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R&D Systems integrin α v β 3
Mechanism of apo(a)-induced effects. (A) SV-SMC were transfected with 25 nM RhoA siRNA; knockdown was confirmed via immunoblotting. Numbers represent densitometry data for RhoA ( n = 6). (B) Number of migrated cells per HP field under basal conditions and in response to apo(a) following RhoA silencing (closed bars) compared to mock transfected cells (open bars, n = 5). (C). Migration under basal conditions and in response to apo(a) following pre-treatment with vehicle control (0.002% dH 2 O; open bars) or 10 μM ROCK inhibitor, Y-27632 (closed bars) for 1 h ( n = 6). (D) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% dH 2 O; open bars) or 1 μM fluvastatin (closed bars) for 2 h ( n = 5). (E). Migration in response to apo(a) following pre-treatment with vehicle control (0.001% PBS; open bars) or 5 μg/mL αvβ 3 <t>integrin</t> neutralising antibody (closed bars) for 5 min ( n = 5). (F) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% DMSO; open bars) or 100 μM genistein (closed bars) for 1 h ( n = 5). *** P < 0.001, ** P < 0.01, * P < 0.05, NS = non-significant.
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R&D Systems nov ccn3 af1640
Mechanism of apo(a)-induced effects. (A) SV-SMC were transfected with 25 nM RhoA siRNA; knockdown was confirmed via immunoblotting. Numbers represent densitometry data for RhoA ( n = 6). (B) Number of migrated cells per HP field under basal conditions and in response to apo(a) following RhoA silencing (closed bars) compared to mock transfected cells (open bars, n = 5). (C). Migration under basal conditions and in response to apo(a) following pre-treatment with vehicle control (0.002% dH 2 O; open bars) or 10 μM ROCK inhibitor, Y-27632 (closed bars) for 1 h ( n = 6). (D) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% dH 2 O; open bars) or 1 μM fluvastatin (closed bars) for 2 h ( n = 5). (E). Migration in response to apo(a) following pre-treatment with vehicle control (0.001% PBS; open bars) or 5 μg/mL αvβ 3 <t>integrin</t> neutralising antibody (closed bars) for 5 min ( n = 5). (F) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% DMSO; open bars) or 100 μM genistein (closed bars) for 1 h ( n = 5). *** P < 0.001, ** P < 0.01, * P < 0.05, NS = non-significant.
Nov Ccn3 Af1640, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Mechanism of apo(a)-induced effects. (A) SV-SMC were transfected with 25 nM RhoA siRNA; knockdown was confirmed via immunoblotting. Numbers represent densitometry data for RhoA ( n = 6). (B) Number of migrated cells per HP field under basal conditions and in response to apo(a) following RhoA silencing (closed bars) compared to mock transfected cells (open bars, n = 5). (C). Migration under basal conditions and in response to apo(a) following pre-treatment with vehicle control (0.002% dH 2 O; open bars) or 10 μM ROCK inhibitor, Y-27632 (closed bars) for 1 h ( n = 6). (D) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% dH 2 O; open bars) or 1 μM fluvastatin (closed bars) for 2 h ( n = 5). (E). Migration in response to apo(a) following pre-treatment with vehicle control (0.001% PBS; open bars) or 5 μg/mL αvβ 3 integrin neutralising antibody (closed bars) for 5 min ( n = 5). (F) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% DMSO; open bars) or 100 μM genistein (closed bars) for 1 h ( n = 5). *** P < 0.001, ** P < 0.01, * P < 0.05, NS = non-significant.

Journal: The International Journal of Biochemistry & Cell Biology

Article Title: Apolipoprotein(a) acts as a chemorepellent to human vascular smooth muscle cells via integrin α V β 3 and RhoA/ROCK-mediated mechanisms

doi: 10.1016/j.biocel.2013.05.021

Figure Lengend Snippet: Mechanism of apo(a)-induced effects. (A) SV-SMC were transfected with 25 nM RhoA siRNA; knockdown was confirmed via immunoblotting. Numbers represent densitometry data for RhoA ( n = 6). (B) Number of migrated cells per HP field under basal conditions and in response to apo(a) following RhoA silencing (closed bars) compared to mock transfected cells (open bars, n = 5). (C). Migration under basal conditions and in response to apo(a) following pre-treatment with vehicle control (0.002% dH 2 O; open bars) or 10 μM ROCK inhibitor, Y-27632 (closed bars) for 1 h ( n = 6). (D) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% dH 2 O; open bars) or 1 μM fluvastatin (closed bars) for 2 h ( n = 5). (E). Migration in response to apo(a) following pre-treatment with vehicle control (0.001% PBS; open bars) or 5 μg/mL αvβ 3 integrin neutralising antibody (closed bars) for 5 min ( n = 5). (F) Migration in response to apo(a) following pre-treatment with vehicle control (0.001% DMSO; open bars) or 100 μM genistein (closed bars) for 1 h ( n = 5). *** P < 0.001, ** P < 0.01, * P < 0.05, NS = non-significant.

Article Snippet: Neutralising antibodies against TGFβRII (AF-241-NA) and integrin α V β 3 (MAB1976 clone LM109) were from R&D Systems and Millipore respectively.

Techniques: Transfection, Knockdown, Western Blot, Migration, Control

Summary figure. Our data suggest that apo(a) interacts with integrin α V β 3 on the surface of vascular SMC. This signals through tyrosine kinases to activate RhoA and induce stress fibre formation, cell spreading and chemorepulsion. These molecular effects may have a negative impact on smooth muscle cell remodelling contributing towards atherosclerosis, vessel stiffness, and impaired vein graft integration and arterialisation.

Journal: The International Journal of Biochemistry & Cell Biology

Article Title: Apolipoprotein(a) acts as a chemorepellent to human vascular smooth muscle cells via integrin α V β 3 and RhoA/ROCK-mediated mechanisms

doi: 10.1016/j.biocel.2013.05.021

Figure Lengend Snippet: Summary figure. Our data suggest that apo(a) interacts with integrin α V β 3 on the surface of vascular SMC. This signals through tyrosine kinases to activate RhoA and induce stress fibre formation, cell spreading and chemorepulsion. These molecular effects may have a negative impact on smooth muscle cell remodelling contributing towards atherosclerosis, vessel stiffness, and impaired vein graft integration and arterialisation.

Article Snippet: Neutralising antibodies against TGFβRII (AF-241-NA) and integrin α V β 3 (MAB1976 clone LM109) were from R&D Systems and Millipore respectively.

Techniques: