2014Journal of Clinical CardiologyRequires access

The expression of connexin in rabbit iliac artery restenosis models

Lei Cao

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Abstract

Objective:To observe the pathological changes and expression of connexin(Cx)in rabbit iliac artery restenosis models.Method:Twenty New Zealand White rabbits were randomly divedied into 2groups:control group(n=10)and restenosis group(n=10).Restenosis group followed high-fat diet combined with double-balloon injury to establish restenosis model.Four weeks later,all rabbits were killed and iliac arteries were then cut down for HE staining,immunohistochemiscal analysis,and detecting the expression of Cx mRNA by RT-PCR as well.Result:Computer-assisted histomorphometric analysis showed the intima thickness of restenosis group increased compared with that of control group[(266.12±70.27)μm vs(2.85±0.19)μm,P0.01].We also observed the stenosis rates of restenosis group were higher than those of controls[(89.32±6.93)% vs(23.00±3.53)%,P0.01].By using immunohistochemistry to detectα-smooth muscle actin(α-SMA),we confirmed that the proliferated cells in neointima were VSMCs in restenosis group.Immuohistochemical analysis indicated Cx43 expressed in all iliac arteries of two groups.Compared with controls,more Cx43 expression was detected in neointima in restenosis group.Additionally,the Cx40 expression of controls was a little lower than that of restenosis group.Compared with control group,the expression of Cx43 mRNA increased in restenosis group(P0.01).As for the expression of Cx40 mRNA,there was no difference between two groups.Conclusion:It is not Cx40 but Cx43in gap junction that contributes to the process of the migration and proliferation of VSMCs in neointima formation,which plays an important role in the pathogenesis of restenosis.

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Objective:To observe the pathological changes and expression of connexin(Cx)in rabbit iliac artery restenosis models.Method:Twenty New Zealand White rabbits were randomly divedied into 2groups:control group(n=10)and restenosis group(n=10).Restenosis group followed high-fat diet combined with double-balloon injury to establish restenosis model.Four weeks later,all rabbits were killed and iliac arteries were then cut down for HE staining,immunohistochemiscal analysis,and detecting the expression of Cx mRNA by RT-PCR as well.Result:Computer-assisted histomorphometric analysis showed the intima thickness of restenosis group increased compared with that of control group[(266.12±70.27)μm vs(2.85±0.19)μm,P0.01].We also observed the stenosis rates of restenosis group were higher than those of controls[(89.32±6.93)% vs(23.00±3.53)%,P0.01].By using immunohistochemistry to detectα-smooth muscle actin(α-SMA),we confirmed that the proliferated cells in neointima were VSMCs in restenosis group.Immuohistochemical analysis indicated Cx43 expressed in all iliac arteries of two groups.Compared with controls,more Cx43 expression was detected in neointima in restenosis group.Additionally,the Cx40 expression of controls was a little lower than that of restenosis group.Compared with control group,the expression of Cx43 mRNA increased in restenosis group(P0.01).As for the expression of Cx40 mRNA,there was no difference between two groups.Conclusion:It is not Cx40 but Cx43in gap junction that contributes to the process of the migration and proliferation of VSMCs in neointima formation,which plays an important role in the pathogenesis of restenosis.

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Available abstract

Objective:To observe the pathological changes and expression of connexin(Cx)in rabbit iliac artery restenosis models.Method:Twenty New Zealand White rabbits were randomly divedied into 2groups:control group(n=10)and restenosis group(n=10).Restenosis group followed high-fat diet combined with double-balloon injury to establish restenosis model.Four weeks later,all rabbits were killed and iliac arteries were then cut down for HE staining,immunohistochemiscal analysis,and detecting the expression of Cx mRNA by RT-PCR as well.Result:Computer-assisted histomorphometric analysis showed the intima thickness of restenosis group increased compared with that of control group[(266.12±70.27)μm vs(2.85±0.19)μm,P0.01].We also observed the stenosis rates of restenosis group were higher than those of controls[(89.32±6.93)% vs(23.00±3.53)%,P0.01].By using immunohistochemistry to detectα-smooth muscle actin(α-SMA),we confirmed that the proliferated cells in neointima were VSMCs in restenosis group.Immuohistochemical analysis indicated Cx43 expressed in all iliac arteries of two groups.Compared with controls,more Cx43 expression was detected in neointima in restenosis group.Additionally,the Cx40 expression of controls was a little lower than that of restenosis group.Compared with control group,the expression of Cx43 mRNA increased in restenosis group(P0.01).As for the expression of Cx40 mRNA,there was no difference between two groups.Conclusion:It is not Cx40 but Cx43in gap junction that contributes to the process of the migration and proliferation of VSMCs in neointima formation,which plays an important role in the pathogenesis of restenosis.

Key concepts: Restenosis, Neointima, Medicine, Connexin, Immunohistochemistry, Intimal hyperplasia, Internal medicine, Artery

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