Phospholipase C and myosin light chain kinase inhibition define a common step in actin regulation during cytokinesis

Wong, Raymond; Fabian, Lacramioara; Forer, Arthur; Brill, Julie A.

doi:10.1186/1471-2121-8-15

Cited by 57 publications

(47 citation statements)

References 43 publications

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“…7 and 8 way, increases cell adhesion and migration (48,49 (50,51), and this appears to be linked to Ca 2ϩ -dependent cell detachment mechanisms such as increased contractility, enzymatic adhesion disassembly, or increased actin severing to the rear (49,52,53). The role of Ca 2ϩ in triggering retraction is particularly evident in cells that display transient increases in [Ca 2ϩ ] i , where Ca 2ϩ transients are often observed immediately before a retraction; this process requires the Ca 2ϩ -dependent protease calpain (54).…”

Section: Discussionmentioning

confidence: 99%

Calcium-sensing Receptor Modulates Cell Adhesion and Migration via Integrins

Tharmalingam

Daulat

Antflick

et al. 2011

Journal of Biological Chemistry

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Background:The calcium-sensing receptor (CaSR) is a nutrient sensor implicated in cell migration. Results:The CaSR is present in a signaling complex with ␤1-containing integrins. Conclusion:The results demonstrate that an ion-sensing G protein-coupled receptor couples to the integrins to promote cellular adhesion and migration in tumor cells. Significance: Identifying components of the CaSR signaling complex is important for understanding the role of the CaSR in cancer cell metastasis.

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Section: Discussionmentioning

confidence: 99%

Calcium-sensing Receptor Modulates Cell Adhesion and Migration via Integrins

Tharmalingam

Daulat

Antflick

et al. 2011

Journal of Biological Chemistry

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“…In the presence of the PLC inhibitor U73122 (10 !M, >20 min), carbachol application significantly increased the mIPSC frequency compared with vehicle-only application (1 mM carbachol, n = 9, vehicle water only, n = 3; frequencies increased by 1.1 ± 1.1 vs. -0.3 ± 0.6 Hz, P = 0.002, U-test).Another PLC inhibitor, 50 !M edelfosine (Horowitz et al, 2005;Wong et al, 2007), also had no significant effect on the carbachol action (20 !M edelfosine, n = 8, vehicle water only, n = 8; frequencies increased by -0.1 ± 0.5 vs. 0.2 ± 0.7 Hz, P = 0.80, U-test) (50 !M edelfosine, n = 6, vehicle water only, n = 5; 200 !M carbachol application in both groups, frequencies increased by 1.1 ± 2.9 vs. 0.1 ± 0.3 Hz, P = 0.56, U-test).…”

Section: Inhibition Of Intracellurar Pathways Such As Plc or Inositolmentioning

confidence: 99%

Muscarinic receptor type 1 (M1) stimulation, probably through KCNQ/Kv7 channel closure, increases spontaneous GABA release at the dendrodendritic synapse in the mouse accessory olfactory bulb

Takahashi

Kaba

2010

Brain Research

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Cholinergic modulation of spontaneous GABAergic currents (mIPSC) was studied using whole-cell patch methods in mouse accessory olfactory bulb slices. Carbachol (above 100 !M) administration produced an increase in the mIPSC frequency in mitral cells, but did not affect the responses of mitral cells to GABA. The carbachol effect persisted in the presence of combined ionotropic and metabotropic glutamatergic receptor antagonists. The carbachol effect was reduced by the muscarinic receptor type-1 and -4 (M1, M4) antagonist pirenzepine (10 !M), but not by the M2 and M4 antagonist himbacine (10 !M). The KCNQ/Kv7 potassium channel openers retigabine (80 !M) and diclofenac (300 !M) blocked the carbachol action, while the KCNQ potassium channel blocker XE-911 (20 !M) increased the mIPSC frequency. XE-911's action persisted in the presence of glutamate receptor blockers. In the presence of carbachol, mIPSCs were abolished by Ni (200 !M), while being insensitive to the calcium channel blocker nimodipine (30 !M), suggesting a role for R-type calcium channels in the GABA release. These results suggest that carbachol closed KCNQ channels by stimulating M1 receptors on granule cell dendrites, and the resulting depolarized and unstable membrane promoted calcium influx, thus increasing the GABA release. The possible role of acetylcholine in facilitating formation of a pheromone memory in mice is also discussed. Classification TermsSection: Neurophysiology

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“…VSMCs were stimulated with bradykinin (10 Ϫ6 mol/l), acutely (10 -30 min) or chronically (1-24 h). In some experiments, cells were preexposed for 30 min to Hoe-140 [bradykinin-2 (B 2) receptor antagonist; 10 Ϫ5 mol/l], chelerythrine (PKC inhibitor; 10 Ϫ5 mol/l), U-73122 (PLC inhibitor; 10 Ϫ5 mol/l) or 2-aminoethoxydiphenyl borate (2-APB; TRPM7 inhibitor; 10 Ϫ5 mol/l, 2 h pretreatment) (18,50,52).…”

Section: Methodsmentioning

confidence: 99%

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Yogi¹,

Callera²,

Tostes³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Yogi A, Callera GE, Tostes R, Touyz RM. Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells. Am J Physiol Regul Integr Comp Physiol 296: R201-R207, 2009. First published September 17, 2008 doi:10.1152/ajpregu.90602.2008.-Transient receptor potential melastatin-7 (TRPM7) channels have recently been identified to be regulated by vasoactive agents acting through G protein-coupled receptors in vascular smooth muscle cells (VSMC). However, downstream targets and functional responses remain unclear. We investigated the subcellular localization of TRPM7 in VSMCs and questioned the role of TRPM7 in proinflammatory signaling by bradykinin. VSMCs from Wistar-Kyoto rats were studied. Cell fractionation by sucrose gradient and differential centrifugation demonstrated that in bradykinin-stimulated cells, TRPM7 localized in fractions corresponding to caveolae. Immunofluorescence confocal microscopy revealed that TRPM7 distributes along the cell membrane, that it has a reticular-type intracellular distribution, and that it colocalizes with flotillin-2, a marker of lipid rafts. Bradykinin increased expression of calpain, a TRPM7 target, and stimulated its cytosol/membrane translocation, an effect blocked by 2-APB (TRPM7 inhibitor) and U-73122 (phospholipase C inhibitor), but not by chelerythrine (PKC inhibitor). Expression of proinflammatory mediators VCAM-1 and cyclooxygenase-2 (COX-2) was time-dependently increased by bradykinin. This effect was blocked by Hoe-140 (B 2 receptor blocker) and 2-APB. Our data demonstrate that in bradykinin-stimulated VSMCs: 1) TRPM7 is upregulated, 2) TRPM7 associates with cholesterol-rich microdomains, and 3) calpain and proinflammatory mediators VCAM-1 and COX2 are regulated, in part, via TRPM7-and phospholipase C-dependent pathways through B 2 receptors. These findings identify a novel signaling pathway for bradykinin, which involves TRPM7. Such phenomena may play a role in bradykinin/B 2 receptor-mediated inflammatory responses in vascular cells.

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Phospholipase C and myosin light chain kinase inhibition define a common step in actin regulation during cytokinesis

Cited by 57 publications

References 43 publications

Calcium-sensing Receptor Modulates Cell Adhesion and Migration via Integrins

Calcium-sensing Receptor Modulates Cell Adhesion and Migration via Integrins

Muscarinic receptor type 1 (M1) stimulation, probably through KCNQ/Kv7 channel closure, increases spontaneous GABA release at the dendrodendritic synapse in the mouse accessory olfactory bulb

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

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