Reduced Expression of Endothelial Connexins 43 and 37 in Hypertensive Rats Is Rectified After 7-Day Carvedilol Treatment

Yeh, Hung‐I; Lee, Ping-Ying; Su, Cheng‐Huang; Tian, Tin-Yi; Ko, Yousang; Tsai, Cheng‐Ho

doi:10.1016/j.amjhyper.2005.08.020

Cited by 40 publications

(36 citation statements)

References 29 publications

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“…Previous studies have shown that direct intercellular communication through cell membrane protein channels made of connexins, called gap junctions, is involved in several steps of atherogenesis (Severs et al 2001;Haefliger et al 2004;Chadjichristos et al 2006). In animal studies, endothelial gap junctions have been reported to be downregulated in the presence of risk factors of atherosclerotic disease, such as aging (Yeh et al 2000a), hypertension (Yeh et al 2006), and hyperlipidemia (Yeh et al 2003b), in which endothelial dysfunction exists (Esper et al 2006). In addition, the downregulation of endothelial gap junctions in hypertension and hyperlipidemia can be, respectively, attenuated by antihypertensive and lipid-lowering drugs (Yeh et al 2003b(Yeh et al ,2006, which are known to improve impaired endothelial function (Esper et al 2006).…”

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confidence: 99%

“…In animal studies, endothelial gap junctions have been reported to be downregulated in the presence of risk factors of atherosclerotic disease, such as aging (Yeh et al 2000a), hypertension (Yeh et al 2006), and hyperlipidemia (Yeh et al 2003b), in which endothelial dysfunction exists (Esper et al 2006). In addition, the downregulation of endothelial gap junctions in hypertension and hyperlipidemia can be, respectively, attenuated by antihypertensive and lipid-lowering drugs (Yeh et al 2003b(Yeh et al ,2006, which are known to improve impaired endothelial function (Esper et al 2006). The evidence has suggested that downregulation of gap junctions in the endothelium reflects endothelial dysfunction.…”

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confidence: 99%

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Diabetes Reduces Aortic Endothelial Gap Junctions in ApoE-deficient Mice: Simvastatin Exacerbates the Reduction

Hou

Tsai

et al. 2008

J Histochem Cytochem.

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(J-JC,M-SS)S U M M A R Y We examined the endothelial gap junctions in diabetic hyperlipidemic mice.Male apolipoprotein E (apoE)-deficient mice were made diabetic by streptozotocin. Three weeks later, the animals were treated with simvastatin for 2 weeks. The expression of aortic gap junctions in the non-diabetic (n=10), untreated diabetic (n=10), and simvastatin-treated diabetic animals (n=6) was analyzed. There was a .4-fold increase in serum cholesterol level and .50% increase in plaque areas in the diabetic mice, regardless of simvastatin treatment. Western blotting of aortae showed reduced expression of connexin37 (Cx37) and Cx40 in the diabetic mice, which were further decreased in the simvastatin-treated diabetic mice. Immunoconfocal microscopy showed that endothelial gap junctions made of Cx37 and Cx40 were both reduced in the untreated diabetic mice compared with the non-diabetic mice (decrease: Cx37, 41%; Cx40, 42%; both p,0.01). The reduction was greater in the simvastatin-treated mice (decrease in treated diabetic vs non-diabetic: Cx37, 61%; Cx40, 79%; both p,0.01; decrease in treated diabetic vs untreated diabetic: Cx37, 34%; Cx40, 63%; both p,0.01). Cx37 and Cx40 were decreased in the endothelium of plaque surface. Cx43 appeared in the medial layer and inner layer of the intima. All three connexins were rarely expressed in monocytes/macrophages inside the plaques. In conclusion, in apoE-deficient mice, streptozotocin-induced diabetes is associated with downregulation of endothelial Cx37 and Cx40 gap junctions. Short-term treatment with simvastatin exacerbates the downregulation. (J Histochem Cytochem 56:745-752, 2008)

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confidence: 99%

Diabetes Reduces Aortic Endothelial Gap Junctions in ApoE-deficient Mice: Simvastatin Exacerbates the Reduction

Hou

Tsai

et al. 2008

J Histochem Cytochem.

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“…In the mesenteric artery of the same rat model, Kansui et al (2004) showed that the Cx37 and Cx40 were downregulated and the Cx43, though scarce and heterogenous, was upregulated. In the tail artery of rat with N-nitro-L-arginine methyl ester-induced hypertension, Yeh et al (2006) demonstrated that the endothelial Cx37 and Cx43 were downregulated and the Cx40 remained unchanged. When compared with the resistant arteries, the baseline pressure of the venous vessels before being anastomosed with the arteries is much lower.…”

Section: Discussionmentioning

confidence: 99%

Differential Endothelial Gap Junction Expression in Venous Vessels Exposed to Different Hemodynamics

Chang

Hsu

et al. 2010

J Histochem Cytochem.

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After being anastomosed with the artery, vein graft is exposed to abruptly increased hemodynamic stresses. These hemodynamic stresses may change the profile of endothelial gap junction expression as demonstrated in the artery, which may subsequently play active roles in physiological adaptation or pathophysiological changes of the vein grafts. We investigated the endothelial expression of gap junction in the venous vessels exposed to different hemodynamic stresses. Immunocytochemical analysis of the endothelial Cx expression was performed by observing the whole mounts of inferior vena cava (IVC) of aortocaval fistula (ACF) rats or IVC-banded ACF rats using confocal microscope. Immunocytochemical analysis demonstrated that in the endothelium of the native vein, the gap-junctional spot numbers (GJSNs) and the total gap-junctional areas (TGJAs) of C×40 and C×43 were lower than those of the thoracic aorta and that C×37 was hardly detectable. In the IVCs of ACF rats, which were demonstrated to be exposed to a hemodynamic condition of high flow velocity and low pressure, the GJSNs and the TGJAs of all three C×5 were increased. In the IVCs of IVC-banded ACF rats, which were exposed to a hemodynamic condition of high pressure and low flow velocity, the GJSNs and the TGJAs of C×37 increased markedly and those of C×40 and C×43 remained without significant changes. In conclusion, the endothelial expressions of gap junctions in the native veins were lower than those of the arteries. When exposed to different hemodynamic stresses, the gap junctions were expressed in specific patterns. (J Histochem Cytochem 58:1083–1092, 2010)

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“…Some special membrane domains composed of aqueous intracellular channels provide direct cytoplasmic connections between cells, and allow for the passage of ions or small molecules between adjacent cells, thus ECs and OBs can communicate and exchange information (Dbouk et al 2009). Several predominant gap junction proteins including Cx43, Cx37 and Cx40 have been identified to express in ECs and OBs (Yeh et al 2006). Similarly, the communication via Cx43 gap junctions can promote the expression of osteoblastic differentiation markers such as alkaline phosphatase (ALP), osteocalcin (OC) and bone sialoprotein in OBs (Guillotin et al 2008).…”

Section: Interaction Between Osteoblasts and Endothelial Cellsmentioning

confidence: 99%

Vascularization in the Bone Repair

Zhou¹,

Dong²

2012

Osteogenesis

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Reduced Expression of Endothelial Connexins 43 and 37 in Hypertensive Rats Is Rectified After 7-Day Carvedilol Treatment

Abstract: The study showed that L-NAME-induced hypertension has differential effects on endothelial connexins, which respond variously to carvedilol and atenolol. In HUVEC carvedilol directly upregulates endothelial Cx43 and the effect is independent of its antioxidant activity.

Cited by 40 publications

References 29 publications

Diabetes Reduces Aortic Endothelial Gap Junctions in ApoE-deficient Mice: Simvastatin Exacerbates the Reduction

Diabetes Reduces Aortic Endothelial Gap Junctions in ApoE-deficient Mice: Simvastatin Exacerbates the Reduction

Differential Endothelial Gap Junction Expression in Venous Vessels Exposed to Different Hemodynamics

Vascularization in the Bone Repair

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