Muscle Cells

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Stefan Offermanns - One of the best experts on this subject based on the ideXlab platform.

  • previously differentiated medial vascular smooth Muscle Cells contribute to neointima formation following vascular injury
    Vascular Cell, 2014
    Co-Authors: Brian Paul Herring, April M Hoggatt, Christopher Burlak, Stefan Offermanns
    Abstract:

    Background The origins of neointimal smooth Muscle Cells that arise following vascular injury remains controversial. Studies have suggested that these Cells may arise from previously differentiated medial vascular smooth Muscle Cells, resident stem Cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth Muscle Cells to the neointima that forms following carotid artery ligation.

  • previously differentiated medial vascular smooth Muscle Cells contribute to neointima formation following vascular injury
    PMC, 2014
    Co-Authors: Brian Paul Herring, April M Hoggatt, Christopher Burlak, Stefan Offermanns
    Abstract:

    The origins of neointimal smooth Muscle Cells that arise following vascular injury remains controversial. Studies have suggested that these Cells may arise from previously differentiated medial vascular smooth Muscle Cells, resident stem Cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth Muscle Cells to the neointima that forms following carotid artery ligation. We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth Muscle myosin heavy chain (Myh11) or smooth Muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth Muscle Cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive Cells to the neointima determined. Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive Cells derived from either Mhy11 or Acta2 tagged medial vascular smooth Muscle Cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth Muscle Cells.

Xinxin Wang - One of the best experts on this subject based on the ideXlab platform.

  • effects of emodin on the activity of k channel in guinea pig taenia coli smooth Muscle Cells
    Acta pharmaceutica Sinica, 1998
    Co-Authors: Jiafang Li, Wenqing Yang, Jiang Wang, W Hu, Xinxin Wang
    Abstract:

    : The effects of emodin, cromakalim (KATP channel opener) glybenclamide (KATP channel inhibitor) Ba2+ and TEA on the electrical and contractive activities of the smooth Muscle Cells in guinea pig taenia coli and the relationship between emodin and four other drugs were studied by using intracellular microelectrode technique and the tension measuring technique. The results are as follows: (1) Emodin enhances the electrical and contractive activities of the smooth Muscle Cells in guinea pig taenia coli. The effects of emodin depend on its concentration. (2) Emodin can resist the inhibition of cromakalim on the electrical and contractive activities of smooth Muscle Cells. On the other hand, cromakalim was shown to suppress the effects of emodin. (3) Ba2+, TEA and glybenclamide all can improve the electrical and contractive activities of smooth Muscle Cells and resist the inhibition of cromakalim. The effects of emodin were found to be similar to that of glybenclamide but different from that of Ba2+ and TEA. The results suggest that the mechanism of action of emodin is to inhibit the activity of KATP channel in the guinea pig taenia coli smooth Muscle Cells.

Brian Paul Herring - One of the best experts on this subject based on the ideXlab platform.

  • previously differentiated medial vascular smooth Muscle Cells contribute to neointima formation following vascular injury
    Vascular Cell, 2014
    Co-Authors: Brian Paul Herring, April M Hoggatt, Christopher Burlak, Stefan Offermanns
    Abstract:

    Background The origins of neointimal smooth Muscle Cells that arise following vascular injury remains controversial. Studies have suggested that these Cells may arise from previously differentiated medial vascular smooth Muscle Cells, resident stem Cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth Muscle Cells to the neointima that forms following carotid artery ligation.

  • previously differentiated medial vascular smooth Muscle Cells contribute to neointima formation following vascular injury
    PMC, 2014
    Co-Authors: Brian Paul Herring, April M Hoggatt, Christopher Burlak, Stefan Offermanns
    Abstract:

    The origins of neointimal smooth Muscle Cells that arise following vascular injury remains controversial. Studies have suggested that these Cells may arise from previously differentiated medial vascular smooth Muscle Cells, resident stem Cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth Muscle Cells to the neointima that forms following carotid artery ligation. We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth Muscle myosin heavy chain (Myh11) or smooth Muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth Muscle Cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive Cells to the neointima determined. Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive Cells derived from either Mhy11 or Acta2 tagged medial vascular smooth Muscle Cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth Muscle Cells.

Tatsuya Tamaoki - One of the best experts on this subject based on the ideXlab platform.

  • the mechanism for the activation of latent tgf beta during co culture of endothelial Cells and smooth Muscle Cells cell type specific targeting of latent tgf beta to smooth Muscle Cells
    Journal of Cell Biology, 1993
    Co-Authors: Yasufumi Sato, Fumio Okada, Mayumi Abe, T Seguchi, Michihiko Kuwano, Seiji Sato, Akiko Furuya, Nobuo Hanai, Tatsuya Tamaoki
    Abstract:

    Transforming growth factor-beta (TGF-beta) is secreted in a latent form and activated during co-culture of endothelial Cells and smooth Muscle Cells. Plasmin located on the surface of endothelial Cells is required for the activation of latent TGF-beta (LTGF-beta) during co-culture, and the targeting of LTGF-beta to the cellular surface is requisite for its activation. In the present study, the cellular targeting of LTGF-beta was examined. We detected the specific binding of 125I-large LTGF-beta 1 isolated from human platelets to smooth Muscle Cells but not to endothelial Cells. A mAb against the latency-associated peptide (LAP) of large LTGF-beta 1 complex, which blocked the binding of 125I-large LTGF-beta 1 to smooth Muscle Cells, inhibited the activation of LTGF-beta during co-culture. The binding of 125I-large LTGF-beta 1 could not be competed either by mannose-6-phosphate (300 microM) or by the synthetic peptide Arg-Gly-Asp-Ser (300 micrograms/ml). These results indicate that the targeting of LTGF-beta to smooth Muscle Cells is required for the activation of LTGF-beta during co-culture of endothelial Cells and smooth Muscle Cells. The targeting of LTGF-beta to smooth Muscle Cells is mediated by LAP, and the domain of LAP responsible for the targeting to smooth Muscle Cells may not be related to mannose-6-phosphate or an Arg-Gly-Asp sequence, both of which have been previously proposed as candidates for the cellular binding domains within LAP.

William T Gerthoffer - One of the best experts on this subject based on the ideXlab platform.