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Mechanisms of connective tissue formation and blocks of mitogen activated protein kinase

Irina A SHURYGINA, Michael G SHURYGIN, Nataliya I AYUSHINOVA, Galina B GRANINA, Nikolay V ZELENIN

《化学科学与工程前沿（英文）》 2012年 第6卷 第2期   页码 232-237 doi: 10.1007/s11705-012-1286-1

摘要： Ninety male Wistar rats were selected under the “Guide for the Care and Use of Laboratory Animals” for skin-muscle wound models. Three groups of animals were examined respectively for inoculation of inhibitor of p38 MAPK (mitogen activated protein kinase) SB 203580 and JNK inhibitor SP 600125, and a control. Light microscopy, immunohistochemistry, and tensometry revealed that the inhibition of p38 or JNK cascades have modified the formation of the connective tissue scar. The degree of connective tissue growth in the area of surgical wound had been significantly reduced by the end of observation (30 d) as the SB 203580 was applied (% volume of collagen 43.60 (41.05 – 60.15) 73.54 (66.87 – 78.01) in control, = 0.002). Conversely, when we have applied the JNK blocker, the density of collagen in scar tissue increased (78.14 (72.77 – 81.14), = 0.022 control). SB203580 inhibits the expression of p38, c-Jun and c-Fos. When we have used the JNK blocker, the expression of c-Fos and c-Jun decreased, but the expression of p38 increased. This determines the high functional activity of fibroblasts after using SP 600125. Obtained results show the importance of studying regulators of cell differentiation as potential drugs, which significantly affect the outcome of the pathological processes.

关键词： connective tissue     mitogen activated protein kinase (MAPK)     p38     JNK    

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Human menstrual blood-derived stem cells alleviate autoimmune hepatitis via JNK/MAPK signaling pathway

《医学前沿（英文）》 2023年 第17卷 第3期   页码 534-548 doi: 10.1007/s11684-022-0953-y

摘要： Autoimmune hepatitis (AIH) is a severe globally distributed liver disease that could occur at any age. Human menstrual blood-derived stem cells (MenSCs) have shown therapeutic effect in acute lung injury and liver failure. However, their role in the curative effect of AIH remains unclear. Here, a classic AIH mouse model was constructed through intravenous injection with concanavalin A (Con A). MenSCs were intravenously injected while Con A injection in the treatment groups. The results showed that the mortality by Con A injection was significantly decreased by MenSCs treatment and liver function tests and histological analysis were also ameliorated. The results of phosphoproteomic analysis and RNA-seq revealed that MenSCs improved AIH, mainly by apoptosis and c-Jun N-terminal kinase/mitogen-activated protein signaling pathways. Apoptosis analysis demonstrated that the protein expression of cleaved caspase 3 was increased by Con A injection and reduced by MenSCs transplantation, consistent with the TUNEL staining results. An AML12 co-culture system and JNK inhibitor (SP600125) were used to verify the JNK/MAPK and apoptosis signaling pathways. These findings suggested that MenSCs could be a promising strategy for AIH.

关键词： autoimmune hepatitis (AIH)     concanavalin A (Con A)     human menstrual blood-derived stem cells (MenSCs)     apoptosis     mitogen-activated protein kinase (MAPK)    

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Mitogen-activated protein kinase pathway inhibitors: inhibitors for diseases?

Xu WANG MS, Xiao-Wei GONG MD, PhD, Yong JIANG MD, PhD, Yu-Hua LI PhD,

《医学前沿（英文）》 2010年 第4卷 第1期   页码 46-53 doi: 10.1007/s11684-010-0010-0

摘要： Mitogen-activated protein kinase (MAPK) signaling pathway, one of the most important signaling pathways in eukaryotic organism, is involved in multiple cellular events such as cell growth, differentiation, and apoptosis. MAPK is of great importance to the normal function of organisms, while its dysfunction results in various diseases. So far, inhibitors specifically against each subfamilies of MAP kinase have been developed, while more endeavors are needed to discover the compounds selectively targeting a particular subfamily member. Most of the kinase inhibitors exert their functions in an ATP-competitive way or a non-ATP-competitive way. Further studies on the effective mechanism of the MAPK inhibitors and their therapeutic roles in the treatment of diseases are helpful for the illumination of MAP kinase function, the development of novel inhibitors, and the therapy of diseases caused by the dysfunction of the MAPK pathway.

关键词： mitogen-activated protein kinase     drug target     inhibitor     signal transduction     disease    

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Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

《医学前沿（英文）》 2007年 第1卷 第3期   页码 248-252 doi: 10.1007/s11684-007-0047-x

摘要： The aim of this study was to investigate the role of p38 mitogen-activated protein kinase (MAPK) in cell migration induced by platelet-derived growth factor (PDGF). Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF. A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of deficiency on this process in a gene knockout (p38) mouse embryonic fibroblast cell line. On the stimulation of PDGF, the migration of NIH3T3 cells was significantly increased (〈0.001) compared to the control and p38 MAP kinase was simultaneously phosphorylated. Furthermore, the PDGF-induced cell migration was significantly blocked in gene knockout (p38) mouse embryonic fibroblasts (MEFs) (〈0.001) as compared with the wild type cells (p38). p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.

关键词： control     stimulation     mitogen-activated     growth factor     process    

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Mechanisms of insulin resistance in obesity

null

《医学前沿（英文）》 2013年 第7卷 第1期   页码 14-24 doi: 10.1007/s11684-013-0262-6

摘要：

Obesity increases the risk for type 2 diabetes through induction of insulin resistance. Treatment of type 2 diabetes has been limited by little translational knowledge of insulin resistance although there have been several well-documented hypotheses for insulin resistance. In those hypotheses, inflammation, mitochondrial dysfunction, hyperinsulinemia and lipotoxicity have been the major concepts and have received a lot of attention. Oxidative stress, endoplasmic reticulum (ER) stress, genetic background, aging, fatty liver, hypoxia and lipodystrophy are active subjects in the study of these concepts. However, none of those concepts or views has led to an effective therapy for type 2 diabetes. The reason is that, there has been no consensus for a unifying mechanism of insulin resistance. In this review article, literature is critically analyzed and reinterpreted for a new energy-based concept of insulin resistance, in which insulin resistance is a result of energy surplus in cells. The energy surplus signal is mediated by ATP and sensed by adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Decreasing ATP level by suppression of production or stimulation of utilization is a promising approach in the treatment of insulin resistance. In support, many of existing insulin sensitizing medicines inhibit ATP production in mitochondria. The effective therapies such as weight loss, exercise, and caloric restriction all reduce ATP in insulin sensitive cells. This new concept provides a unifying cellular and molecular mechanism of insulin resistance in obesity, which may apply to insulin resistance in aging and lipodystrophy.

关键词： type 2 diabetes     energy expenditure     inflammation     lipotoxicity     mitochondria     hyperinsulinemia     adenosine monophosphate-activated protein kinase (AMPK)    

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The role of protein kinase C epsilon in neural signal transduction and neurogenic diseases

null

《医学前沿（英文）》 2011年 第5卷 第1期   页码 70-76 doi: 10.1007/s11684-011-0119-9

摘要：

Protein kinase C epsilon (PKC ?) is one of major isoforms in novel PKC family. Although it has been extensively characterized in the past decade, the role of PKC ? in neuron is still not well understood. Advances in molecular biology have now removed significant barriers to the direct investigation of PKC ? functions in vivo, and PKC ? has been increasingly implicated in the neural biological functions and associated neurogenic diseases. Recent studies have provided important insights into the influence of PKC ? on cortical processing at both the single cell level and network level. These studies provide compelling evidence that PKC ? could regulate distinct aspects of neural signal transduction and suggest that the coordinated actions of a number of molecular signals contribute to the specification and differentiation of PKC ? signal pathway in the developing brain.

关键词： protein kinase C ?     signal transduction     neurogenic disease    

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Effect of inhibiting tyrosine kinase Src expression on protein phosphatase 2A and tau phosphorylation

LIU Rong, ZENG Ji, ZHOU Xinwen, WANG Jianzhi, PEI Jinjing

《医学前沿（英文）》 2008年 第2卷 第3期   页码 235-238 doi: 10.1007/s11684-008-0044-8

摘要： The aim of this study is to investigate the effect of tyrosine kinase Src on Tyrosine 307(Y307) phosphorylation, protein phosphatase 2A (PP2A) activity, and on tau phosphorylation. Specific Src siRNA was transfected into cultured mouse neuroblastoma N2a cells to inhibit the expression of Src protein, and the phosphorylation levels of PP2A Y307 and tau at different sites, as well as PP2A activity were detected at different time points after siRNA transfection. Twelve hours after siRNA transfection, the protein level of Src was dramatically decreased, with decreased PP2A Y307 phosphorylation. However, the total PP2A protein level was also decreased, together with a decreased PP2A activity. Tau was hyperphosphorylated at the Ser198/199/202 sites. Multiple factors may be involved in the cellular regulation of PP2A activity. Inhibiting Src expression could induce inactivation of PP2A and tau hyperphosphorylation.

关键词： hyperphosphorylation     PP2A activity     cellular regulation     siRNA     siRNA transfection    

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Protective effect of tanshinone II A on signal transduction system protein kinase B in rats with myocardial

Enyuan TU MD, Yongjun PAN MM, Kang ZHENG MM, Zhaohua WANG MD, Qiansheng LIANG MD, Guangtian YANG MD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 431-436 doi: 10.1007/s11684-009-0088-4

摘要： The effects of tanshinone II A on cell signal transduction system protein kinase B in rats with myocardial hypertrophy induced by the abdominal aorta partial coarctation were investigated. Rat models of myocardial hypertrophy were established by using abdominal aorta partial coarctation method. Forty-eight rats were randomly divided into sham group (S group), model group (M group), valsartan treatment group (X group), low-dose tanshinone treatment group (LD group), medium-dose tanshinone treatment group (MD group), and high-dose tanshinone treatment group (HD group) (=8 in each group). Left ventricular mass index (LVMI), left ventricular posterior wall (LVPW), and septal thickness (IVS) were detected by high frequency ultrasonography. Myocardial fiber diameter (MFD) was examined by Hematoxylin-Eosin (HE) staining, and the contents of phosphorylated protein kinase B (p-Akt) and p-Gsk3β in myocardium were assayed by Western blot. The results showed that compared with S group, the values of LVMI, LVPW, IVS and MFD were increased in other groups (<0.05), and the contents of p-Akt, and p-Gsk3β were also increased in other groups. As compared with MD group, the values of LVMI, LVPW, IVS and MFD were decreased in all treatment groups (<0.05), and the contents of p-Akt, and p-Gsk3β were also decreased in all treatment groups. However, there were no significant differences among LD, MD, and HD groups (>0.05), and there were no significant differences between X group and tanshinone treatment groups (>0.05). It was suggested that tanshinone II A could prevent myocardial hypertrophy by its action on the Akt signaling pathway.

关键词： tanshinone II A     myocardial hypertrophy     rat     protein kinase B     abdominal aorta coarctation    

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Inhibition of protein kinase B by Palmitate in the insulin signaling of HepG2 cells and the preventive

XIA Yanzhi, WAN Xuedong, DUAN Qiuhong, HE Shansu, WANG Ximing

《医学前沿（英文）》 2007年 第1卷 第2期   页码 200-206 doi: 10.1007/s11684-007-0038-y

摘要： Elevated plasma levels of free fatty acids (FFAs) may contribute to insulin resistance (IR) that is characteristic of type 2 diabetes mellitus. In this study, we investigated the effects of two fatty acids, palmitate (PA) and arach

关键词： palmitate     characteristic     study     plasma     resistance    

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Fate of proteins of waste activated sludge during thermal alkali pretreatment in terms of sludge protein

Xiaoli Song, Zhenghua Shi, Xiufen Li, Xinhua Wang, Yueping Ren

《环境科学与工程前沿（英文）》 2019年 第13卷 第2期 doi: 10.1007/s11783-019-1114-7

摘要：

Maillard reaction between reducing sugars and amides happened during pretreatment.

Over 90 min of TAH at the optimal condition, 67.59% sludge proteins was solubilized.

15.84% soluble proteins broke down to materials with small molecular weight.

关键词： Sludge flocs     Microbial cells     Hydrolysate     Protein breakdown     Melanoidin    

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Effect of PRAK gene knockout on the proliferation of mouse embryonic fibroblasts

Xiaowei GONG MD, PhD, Xiaoyan MING MD, Xu WANG MM, Daan WANG MD, Peng DENG MM, Yong JIANG MD, PhD, Aihua LIU MD, PhD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 379-383 doi: 10.1007/s11684-009-0073-y

摘要： p38 regulated/activated protein kinase (PRAK) plays a key role in cell senescence and tumor suppression. The aim of this study was to investigate if PRAK had effect on cell proliferation. The growth of and mouse embryonic fibroblast (MEF) cells was measured by methylthiazoletetrazolium (MTT) colorimetric assay, and the proportion of the cell number in different phases of the cell cycle was analyzed by flow cytometry. The growth curves showed that the growth rate was notably decreased, and cell double time was elongated in cells; moreover, the number of cells was decreased by 44.5% compared with that of cells cultured for 96h, suggesting that G/M transition is inhibited in cells. Meanwhile, G/S transition was also inhibited in cells, observed with flow cytometry analysis. The ratios of G/G, G/M, and S phases of cells were 44.9%, 12.2%, and 42.9%, respectively, while those of cells were 55.3%, 7.3%, and 37.4%, respectively. There were 23.1% increase and 12.7% decrease of the number of cells in G and S phases comparison with that of cells, respectively. Taken together, gene knockout in MEF cells leads to cell cycle arrest and proliferation inhibition.

关键词： p38 regulated/activated protein kinase     gene knockout     cell cycle     cell proliferation    

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Proteomics study of Mycoplasma pneumoniae pneumonia reveals the Fc fragment of the IgG-binding protein

《医学前沿（英文）》 2022年 第16卷 第3期   页码 378-388 doi: 10.1007/s11684-021-0840-y

摘要： Macrolide and corticosteroid resistance has been reported in patients with Mycoplasma pneumoniae (MP) pneumonia (MPP). MP clearance is difficult to achieve through antibiotic treatment in sensitive patients with severe MPP (SMPP). SMPP in children might progress to airway remodeling and even bronchiolitis/bronchitis obliterans. Therefore, identifying serum biomarkers that indicate MPP progression and exploring new targeted drugs for SMPP treatment require urgency. In this study, serum samples were collected from patients with general MPP (GMPP) and SMPP to conduct proteomics profiling. The Fc fragment of the IgG-binding protein (FCGBP) was identified as the most promising indicator of SMPP. Biological enrichment analysis indicated uncontrolled inflammation in SMPP. ELISA results proved that the FCGBP level in patients with SMPP was substantially higher than that in patients with GMPP. Furthermore, the FCGBP levels showed a decreasing trend in patients with GMPP but the opposite trend in patients with SMPP during disease progression. Connectivity map analyses identified 25 possible targeted drugs for SMPP treatment. Among them, a mechanistic target of rapamycin kinase (mTOR) inhibitor, which is a macrolide compound and a cell proliferation inhibitor, was the most promising candidate for targeting SMPP. To our knowledge, this study was the first proteomics-based characterization of patients with SMPP and GMPP.

关键词： severe Mycoplasma pneumoniae pneumonia     children     proteomics     Fc fragment of the IgG-binding protein     mechanistic target of rapamycin kinase inhibitor    

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Gene and protein expression of proteinase-activated receptor-1, 2 in a murine model of acute graft host

Quan LI MD , Weiming LI MD , Ping ZOU MD , Jian ZHANG BM ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 309-315 doi: 10.1007/s11684-009-0043-4

摘要： Proteinase-activated receptors (PARs) are a novel subclass of seven transmembrane-spanning, G protein-coupled receptors. PAR-1 and PAR-2 are widely expressed in a variety of cells and are found to be involved in many physiological and pathological processes including inflammation and immune response. However, little is known about the function of PAR-1, 2 in acute graft host disease (GVHD). In the present study, we first detected the expression of PAR-1, 2 protein and mRNA in a murine model of acute GVHD using the methods of immunohistochemistry, Western blot and quantitative real-time polymerase chain reaction (PCR). Syngeneic hematopoietic stem cell transplantation (HSCT) mice served as controls. The relative gene expression level of PAR-1 was significantly increased in the skin, liver, small intestine of allogeneic HSCT mice (in skin: 0.039±0.013 0.008±0.002 of controls, =0.009; in liver: 0.165±0.006 0.017±0.006 of controls, =0.004; in small intestine: 0.215±0.009 0.016±0.002 of controls, =0.003), but not in the stomach, lung and kidney of allogeneic HSCT mice (>0.05). PAR-2 mRNA expression in the liver and small intestine of allogeneic HSCT mice (in liver: 0.010±0.002 0.003±0.001 of controls, =0.008; in small intestine: 0.006±0.001 0.003±0.001 of controls, =0.024) was increased significantly, but PAR-2 mRNA expression in the other organs (>0.05) was not found to be significantly elevated. PAR-1, 2 protein expression was in accordance with the mRNA expression, as shown by Western blot. Using immunohistochemistry the present study demonstrated that there was strong PAR-1, 2 immunoreactivity in the epithelial cell and vascular endothelial cell of target organs of acute GVHD. Our findings of markedly increased expression of PAR-1, 2 in target organs of acute GVHD suggest that PAR-1 and PAR-2 may play an important role in the pathogenesis of acute GVHD.

关键词： graft vs host disease     proteinase-activated receptor     murine model     hematopoietic stem cell transplantation    

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Effects of phosphatidylinositol 3-kinase inhibitor on human cervical carcinoma cells

Yuan ZHANG MD , Xiaoyan ZHANG MM , Yanhui LI MM , Xuan DU MM , Zehua WANG MD, PhD , Hongbo WANG MD ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 341-346 doi: 10.1007/s11684-009-0067-9

摘要： Phosphatidylinositol 3-kinase (PI3K) is a crucial cell survival pathway implicated in tumorigenesis because of its role in stimulating cell proliferation and suppressing apoptosis. This study was to investigate the regulation of proliferation and apoptosis by LY294002, an inhibitor of PI3K in cervical cancer cells and the expression of FLICE-like inhibitory protein (c-FLIP) . Human cervical cancer HeLa cells were used in this experiment and cultured. The cultured cells were treated with LY294002 at different concentrations (10, 25, 50 and 100µmol/L) for 6, 12, 24, and 48h before harvesting for evaluation. Cell viability was measured by 3-(4,5)-dimethylthiazol(-2-y1)-3,5-di-phenyltetrazoliumbromide (MTT) assay. Apoptosis was analyzed by flow cytometry. The expression of c-FLIP was detected by Western blot. Cell viability was inhibited by LY294002 significantly (<0.05). Flow cytometry analysis revealed that cell apoptosis was significantly increased in the presence of LY294002 as compared with the control group. Although the expression of c-FLIP was increased in a short time, the expression of c-FLIP was markedly suppressed after the treatment of LY294002 for 48h. These results suggested that the PI3K/Akt signal pathway might be involved in the regulation of cell apoptosis in cervical cancer cells. Moreover, the regulation of c-FLIP expression through PI3K/Akt signal pathway in cervical cancer cells was observed .

关键词： human cervical cancer cells     apoptosis     phosphatidylinositol 3-kinase (PI3K)/Akt     FLICE-like inhibitory protein    

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PAK1 is a novel cardiac protective signaling molecule

null

《医学前沿（英文）》 2014年 第8卷 第4期   页码 399-403 doi: 10.1007/s11684-014-0380-9

摘要：

We review here the novel cardiac protective effects of the multifunctional enzyme, p21-activated kinase 1 (PAK1), a member of a serine/threonine protein kinase family. Despite the large body of evidence from studies in noncardiac tissue indicating that PAK1 activity is key in the regulation of a number of cellular functions, the role of PAK1 in the heart has only been revealed over the past few years. In this review, we assemble an overview of the recent findings on PAK1 signaling in the heart, particularly its cardiac protective effects. We present a model for PAK1 signaling that provides a mechanism for specifically affecting cardiac cellular processes in which regulation of protein phosphorylation states by protein phosphatase 2A (PP2A) predominates. We discuss the anti-adrenergic and antihypertrophic cardiac protective effects of PAK1, as well as its role in maintaining ventricular Ca2+ homeostasis and electrophysiological stability under physiological, β-adrenergic and hypertrophic stress conditions.

关键词： p21-activated kinase 1 (PAK1)     heart    

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标题 作者 时间 类型 操作

Mechanisms of connective tissue formation and blocks of mitogen activated protein kinase

Irina A SHURYGINA, Michael G SHURYGIN, Nataliya I AYUSHINOVA, Galina B GRANINA, Nikolay V ZELENIN

期刊论文

Human menstrual blood-derived stem cells alleviate autoimmune hepatitis via JNK/MAPK signaling pathway

期刊论文

Mitogen-activated protein kinase pathway inhibitors: inhibitors for diseases?

Xu WANG MS, Xiao-Wei GONG MD, PhD, Yong JIANG MD, PhD, Yu-Hua LI PhD,

期刊论文

Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

期刊论文

Mechanisms of insulin resistance in obesity

null

期刊论文

The role of protein kinase C epsilon in neural signal transduction and neurogenic diseases

null

期刊论文

Effect of inhibiting tyrosine kinase Src expression on protein phosphatase 2A and tau phosphorylation

LIU Rong, ZENG Ji, ZHOU Xinwen, WANG Jianzhi, PEI Jinjing

期刊论文

Protective effect of tanshinone II A on signal transduction system protein kinase B in rats with myocardial

Enyuan TU MD, Yongjun PAN MM, Kang ZHENG MM, Zhaohua WANG MD, Qiansheng LIANG MD, Guangtian YANG MD,

期刊论文

Inhibition of protein kinase B by Palmitate in the insulin signaling of HepG2 cells and the preventive

XIA Yanzhi, WAN Xuedong, DUAN Qiuhong, HE Shansu, WANG Ximing

期刊论文

Fate of proteins of waste activated sludge during thermal alkali pretreatment in terms of sludge protein

Xiaoli Song, Zhenghua Shi, Xiufen Li, Xinhua Wang, Yueping Ren

期刊论文

Effect of PRAK gene knockout on the proliferation of mouse embryonic fibroblasts

Xiaowei GONG MD, PhD, Xiaoyan MING MD, Xu WANG MM, Daan WANG MD, Peng DENG MM, Yong JIANG MD, PhD, Aihua LIU MD, PhD,

期刊论文

Proteomics study of Mycoplasma pneumoniae pneumonia reveals the Fc fragment of the IgG-binding protein

期刊论文

Gene and protein expression of proteinase-activated receptor-1, 2 in a murine model of acute graft host

Quan LI MD , Weiming LI MD , Ping ZOU MD , Jian ZHANG BM ,

期刊论文

Effects of phosphatidylinositol 3-kinase inhibitor on human cervical carcinoma cells

Yuan ZHANG MD , Xiaoyan ZHANG MM , Yanhui LI MM , Xuan DU MM , Zehua WANG MD, PhD , Hongbo WANG MD ,

期刊论文

PAK1 is a novel cardiac protective signaling molecule

null

期刊论文