Increased Platelet Volume and Platelet Mass in Patients with Atherosclerotic Renal Artery Stenosis

1994 ◽  
Vol 87 (2) ◽  
pp. 253-257 ◽  
Author(s):  
Philip M. W. Bath ◽  
Constantinos G. Missouris ◽  
Timothy Buckenham ◽  
Graham A. MacGregor

1. Platelet volume was measured in citrated blood in two groups of patients at risk of having atherosclerotic renal artery stenosis, namely (i) 30 patients with severe hypertension, and (ii) 44 patients with peripheral vascular disease. 2. Platelet volume was increased in patients with hypertension who had atherosclerotic renal artery stenosis diagnosed by angiography: no renal artery stenosis, median 7.2 (interquartile range 0.5) × 10−15/l; renal artery stenosis 7.8 (0.8) × 10−15/l; platelet mass also increased with increasing severity of renal artery stenosis. Platelet volume correlated with severity of renal artery stenosis (rs = 0.391, 2p = 0.033, n = 30). Similarly, platelet volume correlated with severity of renal artery stenosis in patients with peripheral vascular disease (rs = 0.319, 2p = 0.035, n = 44). Serum immunoreactive platelet-derived growth factor (predominantly released from platelets) and plasma immunoreactive interleukin-6 (a cytokine which has been postulated to regulate platelet volume) concentrations were not different between hypertensive patients with and without renal artery stenosis. 3. Since large platelets are hyperactive, increased platelet volume may contribute to the development of atherosclerotic renal artery stenosis. However, the present data do not lend support to the hypothesis that platelet-derived growth factor is central to renal artery atherogenesis. Interleukin-6 does not appear to regulate platelet volume.

2006 ◽  
Vol 17 (7) ◽  
pp. 2069-2074 ◽  
Author(s):  
Kwok-Wai Mui ◽  
Mengalvio Sleeswijk ◽  
Huib van den Hout ◽  
Jef van Baal ◽  
Gerjan Navis ◽  
...  

BMJ ◽  
1990 ◽  
Vol 301 (6762) ◽  
pp. 1197-1198 ◽  
Author(s):  
A H Choudhri ◽  
J G Cleland ◽  
P C Rowlands ◽  
T L Tran ◽  
M McCarty ◽  
...  

2001 ◽  
Vol 59 (4) ◽  
pp. 1480-1483 ◽  
Author(s):  
Trude C. Leertouwer ◽  
Peter M.T. Pattynama ◽  
Annette Van Den Berg-Huysmans

1993 ◽  
Vol 85 (s29) ◽  
pp. 25P-25P
Author(s):  
Pmw Bath ◽  
CG Missouris ◽  
T Buckenham ◽  
GA MacGregor

1994 ◽  
Vol 96 (1) ◽  
pp. 10-14 ◽  
Author(s):  
Constantinos G. Missouris ◽  
Tim Buckenham ◽  
Francesco P. Cappuccio ◽  
Graham A. MacGregor

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Busra Isik ◽  
Roman Thaler ◽  
Busra B. Goksu ◽  
Sabena M. Conley ◽  
Hayder Al-Khafaji ◽  
...  

Abstract Background Atherosclerotic renal artery stenosis (ARAS) is a risk factor for ischemic and hypertensive kidney disease (HKD) for which autologous mesenchymal stem cell (MSC) appears to be a promising therapy. However, MSCs from ARAS patients exhibit impaired function, senescence, and DNA damage, possibly due to epigenetic mechanisms. Hypoxia preconditioning (HPC) exerts beneficial effects on cellular proliferation, differentiation, and gene and protein expression. We hypothesized that HPC could influence MSC function and senescence in ARAS by epigenetic mechanisms and modulating gene expression of chromatin-modifying enzymes. Methods Adipose-derived MSC harvested from healthy control (N = 8) and ARAS (N = 8) pigs were cultured under normoxia (20%O2) or hypoxia (1%O2) conditions. MSC function was assessed by migration, proliferation, and cytokine release in conditioned media. MSC senescence was evaluated by SA-β-gal activity. Specific pro-angiogenic and senescence genes were assessed by reverse transcription polymerase chain reaction (RT-PCR). Dot blotting was used to measure global genome 5-hydroxymethylcytosine (5hmC) levels on DNA and Western blotting of modified histone 3 (H3) proteins to quantify tri-methylated lysine-4 (H3K4me3), lysine-9 (H3K9me3), and lysine-27 (H3K27me3) residues. Results Specific pro-angiogenic genes in ARAS assessed by RT-PCR were lower at baseline but increased under HPC, while pro-senescence genes were higher in ARAS at baseline as compared healthy MSCs. ARAS MSCs under basal conditions, displayed higher H3K4me3, H3K27me3, and 5hmC levels compared to healthy MSCs. During HPC, global 5hmC levels were decreased while no appreciable changes occurred in histone H3 tri-methylation. ARAS MSCs cultured under HPC had higher migratory and proliferative capacity as well as increased vascular endothelial growth factor and epidermal growth factor expression compared to normoxia, and SA-β-gal activity decreased in both animal groups. Conclusions These data demonstrate that swine ARAS MSCs have decreased angiogenesis and increased senescence compared to healthy MSCs and that HPC mitigates MSC dysfunction, senescence, and DNA hydroxymethylation in ARAS MSC. Thus, HPC for MSCs may be considered for their optimization to improve autologous cell therapy in patients with nephropathies.


2005 ◽  
Vol 14 (6) ◽  
pp. 386-389 ◽  
Author(s):  
A. Ahmed ◽  
M.R.N. Nampoory ◽  
M. Sheikh ◽  
K.V. Johny

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