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Interference of Y-27632 on the signal transduction of transforming growth factor beta type 1 in ocular Tenon capsule fibroblasts

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International Journal of Ophthalmology(English edition) 2012年第5期5卷 576-581页

作者： Xiao-Hui Zhang, Jian-Ming Wang Department of Ophthalmology the Second Affiliated Hospital College of Medicine Xi'an Jiaotong University Xi'an 710004 Shaanxi Province China Department of Pharmacology Xijing Hospital Fourth Military Medical University Xi'an 710032 Shaanxi Province China

AIM: To investigate the interfering effect of Y-27632, a ROCK-I selective inhibitor, on the signal transduction pathway of transforming growth factor-beta 1 (TGF-beta 1) in ocular Tenon capsule fibroblasts (OTFS) in vitro. METHODS: After OTFS from passages 4 to 6 47 vitro were induced by TGF-beta 1 and then treated by Y-27632, the changes of the OTFS cell cycles were analyzed via flow cytometry, and the proteins expression of the alpha -smooth muscular actin (alpha -SMA), connective tissue growth factor (CTGF), collagen I were calculated by Western blot. After OTFS treated by the different concentrations of Y-27632, the expression levels of the alpha -SMA, CTGF and collagen I mRNA were assayed by RT-PCR. RESULTS: Y-27632 had no markedly effect on the OTFS cell cycles. After treated by TGF-beta 1, OTFS in G1 period significantly increased. The cell cycles distribution by both TGF-beta 1 and Y-27632 had no remarkable difference from that in control group. Y-27632 significantly inhibited the proteins expressions of both alpha -SMA and CTGF, while to some extent inhibited that of collagen I. TGF-beta 1 significantly promoted the proteins expressions of alpha -SMA, CTGF and collagen I. After OTFS treated by both TGF-beta 1 and Y-27632, of alpha -SMA, the protein expression was similar with that in control group (P=0.066>0.05), but the protein expression of CTGF or collagen I, respectively, was significantly different from that in control group (P=0.000<0.01). The differences of expressions of the alpha -SMA, CTGF and collagen I mRNA in 30, 150, 750 mu mol/L Y-27632 group were statistically significant, compared with those in control group, respectively (alpha -SMA, P=0.002, 0.000, 0.000; CTGF, P=0.014, 0.002, 0.001; collagen I,P=0.003, 0.002, 0.000). CONCLUSION: Blocking the Rho/ROCK signaling pathway by using of Y-27632 could inhibit the cellular proliferation and the expression of both CTGF and alpha -SMA whatever OTFS induced by TGF-beta 1 or not. Y-27632 suppressed t

关键词： Y-27632 ocular Tenon's capsule fibroblasts transforming growth factor beta type 1 α-smooth muscular actin connective tissue growth factor collagen I

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Impact of umbelliprenin-containing niosome nanoparticles on VEGF-A and CTGF genes expression in retinal pigment epithelium cells

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International Journal of Ophthalmology(English edition) 2024年第1期17卷 7-15页

作者： Farzad Dastaviz Akram Vahidi Teymoor Khosravi Ayyoob Khosravi Mehdi Sheikh Arabi Abouzar Bagheri Mohsen Rashidi Morteza Oladnabi Stem Cell Research Center Golestan University of Medical SciencesGorgan ***Iran Department of Medical Genetics School of Advanced Technologies in MedicineGolestan University of Medical SciencesGorgan ***Iran Student Research Committee Golestan University of Medical SciencesGorgan ***Iran Department of Molecular Medicine Faculty of Advanced Medical TechnologiesGolestan University of Medical SciencesGorgan ***Iran Department of Medical Nanotechnology Faculty of Advanced Medical TechnologiesGolestan University of Medical SciencesGorgan ***Iran Department of Clinical Biochemistry and Genetics Faculty of MedicineMazandaran University of Medical SciencesSari ***Iran Department Pharmacology Faculty of MedicineMazandaran University of Medical SciencesSari ***Iran Gorgan Congenital Malformations Research Center Golestan University of Medical SciencesGorgan ***Iran

AIM:To investigate the impact of niosome nanoparticles carrying umbelliprenin(UMB),an anti-angiogenic and anti-inflammatory plant compound,on the expression of vascular endothelial growth factor(VEGF-A)and connective tissue growth factor(CTGF)genes in a human retinal pigment epithelium(RPE)-like retina-derived cell ***:UMB-containing niosomes were created,optimized,and ***-like cells were treated with free UMB and UMB-containing *** IC_(50)values of the treatments were determined using an MTT *** expression of VEGF-A and CTGF was evaluated using real-time polymerase chain reaction after RNA extraction and cDNA ***’characteristics,including drug entrapment efficiency,size,dispersion index,and zeta potential were *** UMB had an IC_(50)of 96.2μg/mL,while UMB-containing niosomes had an IC_(50)of 25μg/***:Treatment with UMB-containing niosomes and free UMB resulted in a significant reduction in VEGF-A expression compared to control cells(P=0.001).Additionally,UMB-containing niosomes demonstrated a significant reduction in CTGF expression compared to control cells(P=0.05).However,there was no significant reduction in the expression of both genes in cells treated with free ***:Both free UMB and niosome-encapsulated UMB inhibits VEGF-A and CTGF genes ***,the latter demonstrates significantly greater efficacy,potentially due to the lower UMB dosage and gradual *** findings have implications for anti-angiogenesis therapeutic approaches targeting age-related macular degeneration.

关键词： umbelliprenin niosome age-related macular degeneration vascular endothelial growth factor-A connective tissue growth factor

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Expression of Serum and Glucocorticoid-inducible Kinase1 in Diabetic Rats and Its Modulation by Fluvastatin

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2005年第6期25卷 651-654页

作者：王学彬罗长青刘建社张春王玉梅朱忠华 Department of Nephrology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulation by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group （n = 8）, diabetic nephropathy group （n = 8） and fluvastatin-treated diabetic nephropathy group （15 mg/kg/d, n=8）. The metabolic parameters were measured at the 8th week. The expression of transforming growth factor β1 （TGF-β1） and fibronectin （FN） was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose, 24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-β1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-β1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGKlmRNA expression in renal cortex and postponed the development of diabetic nephropathy.

关键词： serum and glucocorticoid-inducible kinase connective tissue growth factor diabetic nephropathy fluvastatin

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Effects of Mycophenolic Acid on High Glucose-induced Expression of TGF-β and CTGF in Mesangial Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第3期26卷 292-293,304页

作者：吕永曼陈俊英邵菊芳 Department of Nephrology Tongji Hospital Huazhong University of Science and Technology Wuhan 430030 China

The effects of mycophenolic acid （MPA） on high glucose-induced expression of transforming growth factor-β （TGF-β） and connective tissue growth factor （CTGF） in mesangial cells （MC） were investigated. Rat MC were cultured in the presence of different concentrations of MPA （1.0 and 10.0 μmol/L） or MPA plus high glucose for 72 h. The expression of TGF-β and CTGF was detected by Western blot. The results showed that high glucose could induce the expression of TGF-β and CTGF in MC, but MPA could inhibit this effects. MPA did not influence the expression of TGF-β and CTGF in normal glucose. It was concluded that MPA might prevent the progression of diabetic nephropathy by inhibiting the expression of TGF-β and CTGF in MC.

关键词： mycophenolic acid transforming growth factor-β connective tissue growth factor mesangial cell diabetic nephropathy

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Epithelial to mesenchymal transition in the progression of tubulointerstitial fibrosis

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Chinese Medical Journal 2007年第21期120卷 1925-1930页

作者： LI Min-xia LIU Bi-cheng Institute of Nephrology Zhong Da Hospital Southeast University Nanjing 210009 China

Objective To review the mechanisms of epithelial to mesenchymal transition （EMT） and its role in the progression of tubulointerstitial fibrosis. Data sources The data used in this review were obtained mainly from the studies of EMT reported from 2000-2006. Study selection Relevant articles on studies of EMT in tubulointerstitial fibrosis were selected. Data were mainly extracted from the 45 articles listed in the reference section of this review. Results The process of EMT has gained wide recognition as candidate mechanism in progression of chronic fibrotic disorders. New markers were identified and facilitate the observation of EMT. EMT is regulated by many factors through activation of kinase-dependent signaling cascades. Recent findings suggest that EMT is a reversible process, which can be controlled by factors for their epithelial inducing activities. Conclusion Remarkable progresses of EMT research have been made recently. Preventing or reversing EMT is a promising strategy against renal fibrosis.

关键词： epithelial to mesenchymal transition connective tissue growth factor transforming growth factor integrin-linked kinase tubulointerstitial fibrosis

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Effect of anaphylatoxin C3a, C5a on the tubular epithelial-myofibroblast transdifferentiation in vitro

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Chinese Medical Journal 2011年第23期124卷 4039-4045页

作者： LIU Fang GOU Rong HUANG Jun FU Ping CHEN Feng FAN Wen-xing HUANG You-qun ZANG Li WU Min QIU Hong-yu WEI Da-peng Division of Nephrology West China Hospital of Sichuan University Chengdu Sichuan 610041 China

Background Tubulointerstitial renal fibrosis is the common end point of progressive kidney diseases, and tubular epithelial-myofibroblast transdifferentiation （TEMT） plays a key role in the progress of tubulointerstitial renal fibrosis. Anaphylatoxin C3a and C5a are identified as novel profibrotic factors in renal disease and as potential new therapeutic targets. The aim of this study was to investigate whether C3a, C5a can regulate TEMT by transforming growth factor-β1 （TGF-β1）/connective tissue growth factor （CTGF） signaling pathway and the effects of C3a and C5a receptor antagonists （C3aRA and C5aRA） on C3α- and C5α-induced TEMT. Methods HK-2 cells were divided into C3a and C5a groups which were subdivided into four subgroups： control group, 10 ng/ml TGF-I31 group, 50 nmol/L C3a group, 50 nmol/L C3a plus 1 pmol/L C3aRA group; control group, 10 ng/ml TGF-I^I group, 50 nmol/L C5a group, 50 nmol/L C5a plus 2.5 pmol/L C5aRA group. TGF-β1 receptor antagonist （TGF-β1 RA） 10 IJg/ml was used to investigate the mechanism of C3α- and C5α-induced TEMT. Electron microscopy was used to observe the morphological changes. Immunocytochemistry staining, real-time PCR and Western blotting were used to detect the expressions of a smooth muscle actin （α-SMA）, E-cadherin, Col-I, C3a receptor （C3aR）, C5aR, CTGF and TGF-β1. Results HK-2 cells cultured with C3a and C5a for 72 hours exhibited strong staining of α-SMA, lost the positive staining of E-cadherin, and showed a slightly spindle-like shape and loss of microvilli on the cell surface. The expressions of α-SMA, E-cadherin, Col-I, C3aR, C5aR, TGF-β1 and CTGF in C3α- and C5α-treated groups were higher than normal control group （P 〈0.05）. C3aRA and C5aRA inhibited the expressions of α-SMA, Col-I, C3aR, C5aR, and up-regulated the expression of E-cadherin （P 〈0.05）. TGF-β1 and CTGF mRNA expressions induced by C3a and C5a were partly blocked by TGF-β1 RA （P 〈0.05）. Conclusion C3a and C5a can induce TEMT via the up-regulations of C3aR an

关键词： C3a C5a tubular epithelial-myofibroblast transdifferentiation transforming growth factor-ill connective tissue growth factor

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Simvastatin attenuates bleomycin-induced pulmonary fibrosis in mice

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Chinese Medical Journal 2008年第18期121卷 1821-1829页

作者： OU Xue-mei FENG Yu-lin WEN Fu-qiang HUANG Xiang-yang XIAO Jun WANG Ke WANG Tao Division of Pulmonary Diseases State Key Laboratory of Biotherapy of China Department of Respiratory Medicine West China Hospital Sichuan University Chengdu Sichuan 610041 China

Background Bleomycin-induced fibrosis is extensively used to model aspects of the pathogenesis of interstitial pulmonary fibrosis. This study aimed to determine the benefic effects and mechanisms of simvastatin on bleomycininduced pulmonary fibrosis in mice. Methods Bleomycin-induced pulmonary fibrosis mice were administered with simvastatin in different doses for 28 days. We measured inflammatory response, fibrogenic cytokines and profibrogenic markers in both bleomycin-stimulated and control lungs, and correlated these parameters with pulmonary fibrosis. Results Simvastatin attenuated the histopathological change of bleomycin-induced pulmonary fibrosis and prevented the increase of lung hydroxyproline content and collagen （Ⅰ and Ⅲ） mRNA expression induced by bleomycin. Moreover, simvastatin down-regulated the increased expression of transforming growth factor-β1 （TGF-β1） and connective tissue growth factor （CTGF） induced by bleomycin at both gene and protein levels. Simultaneously, the accumulation of neutrophils and lymphocytes and the increased production of tumor necrosis factor-a （TNF-α） in bronchial alveolar lavage fluid were inhibited by simvastatin in early inflammatory phase after bleomycin infusion. The higher dose of simvastatin was associated with a more significant reduction in these inflammatory and fibrotic parameters. Furthermore, the inactivation of p38, RhoA and Smad2/3 signaling pathways was observed during simvastatin administration. Conclusions Simvastatin attenuated bleomycin-induced pulmonary fibrosis, as indicated by decreases in Ashcroft score and lung collagen accumulation. The inhibitory effect of simvastatin on the progression of pulmonary fibrosis may be demonstrated by reducing inflammatory response and production of TGF-β1 and CTGR These findings indicate that simvastatin may be used in the treatment of pulmonary fibrosis.

关键词： pulmonary fibrosis simvastatin transforming growth factor-β1 connective tissue growth factor

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Combined expression of CTGF and tissue inhibitor of metalloprotease-1 promotes synthesis of proteoglycan and collagen type Ⅱ in rhesus monkey lumbar intervertebral disc cells in vitro

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Chinese Medical Journal 2010年第15期123卷 2082-2087页

作者： LIU Yong KONG Jie CHEN Bo-hua HU You-gu Department of Orthopaedic Surgery Affiliated Hospital of Medical College Qingdao University Qingdao Shandong 266003 China

Background Low back pain has emerged as a widespread disease often caused by intervertebral disc *** study aimed to establish an in vitro cell culture model of rhesus monkey lumbar intervertebral discs and to investigate the effect of combined connective tissue growth factor （CTGF） and tissue inhibitor of metalloprotease-1（TIMP-1） expression mediated by adeno-associated virus （AAV） on collagen type Ⅱ and proteoglycan *** purpose of these investigations was to explore potential methods for relieving the degeneration of lumbar intervertebral disc *** Rhesus monkey lumbar intervertebral disc nucleus pulposus cells （NPCs） were isolated by enzyme digestion,cultured, and transduced with rAAV2-CTGF-IRES-TIMP-1, rAAV2-CTGF, or rAAV2-TIMP-1 at a multiplicity of infection （MOl） of *** expression of collagen type Ⅱ and proteoglycan was measured using RT-PCR and Western *** synthetic rate of proteoglycan was measured using 35S *** Rhesus monkey lumbar intervertebral disc NPCs were transduced with rAAV2-CTGF-IRES-TIMP-1,rAAV2-CTGF, and rAAV2-TIMP-1 and the transduced genes were expressed and *** to the control,CTGF promoted the synthesis of collagen type Ⅱ and ***-1 showed an enhancing effect on the expression of proteoglycan but no effect on collagen type Ⅱ.Expression of both genes in rhesus monkey lumbar intervertebral disc NPCs significantly enhances the synthesis of proteoglycan and collagen type Ⅱ.Conclusions Single gene transduction of CTGF or TIMP-1 can enhanced synthesis of *** expression can also enhance collagen type Ⅱ protein *** transduction of both CTGF and TIMP1 can significantly promote the expression of proteoglycan and collagen type Ⅱ to levels greater than transduction of a single gene *** study provides a good basis for multi-gene therapy to treat lumbar intervertebral disc degeneration.

关键词： connective tissue growth factor tissue inhibitor of metalloprotease-1 collagen type Ⅱ proteoglycan intervertebral disc

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Role of connective growth factor in plasminogen activator inhibitor-1 and fibronectin expression induced by transforming growth factor β1 in renal tubular cells

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Chinese Medical Journal 2004年第7期117卷 990-996页

作者：张春孟宪芳朱忠华杨晓邓安国 Department of Nephrology Department of Neuroscience

Background connective tissue growth factor (CTGF) contributes greatly to renal tubulointerstitial fibrosis, which is the final event leading to end-stage renal failure. This study was designed to investigate the effects of CTGF antisense oligodeoxynucleotides (ODNs) on the expressions of plasminogen activator inhibitor-1 (PAI-1) and fibronectin in renal tubular cells induced by transforming growth factor β1 (TGF-β1) in addition to the role of CTGF in the accumulation and degradation of renal extracellular matrix (ECM).Methods A human proximal tubular epithelial cell line (HKC) was cultured in vitro. Cationic lipid-mediated CTGF antisense ODNs were transfected into HKC cells. After HKC cells were stimulated with TGF-β1 (5 μg/L), the mRNA levels of PAI-1 and fibronectin were measured by RT-PCR. Intracellular PAI-1 protein synthesis was assessed by flow cytometry. The secreted PAI-1 and fibronectin in the medium were determined by Western blot and ELISA, *** TGF-β1 was found to induce tubular CTGF, PAI-1, and fibronectin mRNA expression. PAI-1 and fibronectin mRNA expression induced by TGF-β1 was significantly inhibited by CTGF antisense ODNs. CTGF antisense ODNs also inhibited intracellular PAI-1 protein synthesis and lowered the levels of PAI-1 and fibronectin protein secreted into the *** CTGF may play a crucial role in the accumulation and degradation of excessive ECM during tubulointerstitial fibrosis, and transfecting CTGF antisense ODNs may be an effective way to prevent renal fibrosis.

关键词： connective tissue growth factor antisense oligodeoxynucleotide plasminogen activator inhibitor-1 fibronectin renal tubular epithelial cells

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Botulinum Toxin Type A and Its Possible Mechanisms on Wound Healing

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Modern Plastic Surgery 2020年第3期10卷 38-55页

作者： Khushboo Gurung Qian Tan Ye Xu Bingchen Duan Department of Burns Plastic and Reconstructive Surgery Nanjing Drum Tower Hospital Affiliated to Medical School of Southeast University Nanjing China Department of Burns Plastic and Reconstructive Surgery Nanjing Drum Tower Hospital Affiliated Hospital of Nanjing University Nanjing China Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University Nanjing China

Botulinum toxin type-A (BTX-A), a subtype from known seven types of botulinum neurotoxin (serotype A-G), is produced by a gram-positive bacterium, Clostridium botulinum. The toxin is now widely and efficiently used in treating a plethora of diverse symptoms and conditions. Recent evidence in the literature also shows that BTX-A exhibits a wide range of effects on non-neuronal cells. Its potential has markedly expanded to clinical applications other than the treatment of neurological and muscular conditions that are characterized by neuronal hyperactivity. A number of studies have shown BTX-A to improve the quality of scar outcome and prevent the formation of keloids and HTS. Although the mechanism of action of BTX-A on wound healing is still not clearly understood, lately there has been extensive research to grasp the underlying mechanisms of this multifunctional toxin. BTX-A seems to affect wound healing by a number of mechanisms that include action on tensile forces, inhibition of fibroblasts differentiation, downregulation of TGF-β1 and collagen expression. This review will explore the responses of Botulinum toxin type-A on wound healing and preventing pathological scars like HTS and keloids, and comprehend the overall effect BTX-A has on wound healing.

关键词： Wound Healing Botulinum Toxin Type-A Hypertrophic Scar Keloid Fibroblast Myofibroblasts Transforming growth factor β-1 Collagen Metalloproteinases connective tissue growth factor

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