The Rho-Kinase Inhibitor H-1152P Suppresses the Wound-Healing Activities of Human Tenon’s Capsule Fibroblasts In Vitro

2007 ◽  
Vol 48 (5) ◽  
pp. 2152 ◽  
Author(s):  
Aysegu¨l Tura ◽  
Salvatore Grisanti ◽  
Katrin Petermeier ◽  
Sigrid Henke-Fahle
Keyword(s):  
Wound Healing ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Tenon’S Capsule ◽  
Rho Kinase Inhibitor ◽  
Tenon's Capsule

In Vitro Effect of Ascorbic Acid on the Proliferation of Bovine Scleral and Tenon's Capsule Fibroblasts

1998 ◽  
Vol 8 (1) ◽  
pp. 37-41 ◽  
Author(s):  
P.O. Denk ◽  
M. Knorr
Keyword(s):  
Wound Healing ◽  
Ascorbic Acid ◽  
Healing Process ◽  
Wound Healing Process ◽  
Filtration Surgery ◽  
Glaucoma Filtration Surgery ◽  
Tenon’S Capsule ◽  
Tenon's Capsule ◽  
Vitro Effect

The success of glaucoma filtration surgery depends mainly on an incomplete wound healing process in the area of the fistula. Since Kornblueth and Tenenbaum's investigations in 1956 it has been known that aqueous humour has intrinsic antiproliferative properties. It is assumed that ascorbic acid is involved in the regulation of the wound healing process after filtration surgery. To evaluate the antiproliferative effect of ascorbic acid in vitro, we used cultured fibroblasts of bovine Tenon's capsule and bovine sclera. Incubation of these cells with ascorbic acid at concentrations ranging from 0.5 to 3 mM/L led to dose-dependent inhibition of cell proliferation. The half-maximal inhibitory concentration was 1.0 mM/L for both cell types. Physiological concentrations of ascorbic acid may be valuable in the pharmacological prevention of failure of glaucoma filtration surgery. However, extensive clinical investigations are needed to clarify whether topical intraoperative or postoperative as well as oral administration of ascorbic acid inhibits fibroblast proliferation after glaucoma filtration surgery.

Animal model for angiotensin II effects in the internal anal sphincter smooth muscle: mechanism of action

2002 ◽  
Vol 282 (3) ◽  
pp. G461-G469 ◽  
Author(s):  
Ya-Ping Fan ◽  
Rajinder N. Puri ◽  
Satish Rattan
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Ang Ii ◽  
Kinase C ◽  
Rho Kinase Inhibitor ◽  
Isolated Smooth Muscle Cells

Effect of ANG II was investigated in in vitro smooth muscle strips and in isolated smooth muscle cells (SMC). Among different species, rat internal and sphincter (IAS) smooth muscle showed significant and reproducible contraction that remained unmodified by different neurohumoral inhibitors. The AT1antagonist losartan but not AT2 antagonist PD-123319 antagonized ANG II-induced contraction of the IAS smooth muscle and SMC. ANG II-induced contraction of rat IAS smooth muscle and SMC was attenuated by tyrosine kinase inhibitors genistein and tyrphostin, protein kinase C (PKC) inhibitor H-7, Ca2+ channel blocker nicardipine, Rho kinase inhibitor Y-27632 or p44/42mitogen-activating protein kinase (MAPK44/42) inhibitor PD-98059. Combinations of nicardipine and H-7, Y-27632, and PD-98059 caused further attenuation of the ANG II effects. Western blot analyses revealed the presence of both AT1 and AT2receptors. We conclude that ANG II causes contraction of rat IAS smooth muscle by the activation of AT1 receptors at the SMC and involves multiple intracellular pathways, influx of Ca2+, and activation of PKC, Rho kinase, and MAPK44/42.

scholarly journals Rho-kinase inhibitor, fasudil, suppresses glioblastoma cell line progression in vitro and in vivo

2010 ◽  
Vol 9 (11) ◽  
pp. 875-884 ◽  
Author(s):  
Lin Deng ◽  
Gang Li ◽  
Ronghui Li ◽  
Qinglin Liu ◽  
Qiaowei He ◽  
...  
Keyword(s):  
Cell Line ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Glioblastoma Cell Line ◽  
Glioblastoma Cell ◽  
Rho Kinase Inhibitor

scholarly journals An in vitro study of scarring formation mediated by human Tenon fibroblasts: Effect of Y‐27632, a Rho kinase inhibitor

2019 ◽  
Vol 37 (2) ◽  
pp. 113-124 ◽  
Author(s):  
Diah Gemala Ibrahim ◽  
Ji‐Ae Ko ◽  
Wakana Iwata ◽  
Hideaki Okumichi ◽  
Yoshiaki Kiuchi
Keyword(s):  
Kinase Inhibitor ◽  
Rho Kinase ◽  
In Vitro Study ◽  
Vitro Study ◽  
Rho Kinase Inhibitor

scholarly journals Rho Kinase Inhibitor Fasudil Suppresses the Vasculogenic Mimicry of B16 Mouse Melanoma Cells Both In Vitro and In Vivo

2015 ◽  
Vol 14 (7) ◽  
pp. 1582-1590 ◽  
Author(s):  
Yun Xia ◽  
Xian-Yi Cai ◽  
Ji-Quan Fan ◽  
Li-Ling Zhang ◽  
Jing-Hua Ren ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Vasculogenic Mimicry ◽  
Rho Kinase ◽  
Melanoma Cells ◽  
Mouse Melanoma ◽  
Rho Kinase Inhibitor ◽  
B16 Mouse Melanoma

Abstract 4461: Rho-kinase Pathway Plays an Important Role in the Pathogenesis of Coronary Hyperconstricting Responses Induced by Drug-Eluting Stent

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takashi Shiroto ◽  
Satoshi Yasuda ◽  
Ryuji Tsuburaya ◽  
Yoshitaka Ito ◽  
Hatsue Ishibashi-Ueda ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Bare Metal Stent ◽  
Drug Eluting Stent ◽  
Rho Kinase Inhibitor ◽  
Drug Eluting ◽  
Kinase Expression ◽  
Kinase Pathway

It has recently been reported that coronary vasoconstricting responses are enhanced at the edge of coronary segment implanted with drug-eluting stent (DES) as compared with bare-metal stent (BMS) in humans. We have previously demonstrated in animal models and humans that activation of Rho-kinase plays a key role in the molecular mechanism of coronary vasospasm. In this study, we thus examined whether Rho-kinase pathway also is involved in the DES-induced coronary hyperconstriction in vitro and in vivo. In cultured human coronary vascular smooth muscle cells, paclitaxel (10 –1000 nM, comparable tissue concentrations in humans, 24 hours) concentration-dependently up-regulated Rho-kinase expression (n=9) and increased Rho-kinase activity (10 nM, n=6). In a porcine model in vivo, DES (Taxus ™ ) and BMS (Express ™ ) were randomly implanted in the left anterior descending and circumflex coronary arteries (n=5). Four weeks after the implantation, coronary vasoconstricting responses to serotonin (5-HT, 50 and 100 μg/kg, IC) were significantly enhanced at the DES site compared with the BMS site (DES −52±4 vs. BMS −31±5%, P<0.01), and the enhanced responses were prevented by hydroxyfasudil (HF, 90 and 300 μg/kg, IC), a selective Rho-kinase inhibitor ( Figure A ). The same in vivo findings also were noted in another comparison between DES (Cypher ™ ) and BMS (Velocity ™ ) (DES −62±3% vs. BMS −41±3%, n=6, P<0.01) ( Figure B ). Histological analysis showed microthrombus formation only at the DES site. These results suggest that Rho-kinase pathway also plays an important pathogenetic role in the DES-induced coronary hyperconstricting responses.

Effect of the Rho Kinase Inhibitor Y-27632 on Corneal Endothelial Wound Healing

2015 ◽  
Vol 56 (10) ◽  
pp. 6067 ◽  
Author(s):  
Naoki Okumura ◽  
Ryota Inoue ◽  
Yugo Okazaki ◽  
Shinichiro Nakano ◽  
Hiroko Nakagawa ◽  
...  
Keyword(s):  
Wound Healing ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Rho Kinase Inhibitor ◽  
Endothelial Wound Healing

Rho-kinase inhibitor prevents hepatocyte damage in acute liver injury induced by carbon tetrachloride in rats

2007 ◽  
Vol 293 (4) ◽  
pp. G911-G917 ◽  
Author(s):  
Hitoshi Ikeda ◽  
Yukio Kume ◽  
Kazuaki Tejima ◽  
Tomoaki Tomiya ◽  
Takako Nishikawa ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Protective Effect ◽  
Kinase Inhibitor ◽  
Acute Liver Injury ◽  
Rho Kinase ◽  
Akt Pathway ◽  
Rho Kinase Inhibitor ◽  
Hepatocyte Damage

A protective effect of Rho-kinase inhibitor on various organ injuries is gaining attention. Regarding liver injury, Rho-kinase inhibitor is reported to prevent carbon tetrachloride (CCl4)- or dimethylnitrosamine-induced liver fibrosis and hepatic ischemia-reperfusion injury in rats. Because Rho-kinase inhibitor not only improved liver fibrosis but also reduced serum alanine aminotransferase (ALT) level in CCl4-induced liver fibrosis, we wondered whether Rho-kinase inhibitor might exert a direct hepatocyte-protective effect. We examined this possibility in acute CCl4 intoxication in rats. Rho-kinase inhibitor, HA-1077, reduced serum alanine ALT level in rats with acute liver injury induced by CCl4 with the improvement of histological damage and the reduction of the number of apoptotic cells. In cultured rat hepatocytes in serum-free condition, HA-1077 reduced apoptosis evaluated by quantitative determination of cytoplasmic histone-associated DNA oligonucleosome fragments with the reduction of caspase-3 activity and the enhancement of Bcl-2 expression. HA-1077 stimulated phosphorylation of Akt, and wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3-kinase)/Akt pathway, abrogated the reduction of hepatocyte apoptosis by HA-1077 in vitro. Furthermore, wortmannin abrogated the reduction of serum ALT level by HA-1077 in rats with acute liver injury induced by CCl4, suggesting that the activation of PI3-kinase/Akt pathway may be involved in the hepatocyte-protective effect by Rho-kinase inhibitor in vivo. In conclusion, Rho-kinase inhibitor prevented hepatocyte damage in acute liver injury induced by CCl4 in rats and merits consideration as a hepatocyte-protective agent in liver injury, considering its direct antiapoptotic effect on hepatocytes in vitro.

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