Cytosolic Ca profile of resting and tnrombin-stimulated platelets from black women with NIDDM

Zentay, Zoltan; Raguwanshi, Maya; Reddi, Alluru S.; Lasker, Norman; Dasmahapatra, Amita; Aviv, Abraham

doi:10.1016/1056-8727(94)00007-b

Cited by 6 publications

(5 citation statements)

References 23 publications

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“…This result can be explained by a decrease of platelet NO due to decreased intraplatelet synthesis of endogenous NO or diminished release of NO from the vascular endothelium or by quenching of NO by advanced glycosylation products. The findings of elevated intracellular platelet Ca ++ in diabetes mellitus (25,26) are in line with the hypothesis of reduced intraplatelet NO levels.…”

Section: Introductionsupporting

confidence: 79%

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Martina¹,

Ga²,

Trucco³

et al. 1998

Thromb Haemost

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SummarySeveral studies in vitro and in vivo suggest that the nitric oxide (NO) production is impaired in diabetes mellitus. Reduced levels of NO could contribute to vascular alteration facilitating platelet-vascular wall interaction, adhesion of monocytes to endothelium, vascular smooth muscle proliferation and by decreasing endothelium-dependent vasodilation. In this study we evaluated the activity of the constitutive nitric oxide synthase (cNOS) in platelets of patients with insulin-dependent diabetes mellitus (IDDM) and with non-insulin-dependent diabetes mellitus (NIDDM). When compared to that of normal subjects, cNOS activity is significantly lower in patients with IDDM and with NIDDM (1.57 ± 0.25 vs. 0.66 ± 0.10 fmol/min/10 9 PLTs and 1.57 ± 0.25 vs. 0.67 ± 0.08, respectively; p <0.005). These data demonstrate that the platelet cNOS activity is decreased in diabetes mellitus.

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Section: Introductionsupporting

confidence: 79%

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Martina¹,

Ga²,

Trucco³

et al. 1998

Thromb Haemost

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“…Several studies have demonstrated elevated Ca/ in cells from diabetic and/or hypertensive individualsI10, [21][22][23][24][25][26][27][28] and a reduction in Ca/ associated with a combination drug therapy. L291…”

Section: Discussionmentioning

confidence: 99%

Evidence for Mechanistic Alterations of Ca²⁺Homeostasis in Type 2 Diabetes Mellitus

Balasubramanyam

Balaji

Subashini

et al. 2000

Journal of Diabetes Research

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Altered cytosolic Ca2+ is implicated in the aetiology of many diseases including diabetes but there are few studies on the mechanism(s) of the altered Ca2+ regulation. Using human lymphocytes, we studied cytosolic calcium (Cai) and various Ca2+ transport mechanisms in subjects with Type 2 diabetes mellitus and control subjects. Ca2+-specific fluorescent probes (Fura-2 and Fluo-3) were used to monitor the Ca2+ signals. Thapsigargin, a potent and specific inhibitor of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), was used to study Ca2+- store dependent Ca2+ fluxes. Significant (P < 0.05) elevation of basal Cai levels was observed in lymphocytes from diabetic subjects. Cai levels were positively correlated with fasting, plasma glucose and HbAlc. There was also a significant (P < 0.05) reduction in plasma membrane calcium (PMCA) ATPase activity in diabetic subjects compared to controls. Cells from Type 2 diabetics exhibited an increased Ca2+ influx (as measured both by Fluo-3 fliorescence and C45a assays) as a consequence of of thapsigargin-mediated Ca2+ store depletion. Upon addition of Mn2+ (a surrogate of Ca2+), the fura-2 fluorescence decayed in an exponential fashion and the rate and extent of this decline was steeper and greater in cells from type 2 diabetic patients. There was also a significant (P < 0.05) difference in the Na+/Ca2+ exchange activity in Type 2 diabetic patients, both under resting conditions and after challenging the cells with thapsigargin, when the internal store Ca2+ sequestration was circumvented. Pharmacological activation of protein kinase C (PKC) in cells from patients resulted in only partial inhibition of Ca2+ entry. We conclude that cellular Ca2+ accumulation in cells from Type 2 diabetes results from (a) reduction in PMCA ATPase activity, (b) modulation of Na+/Ca2+ exchange and (3) increased Ca2+ influx across the plasma membrane.

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“…Activation of platelets occurs in association with both type 1 and type 2 diabetes. Emersion of platelets from normal subjects in plasma from patients with diabetes alters platelet function (15)(16)(17). Emersion of platelets from patients with diabetes in plasma from normal subjects normalizes platelet function to some extent.…”

Section: Platelet-mediated Effectsmentioning

confidence: 99%

Fibrinolysis and diabetes

Sobel¹

2003

Front Biosci

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Diabetes is characterized by impaired fibrinolysis. This phenomenon reflects augmented concentrations of plasminogen activator inhibitor type-1 in tissues and in blood. The derangement appears to depend in part on elevated concentrations of free fatty acids, triglycerides, and insulin in association with the insulin resistance syndrome. Impaired fibrinolysis may exacerbate already existing coronary artery disease and potentiate its evolution. Several measures are available to favorably modify fibrinolytic system capacity. They include inhibition of the renin angiotensin system, attenuation of dyslipidemia, and enhancement of insulin sensitivity. Accordingly, normalization of the derangement in fibrinolysis typical of diabetes is an important and achievable therapeutic objective.

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Cytosolic Ca profile of resting and tnrombin-stimulated platelets from black women with NIDDM

Cited by 6 publications

References 23 publications

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Evidence for Mechanistic Alterations of Ca²⁺Homeostasis in Type 2 Diabetes Mellitus

Fibrinolysis and diabetes

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Cytosolic Ca profile of resting and tnrombin-stimulated platelets from black women with NIDDM

Cited by 6 publications

References 23 publications

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Platelet cNOS Activity Is Reduced in Patients with IDDM and NIDDM

Evidence for Mechanistic Alterations of Ca2+Homeostasis in Type 2 Diabetes Mellitus

Fibrinolysis and diabetes

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Product

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Evidence for Mechanistic Alterations of Ca²⁺Homeostasis in Type 2 Diabetes Mellitus