scholarly journals CNP-pGC-cGMP-PDE3-cAMP Signal Pathway Upregulated in Gastric Smooth Muscle of Diabetic Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Ying-Lan Cai ◽  
Mo-Han Zhang ◽  
Xu Huang ◽  
Jing-Zhi Jiang ◽  
Li-Hua Piao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Tissue ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Signal Pathway ◽  
Diabetic Rat ◽  
Rt Pcr ◽  
Smooth Muscle Tissue ◽  
Circular Smooth Muscle ◽  
Gastric Smooth Muscle

Our previous studies have shown that CNP-NPR-B/pGC-cGMP is upregulated in the diabetic rats. The present study was designed to determine whether the upregulation of CNP-NPR-B/pGC-cGMP signal pathway affects cGMP-PDE3-cAMP signal pathway in diabetic gastric smooth muscle. The gastric smooth muscle motility was observed by using isometric measurement. PDEs expressions in diabetic gastric smooth muscle tissue were observed by using immunohistochemistry, Western blotting, and RT-PCR methods. The results demonstrated that the inhibitory effect of CNP on the spontaneous contraction of gastric antral circular smooth muscle was potentiated in STZ-induced diabetic rat. CNP-induced increase of cGMP and cAMP was much higher in diabetic gastric smooth muscle tissue than in controls. The expression of PDE3 is downregulated while the levels of gene expression of PDE1, PDE2, PDE4, and PDE5 were not altered in the diabetic gastric smooth muscle tissue. The results suggest that the sensitivity of gastric smooth muscle to CNP is potentiated via activation of CNP-pGC-cGMP-PDE3-cAMP signal pathway in STZ-induced diabetic rats, which may be associated with diabetes-induced gastric motility disorder.

scholarly journals Effect ofAurantii Fructus Immaturus Flavonoidon the Contraction of Isolated Gastric Smooth Muscle Strips in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Zhenyu Wu ◽  
Shengsheng Zhang ◽  
Peicai Li ◽  
Xiaofang Lu ◽  
Jiajia Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cyclic Guanosine Monophosphate ◽  
Inhibitory Effect ◽  
Guanosine Monophosphate ◽  
Muscle Strip ◽  
Circular Smooth Muscle ◽  
Gastric Smooth Muscle ◽  
Underlying Mechanisms ◽  
Oxide Synthase ◽  
Dose Dependent

This study was designed to investigate the effect ofAurantii fructus immaturus flavonoid(AFIF) on the contraction of isolated gastric smooth muscle in rats and explore its underlying mechanisms. Isolated antral longitudinal smooth muscle strip (ALSMS) and pyloric circular smooth muscle strip (PCSMS) of rats were suspended in tissue chambers. The responses of ALSMS and PCSMS to administration of AFIF were observed. Cyclic guanosine monophosphate (cGMP) and protein kinase G (PKG) levels of PCSMS were measured by ELISA kits. In this study, AFIF showed no significant effect on ALSMS contraction, but it dose-dependently reduced the mean contraction amplitude of PCSMS. When the concentration of AFIF reached 3000 μg/mL, 6000 μg/mL, and 10000 μg/mL, its inhibitory effect on PCSMS contraction was significant. This effect of AFIF was weakened in Ca2+-rich environment. And Nω-nitro-L-arginine methyl (L-NAME), the inhibitor of nitric oxide synthase (NOS), significantly inhibited AFIF’s action in comparison with control (P<0.05). After incubation with AFIF for 30 min, levels of cGMP and PKG in PCSMS were significantly increased compared with control (P<0.05). Our results suggest that AFIF has a dose-dependent diastolic effect on PCSMS in rats, which may be related to the regulatory pathway of NO/cGMP/PKG/Ca2+.

A collagen matrix derived from bladder can be used to engineer smooth muscle tissue

2008 ◽  
Vol 26 (4) ◽  
pp. 307-314 ◽  
Author(s):  
Byung-Soo Kim ◽  
Anthony Atala ◽  
James J. Yoo
Keyword(s):  
Smooth Muscle ◽  
Muscle Tissue ◽  
Collagen Matrix ◽  
Smooth Muscle Tissue

scholarly journals Microarray analysis reveals novel gene expression changes associated with erectile dysfunction in diabetic rats

2005 ◽  
Vol 23 (2) ◽  
pp. 192-205 ◽  
Author(s):  
Chris J. Sullivan ◽  
Thomas H. Teal ◽  
Ian P. Luttrell ◽  
Khoa B. Tran ◽  
Mette A. Peters ◽  
...  
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Erectile Dysfunction ◽  
Splice Variants ◽  
Full Range ◽  
Diabetic Rats ◽  
Differentially Expressed ◽  
Diabetic Rat ◽  
Literature Mining ◽  
Mrna Levels

To investigate the full range of molecular changes associated with erectile dysfunction (ED) in Type 1 diabetes, we examined alterations in penile gene expression in streptozotocin-induced diabetic rats and littermate controls. With the use of Affymetrix GeneChip arrays and statistical filtering, 529 genes/transcripts were considered to be differentially expressed in the diabetic rat cavernosum compared with control. Gene Ontology (GO) classification indicated that there was a decrease in numerous extracellular matrix genes (e.g., collagen and elastin related) and an increase in oxidative stress-associated genes in the diabetic rat cavernosum. In addition, PubMatrix literature mining identified differentially expressed genes previously shown to mediate vascular dysfunction [e.g., ceruloplasmin ( Cp), lipoprotein lipase, and Cd36] as well as genes involved in the modulation of the smooth muscle phenotype (e.g., Kruppel-like factor 5 and chemokine C-X3-C motif ligand 1). Real-time PCR was used to confirm changes in expression for 23 relevant genes. Further validation of Cp expression in the diabetic rat cavernosum demonstrated increased mRNA levels of the secreted and anchored splice variants of Cp. CP protein levels showed a 1.9-fold increase in tissues from diabetic rats versus controls. Immunohistochemistry demonstrated localization of CP protein in cavernosal sinusoids of control and diabetic animals, including endothelial and smooth muscle layers. Overall, this study broadens the scope of candidate genes and pathways that may be relevant to the pathophysiology of diabetes-induced ED as well as highlights the potential complexity of this disorder.

Regulation of lipoprotein lipase activity in cardiac myocytes from control and diabetic rat hearts by plasma lipids

1992 ◽  
Vol 70 (9) ◽  
pp. 1271-1279 ◽  
Author(s):  
Brian Rodrigues ◽  
Janice E. A. Braun ◽  
Michael Spooner ◽  
David L. Severson
Keyword(s):  
Lipoprotein Lipase ◽  
Cardiac Myocytes ◽  
Lipase Activity ◽  
Plasma Lipids ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Lipoprotein Lipase Activity ◽  
Triton Wr 1339 ◽  
Plasma Triacylglycerol

The objective of this investigation was to test the hypothesis that the diabetes-induced reduction in lipoprotein lipase activity in cardiac myocytes may be due to hypertriglyceridemia. Administration of 4-aminopyrazolopyrimidine (50 mg/kg) to control rats for 24 h reduced plasma triacylglycerol levels and increased the heparin-induced release of lipoprotein lipase into the incubation medium of cardiac myocytes. The acute (3–5 days) induction of diabetes by streptozotocin (100 mg/kg) produced hypertriglyceridemia and reduced heparin-releasable lipoprotein lipase activity in cardiac myocytes. Treatment of diabetic rats with 4-aminopyrazolopyrimidine resulted in a fall in plasma triacylglycerol content and increased heparin-releasable lipoprotein lipase activity. Administration of Triton WR-1339 also resulted in hypertriglyceridemia, but the heparin-induced release of lipoprotein lipase from control cardiac myocytes was not reduced in the absence of lipolysis of triacylglycerol-rich lipoproteins. Treatment with Triton WR-1339 did, however, increase the heparin-induced release of lipoprotein lipase from diabetic cardiac myocytes. Preparation of cardiac myocytes with 0.9 mM oleic acid resulted in a decrease in both total cellular and heparin-releasable lipoprotein lipase activities. These results suggest that the diabetes-induced reduction in heart lipoprotein lipase activity may, at least in part, be due to an inhibitory effect of free fatty acids, derived either from lipoprotein degradation or from adipose tissue lipolysis, on lipoprotein lipase activity in (and (or) release from) cardiac myocytes.Key words: diabetes, plasma triacylglycerols, cardiac myocytes, lipoprotein lipase.

scholarly journals Ultrastructural Pathology of Smooth Muscle Tissue Surrounding Prostatic Adenocarcinoma

2003 ◽  
Vol 9 (S02) ◽  
pp. 1400-1401
Author(s):  
H.J. Finol ◽  
T. Gledhill ◽  
D. Parada ◽  
C. López ◽  
O. Moreira
Keyword(s):  
Smooth Muscle ◽  
Muscle Tissue ◽  
Prostatic Adenocarcinoma ◽  
Smooth Muscle Tissue ◽  
Ultrastructural Pathology
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