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. 2008 Jun 21;47(9):1299–1310. doi: 10.1093/rheumatology/ken225

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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Fig. 8. — CypA-mediated Ca²⁺ increase and adhesion of the THP-1 cells. (a) Ca²⁺ mobilization in the Fluo-3-loaded uTHP-1 (a ∼ d) and dTHP-1 (e ∼ h) cells was measured in the presence of CypA (200 ng/ml) (a, e), CypA/CSA (b, f), HAb18 pre-incubation (d, h) or pre-stimulation (c, g). The arrows indicate the addition of the agonist. The calcium intensity that was detected by intensity of green fluorescence correlated well with cytosolic Ca²⁺ concentration and showed the changing of Ca²⁺ levels in THP-1 cells. CypA-induced Ca²⁺ mobilization in both uTHP-1 (a) and dTHP-1 (e) cells while HAb 18 and CSA inhibited CypA-induced Ca²⁺ mobilization. (b) The uTHP-1 and dTHP-1 cells were pre-treated with HAb18 antibody or CSA and then were stimulated with CypA in Matrigel Matrix-coated 96-well microtitre plates. A significant increase in both uTHP-1 and dTHP-1 cell adhesion was observed with CypA. In contrast, CSA or HAb18 dramatically reduced THP-1 cell adhesion respectively, both in the absence or presence of CypA. Data are expressed as means ± s.d. (n = 3). P < 0.05 vs the normal negative uTHP-1 cells. *P < 0.05 vs the normal negative dTHP-1 cells.

Fig. 8. — CypA-mediated Ca²⁺ increase and adhesion of the THP-1 cells. (a) Ca²⁺ mobilization in the Fluo-3-loaded uTHP-1 (a ∼ d) and dTHP-1 (e ∼ h) cells was measured in the presence of CypA (200 ng/ml) (a, e), CypA/CSA (b, f), HAb18 pre-incubation (d, h) or pre-stimulation (c, g). The arrows indicate the addition of the agonist. The calcium intensity that was detected by intensity of green fluorescence correlated well with cytosolic Ca²⁺ concentration and showed the changing of Ca²⁺ levels in THP-1 cells. CypA-induced Ca²⁺ mobilization in both uTHP-1 (a) and dTHP-1 (e) cells while HAb 18 and CSA inhibited CypA-induced Ca²⁺ mobilization. (b) The uTHP-1 and dTHP-1 cells were pre-treated with HAb18 antibody or CSA and then were stimulated with CypA in Matrigel Matrix-coated 96-well microtitre plates. A significant increase in both uTHP-1 and dTHP-1 cell adhesion was observed with CypA. In contrast, CSA or HAb18 dramatically reduced THP-1 cell adhesion respectively, both in the absence or presence of CypA. Data are expressed as means ± s.d. (n = 3). P < 0.05 vs the normal negative uTHP-1 cells. *P < 0.05 vs the normal negative dTHP-1 cells.