The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform

Martin Tepel - One of the best experts on this subject based on the ideXlab platform.

  • increased migration of monocytes in essential hypertension is associated with increased transient receptor potential channel canonical type 3 channels
    PLOS ONE, 2012
    Co-Authors: Zhigang Zhao, Jing Chen, Jian Zhong, Zhencheng Yan, Alexandra Scholze, Daoyan Liu, Zhiming Zhu, Martin Tepel
    Abstract:

    Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed in a microchemotaxis chamber using chemoattractants formylated peptide Met-Leu-Phe (fMLP) and tumor necrosis factor-α (TNF-α). Proteins were identified by immunoblotting and quantitative in-cell Western assay. The effects of TRP channel-inhibitor 2–Aminoethoxydiphenylborane (2-APB) and small interfering RNA knockdown of TRPC3 were investigated. We observed an increased fMLP-induced migration of monocytes from hypertensive patients compared with normotensive control subjects (246±14% vs 151±10%). The TNF-α-induced migration of monocytes in patients with essential hypertension was also significantly increased compared to normotensive control subjects (221±20% vs 138±18%). In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked. The fMLP-induced changes of cytosolic calcium were significantly increased in monocytes from hypertensive patients compared to normotensive control subjects. The fMLP-induced monocyte migration was significantly reduced in the presence of inhibitors of tyrosine kinase and phosphoinositide 3-kinase. We conclude that increased monocyte migration in patients with essential hypertension is associated with increased TRPC3 channels.

Christian Stricker - One of the best experts on this subject based on the ideXlab platform.

  • the contribution of intracellular calcium stores to mepscs recorded in layer ii neurones of rat barrel cortex
    The Journal of Physiology, 2002
    Co-Authors: Christopher R L Simkus, Christian Stricker
    Abstract:

    Loading slices of rat barrel cortex with 50 μm BAPTA-AM while recording from pyramidal cells in layer II induces a marked reduction in both the frequency and amplitudes of mEPSCs. These changes are due to a presynaptic action. Blocking the refilling of Ca2+ stores with 20 μm cyclopiazonic acid (CPA), a SERCA pump inhibitor, in conjunction with neuronal depolarisation to activate Ca2+ stores, results in a similar reduction of mEPSCs to that observed with BAPTA-AM, indicating that the source for intracellular Ca2+ is the endoplasmic reticulum. Block or activation of ryanodine receptors by 20 μm ryanodine or 10 mm caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca2+ release from ryanodine stores. Blocking IP3 receptors with 14 μm 2-Aminoethoxydiphenylborane (2APB) also reduces the frequency and amplitude of mEPSCs, indicating the involvement of IP3 stores in the generation of mEPSCs. Activation of group I metabotropic receptors with 20 μm (RS)-3,5-dihydroxyphenylglycine (DHPG) results in a significant increase in the frequency of mEPSCs, further supporting the role of IP3 receptors and indicating a role of group I metabotropic receptors in causing transmitter release. Statistical evidence is presented for Ca2+-induced Ca2+ release (CICR) from ryanodine stores after the spontaneous opening of IP3 stores.

Zhigang Zhao - One of the best experts on this subject based on the ideXlab platform.

  • Increased Migration of Monocytes in Essential Hypertension Is Associated with Increased Transient Receptor Potential Channel Canonical Type 3 Channels
    2013
    Co-Authors: Zhigang Zhao, Jian Zhong, Zhencheng Yan, Daoyan Liu, Ra Scholze, Zhiming Zhu
    Abstract:

    Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed in a microchemotaxis chamber using chemoattractants formylated peptide Met-Leu-Phe (fMLP) and tumor necrosis factor-a (TNF-a). Proteins were identified by immunoblotting and quantitative in-cell Western assay. The effects of TRP channel-inhibitor 2–Aminoethoxydiphenylborane (2-APB) and small interfering RNA knockdown of TRPC3 were investigated. We observed an increased fMLP-induced migration of monocytes from hypertensive patients compared with normotensive control subjects (246614 % vs 151610%). The TNF-ainduced migration of monocytes in patients with essential hypertension was also significantly increased compared to normotensive control subjects (221620 % vs 138618%). In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked. The fMLP-induced changes of cytosolic calcium were significantly increased in monocytes from hypertensive patients compared to normotensive control subjects. The fMLPinduced monocyte migration was significantly reduced in the presence of inhibitors of tyrosine kinase and phosphoinositide 3-kinase. We conclude that increased monocyte migration in patients with essential hypertension is associated wit

  • increased migration of monocytes in essential hypertension is associated with increased transient receptor potential channel canonical type 3 channels
    PLOS ONE, 2012
    Co-Authors: Zhigang Zhao, Jing Chen, Jian Zhong, Zhencheng Yan, Alexandra Scholze, Daoyan Liu, Zhiming Zhu, Martin Tepel
    Abstract:

    Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed in a microchemotaxis chamber using chemoattractants formylated peptide Met-Leu-Phe (fMLP) and tumor necrosis factor-α (TNF-α). Proteins were identified by immunoblotting and quantitative in-cell Western assay. The effects of TRP channel-inhibitor 2–Aminoethoxydiphenylborane (2-APB) and small interfering RNA knockdown of TRPC3 were investigated. We observed an increased fMLP-induced migration of monocytes from hypertensive patients compared with normotensive control subjects (246±14% vs 151±10%). The TNF-α-induced migration of monocytes in patients with essential hypertension was also significantly increased compared to normotensive control subjects (221±20% vs 138±18%). In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked. The fMLP-induced changes of cytosolic calcium were significantly increased in monocytes from hypertensive patients compared to normotensive control subjects. The fMLP-induced monocyte migration was significantly reduced in the presence of inhibitors of tyrosine kinase and phosphoinositide 3-kinase. We conclude that increased monocyte migration in patients with essential hypertension is associated with increased TRPC3 channels.

Zhiming Zhu - One of the best experts on this subject based on the ideXlab platform.

  • Increased Migration of Monocytes in Essential Hypertension Is Associated with Increased Transient Receptor Potential Channel Canonical Type 3 Channels
    2013
    Co-Authors: Zhigang Zhao, Jian Zhong, Zhencheng Yan, Daoyan Liu, Ra Scholze, Zhiming Zhu
    Abstract:

    Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed in a microchemotaxis chamber using chemoattractants formylated peptide Met-Leu-Phe (fMLP) and tumor necrosis factor-a (TNF-a). Proteins were identified by immunoblotting and quantitative in-cell Western assay. The effects of TRP channel-inhibitor 2–Aminoethoxydiphenylborane (2-APB) and small interfering RNA knockdown of TRPC3 were investigated. We observed an increased fMLP-induced migration of monocytes from hypertensive patients compared with normotensive control subjects (246614 % vs 151610%). The TNF-ainduced migration of monocytes in patients with essential hypertension was also significantly increased compared to normotensive control subjects (221620 % vs 138618%). In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked. The fMLP-induced changes of cytosolic calcium were significantly increased in monocytes from hypertensive patients compared to normotensive control subjects. The fMLPinduced monocyte migration was significantly reduced in the presence of inhibitors of tyrosine kinase and phosphoinositide 3-kinase. We conclude that increased monocyte migration in patients with essential hypertension is associated wit

  • increased migration of monocytes in essential hypertension is associated with increased transient receptor potential channel canonical type 3 channels
    PLOS ONE, 2012
    Co-Authors: Zhigang Zhao, Jing Chen, Jian Zhong, Zhencheng Yan, Alexandra Scholze, Daoyan Liu, Zhiming Zhu, Martin Tepel
    Abstract:

    Increased transient receptor potential canonical type 3 (TRPC3) channels have been observed in patients with essential hypertension. In the present study we tested the hypothesis that increased monocyte migration is associated with increased TRPC3 expression. Monocyte migration assay was performed in a microchemotaxis chamber using chemoattractants formylated peptide Met-Leu-Phe (fMLP) and tumor necrosis factor-α (TNF-α). Proteins were identified by immunoblotting and quantitative in-cell Western assay. The effects of TRP channel-inhibitor 2–Aminoethoxydiphenylborane (2-APB) and small interfering RNA knockdown of TRPC3 were investigated. We observed an increased fMLP-induced migration of monocytes from hypertensive patients compared with normotensive control subjects (246±14% vs 151±10%). The TNF-α-induced migration of monocytes in patients with essential hypertension was also significantly increased compared to normotensive control subjects (221±20% vs 138±18%). In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked. The fMLP-induced changes of cytosolic calcium were significantly increased in monocytes from hypertensive patients compared to normotensive control subjects. The fMLP-induced monocyte migration was significantly reduced in the presence of inhibitors of tyrosine kinase and phosphoinositide 3-kinase. We conclude that increased monocyte migration in patients with essential hypertension is associated with increased TRPC3 channels.

Christopher R L Simkus - One of the best experts on this subject based on the ideXlab platform.

  • the contribution of intracellular calcium stores to mepscs recorded in layer ii neurones of rat barrel cortex
    The Journal of Physiology, 2002
    Co-Authors: Christopher R L Simkus, Christian Stricker
    Abstract:

    Loading slices of rat barrel cortex with 50 μm BAPTA-AM while recording from pyramidal cells in layer II induces a marked reduction in both the frequency and amplitudes of mEPSCs. These changes are due to a presynaptic action. Blocking the refilling of Ca2+ stores with 20 μm cyclopiazonic acid (CPA), a SERCA pump inhibitor, in conjunction with neuronal depolarisation to activate Ca2+ stores, results in a similar reduction of mEPSCs to that observed with BAPTA-AM, indicating that the source for intracellular Ca2+ is the endoplasmic reticulum. Block or activation of ryanodine receptors by 20 μm ryanodine or 10 mm caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca2+ release from ryanodine stores. Blocking IP3 receptors with 14 μm 2-Aminoethoxydiphenylborane (2APB) also reduces the frequency and amplitude of mEPSCs, indicating the involvement of IP3 stores in the generation of mEPSCs. Activation of group I metabotropic receptors with 20 μm (RS)-3,5-dihydroxyphenylglycine (DHPG) results in a significant increase in the frequency of mEPSCs, further supporting the role of IP3 receptors and indicating a role of group I metabotropic receptors in causing transmitter release. Statistical evidence is presented for Ca2+-induced Ca2+ release (CICR) from ryanodine stores after the spontaneous opening of IP3 stores.