY, Issue 3 2006
    Donatella Stilli
    We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source]

    CCR2 promotes hepatic fibrosis in mice,

    HEPATOLOGY, Issue 1 2009
    Ekihiro Seki
    Chemokines and chemokine receptors contribute to the migration of hepatic stellate cells (HSCs) and Kupffer cells, two key cell types in fibrogenesis. Here, we investigate the role of CCR2, the receptor for monocyte chemoattractant protein (MCP)-1, MCP-2, and MCP-3, in hepatic fibrosis. Hepatic CCR2, MCP-1, MCP-2, and MCP-3 messenger RNA expression was increased after bile duct ligation (BDL). Both Kupffer cells and HSCs, but not hepatocytes, expressed CCR2. BDL- and CCl4 -induced fibrosis was markedly reduced in CCR2,/, mice as assessed through collagen deposition, ,-smooth muscle actin expression, and hepatic hydroxyproline content. We generated CCR2 chimeric mice by the combination of clodronate, irradiation, and bone marrow (BM) transplantation allowing full reconstitution of Kupffer cells, but not HSCs, with BM cells. Chimeric mice containing wild-type BM displayed increased macrophage recruitment, whereas chimeric mice containing CCR2,/, BM showed less macrophage recruitment at 5 days after BDL. Although CCR2 expressed in the BM enhanced macrophage recruitment in early phases of injury, CCR2 expression on resident liver cells including HSCs, but not on the BM, was required for fibrogenic responses in chronic fibrosis models. In vitro experiments demonstrated that HSCs deficient in CCR2,/, or its downstream mediator p47phox,/, did not display extracellular signal-regulated kinase and AKT phosphorylation, chemotaxis, or reactive oxygen species production in response to MCP-1, MCP-2, and MCP-3. Conclusion: Our results indicate that CCR2 promotes HSC chemotaxis and the development of hepatic fibrosis. (HEPATOLOGY 2009.) [source]

    Differential activation of stress-responsive signalling proteins associated with altered loading in a rat skeletal muscle

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2005
    Inho Choi
    Abstract Skeletal muscle undergoes a significant reduction in tension upon unloading. To explore intracellular signalling mechanisms underlying this phenomenon, we investigated twitch tension, the ratio of actin/myosin filaments, and activities of key signalling molecules in rat soleus muscle during a 3-week hindlimb suspension and 2-week reloading. Twitch tension and myofilament ratio (actin/myosin) gradually decreased during unloading but progressively recovered to initial levels during reloading. To study the involvement of stress-responsive signalling proteins during these changes, the activities of protein kinase C alpha (PKC,) and three mitogen-activated protein kinases (MAPKs),c-Jun NH2 -terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), and p38 MAPK,were examined using immunoblotting and immune complex kinase assays. PKC, phosphorylation correlated positively with the tension (Pearson's r,=,0.97, P,<,0.001) and the myofilament ratio (r,=,0.83, P,<,0.01) over the entire unloading and reloading period. Treatment of the soleus muscle with a PKC activator resulted in a similar paralleled increment in both PKC, phosphorylation and the ,-sarcomeric actin expression. The three MAPKs differed in the pattern of activation in that JNK activity peaked only for the first hours of reloading, whereas ERK and p38 MAPK activities remained elevated during reloading. These results suggest that PKC, may play a pivotal role in converting loading stress to intracellular changes in contractile proteins that determine muscle tension. Differential activation of MAPKs may also help alleviate muscle damage, modulate energy transport and/or regulate the expression of contractile proteins upon altered loading. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source]

    Hobnail hemangiomas (targetoid hemosiderotic hemangiomas) are true lymphangiomas

    JOURNAL OF CUTANEOUS PATHOLOGY, Issue 5 2004
    Folker E. Franke
    Background:, Hobnail hemangioma (targetoid hemosiderotic hemangioma) is a small benign vascular tumor of the superficial and mid-dermis. In contrast to its well-characterized histology, it has been unclear whether this tumor arises from blood vessel endothelial cells (BECs) or lymphatic vessel endothelial cells (LECs). Methods:, We analyzed 10 hobnail hemangiomas by immunohistochemistry, using the recently described lymphatic endothelial cell marker, D2-40. For comparison, CD31, CD34, and ,-smooth muscle actin expression were studied in consecutive sections of the paraffin-embedded tissues. Results:, In all analyzed vessels, D2-40 labeled exclusively LECs, whereas BECs were consistently negative. In contrast to capillary BECs, either neighboring the tumors or intermingled, neoplastic endothelial cells of all 10 hobnail hemangiomas were strongly labeled by D2-40. Conclusions:, The results suggest a lymphatic origin for hobnail hemangiomas. This view is further supported by the CD34 negativity of endothelial cells and the lack of actin-labeled pericytes in hobnail hemangiomas, both characteristic of lymphatic vessels. Moreover, our analysis revealed that microshunts between neoplastic lymphatic vascular channels and small blood vessels occur, explaining some features of hobnail hemangiomas, such as aneurysmatic microstructures, erythrocytes within and beneath neoplastic vascular spaces, inflammatory changes, scarring, and interstitial hemosiderin deposits. [source]

    Alcohol Primes the Airway for Increased Interleukin-13 Signaling

    ALCOHOLISM, Issue 3 2009
    Patrick O. Mitchell
    Background:, Using an experimental model of airway fibrosis following lung transplantation, we recently showed that chronic alcohol ingestion by donor rats amplifies airway fibrosis in the recipient. Associated with alcohol-mediated amplification of airway fibrosis is increased transforming growth factor ,-1(TGF,1) and ,-smooth muscle actin expression. Other studies have shown that interleukin-13 (IL-13) modulates TGF,1 signaling during experimentally-induced airway fibrosis. Therefore, we hypothesized that IL-13 is a component of alcohol-mediated amplification of pro-fibrotic mediators in the alcoholic lung. Methods:, To test this hypothesis, we analyzed tracheal epithelial cells and type II alveolar cells from control- or alcohol-fed rats, alcohol-treated mouse lung fibroblasts, and human bronchial epithelial cells in vitro for expression of various components of the IL-13 signaling pathway. Signaling via the IL-13 pathway was assessed by measuring levels of phosphorylated signal transducers and activators of transcription-6 (STAT6). In addition, we performed heterotopic tracheal transplantation using control-fed and alcohol-fed donor rats and analyzed tracheal allografts for expression of components of the IL-13 signaling pathway by RT-PCR and immunocytochemical analyses. Results:, Interleukin-13 expression was detected in type II alveolar epithelial cells and human bronchial epithelial cells, but not in lung fibroblasts. IL-13 expression was decreased in whole lung and type II cells in response to alcohol exposure. In all cell types analyzed, expression of IL-13 signaling receptor (IL-13R,1) mRNA was markedly increased. In contrast, mRNA and protein expression of the IL-13 decoy receptor (IL-13R,2) were decreased in all cells analyzed. Exposure to alcohol also increased STAT6 phosphorylation in response to IL-13 and lipopolysaccharide. Conclusions:, Data from multiple cell types in the pulmonary system suggest that IL-13 and its receptors play a role in alcohol-mediated activation of pro-fibrotic pathways. Taken together, these data suggest that alcohol primes the airway for increased IL-13 signaling and subsequent tissue remodeling upon injury such as transplantation. [source]

    Effects of interleukin 18 on injury and activation of human proximal tubular epithelial cells

    NEPHROLOGY, Issue 1 2007
    DONG LIANG
    SUMMARY: Background/Aims: Injury and activation of tubular proximal epithelial cells (TEC) play central roles in renal tubulointerstitial fibrosis (TIF), but its mechanisms remain obscure. Interleukin 18 (IL-18) is overproduced during chronic kidney diseases (CKD), but how IL-18 affects the biological behaviour of TEC is not clear. The aim of the present study is to reveal the role of IL-18 in renal TIF. Methods: The expressions of IL-18 and IL-18 receptor in TEC were detected by immunohistochemical staining in vivo and by reverse transcriptase polymerase chain reaction (RT-PCR) in vitro. TEC line (HK-2 cells) were incubated without or with IL-18. Cell proliferation and cell cycle were evaluated by methyl thiazolyl tetrazolium assay and flow cytometric analysis, respectively. Cell apoptosis was assessed by Hoechst 33258 staining. Expression of ,-smooth muscle actin was evaluated by RT-PCR, immunocytochemical staining and flow cytometric analysis, respectively. Type I collagen, fibronectin, MCP-1 and RANTES in cultured supernatants were measured by enzyme-linked immunosorbent assay. Results: IL-18 expression in TEC increased significantly in CKD state. IL-18 receptor was constitutively expressed in normal proximal TEC, and its expression increased strongly in CKD state. Proliferation and cell cycle of HK-2 cells were not affected by IL-18. Cell apoptosis, ,-smooth muscle actin expression, type I collagen and fibronectin production as well as MCP-1 secretion were promoted by IL-18 in dosage- and/or time-dependent manners, but RANTES secretion was not affected. Conclusion: IL-18 may play a crucial role in the process of TIF by promoting TEC injury and activation, and could be a target of the therapeutic approaches against TIF. [source]

    Upregulation of heparin-binding epidermal growth factor-like growth factor and osteopontin in experimental hydronephrosis

    NEPHROLOGY, Issue 3 2000
    M Katerelos
    SUMMARY This study examined the expression of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and osteopontin in unilateral ureteral obstruction (UUO) in the rat, a model of obstructive uropathy. HB-EGF mRNA was upregulated 5.5-fold at 4 h post-obstruction (P < 0.05) and 4.5-fold after 12 h (P < 0.05). Immunohistochemical staining for HB-EGF demonstrated an increase in protein in the distended tubules. To determine what effects increased HB-EGF might have in the obstructed kidney, we attempted to determine whether HB-EGF upregulates osteopontin and ,-smooth muscle actin (,-SMA) in the tubular line NRK-52E. Both of these molecules are increased in UUO. Osteopontin mRNA was upregulated in NRK-52E cells after 24, 48 and 72 h HB-EGF stimulation. In contrast, HB-EGF caused a downregulation of ,-SMA protein by Western blot in NRK-52E cells. When a blocking mAb against secreted HB-EGF was administered, however, there was no effect on osteopontin mRNA levels or immunohistochemical staining for ,-smooth muscle actin. These data suggest that the action of HB-EGF in UUO may be to increase osteopontin and reduce ,-smooth muscle actin expression by tubular epithelial cells by an autocrine or intracrine mechanism. By reducing ,-SMA expression, HB-EGF may also act to maintain epithelial cell morphology in this model. [source]

    Identification and expression analysis of an actin gene from the soft tick, Ornithodoros moubata (Acari: Argasidae)

    ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 4 2007
    Mari Horigane
    Abstract Actin genes are found in all living organisms and highly conserved in various animals as shown by numerous studies on actin gene expression and function. Because of this ubiquitous nature of actin, it is often used as an internal control in gene expression studies. To clarify the suitability of actin gene as an internal control in soft ticks, isolation and expression analyses of an actin gene from Ornithodoros moubata was performed. An actin gene of Ornithodoros moubata (OmAct2, GenBank accession no. AB208021) with 1,131 bp and 376 amino acid residues was identified. The homology of OmAct2 with other arthropod actin genes was greater than 80% in nucleotides and 99% in amino acids. OmAct2 gene was classified as a cytoskeletal actin type by absence of muscle-specific amino acids commonly found in insects and ubiquitous expression in all stages and both sexes. Southern blot revealed that O. moubata has four to seven actin genes. In addition, actin expression analyzed by real-time PCR before and after blood feeding was not significantly different indicating OmAct2 is an appropriate internal control for the analysis of gene expression in these ticks. Arch. Insect Biochem. Physiol. 64:186,199, 2007. © 2007 Wiley-Liss, Inc. [source]

    Requirement of transforming growth factor ,,activated kinase 1 for transforming growth factor ,,induced ,-smooth muscle actin expression and extracellular matrix contraction in fibroblasts

    ARTHRITIS & RHEUMATISM, Issue 1 2009
    Xu Shi-Wen
    Objective Fibrosis is believed to occur through normal tissue remodeling failing to terminate. Tissue repair intimately involves the ability of fibroblasts to contract extracellular matrix (ECM), and enhanced ECM contraction is a hallmark of fibrotic cells in various conditions, including scleroderma. Some fibrogenic transcriptional responses to transforming growth factor , (TGF,), including ,-smooth muscle actin (,-SMA) expression and ECM contraction, require focal adhesion kinase/Src (FAK/Src). The present study was undertaken to assess whether TGF,-activated kinase 1 (TAK1) acts downstream of FAK/Src to mediate fibrogenic responses in fibroblasts. Methods We used microarray, real-time polymerase chain reaction, Western blot, and collagen gel contraction assays to assess the ability of wild-type and TAK1-knockout fibroblasts to respond to TGF,1. Results The ability of TGF to induce TAK1 was blocked by the FAK/Src inhibitor PP2. JNK phosphorylation in response to TGF,1 was impaired in the absence of TAK1. TGF, could not induce matrix contraction or expression of a group of fibrotic genes, including ,-SMA, in the absence of TAK1. Conclusion These results suggest that TAK1 operates downstream of FAK/Src in mediating fibrogenic responses and that targeting of TAK1 may be a viable antifibrotic strategy in the treatment of certain disorders, including scleroderma. [source]