Wyniki wyszukiwania - Biblioteka Nauki

1

Mechanizmy transdukcji sygnału w procesie aktywacji płytek krwi

100%

Tomasiak M.

|

tom 17

|

nr 3

2

Protein kinase c-mediated activation of Na - H exchanger in porcine blood platelets

100%

Tomasiak M.

|

nr 3

3

Inhibitory effect of quercetin on glycolysis in blood platelets

100%

Tomasiak M.

|

nr 1

4

Relationship between intracellular pH and aggregation in porcine blood platelets

100%

Tomasiak M.

|

tom 02

|

nr 2

5

The involvement of Na+/H+ exchanger in the desmopressin-induced platelet procoagulant response

71%

Tomasiak M. , Stelmach H. , Bodzenta A. , Tomasiak M.

|

nr Supplement 1

6

The role of the Na+/K+ -ATPase the generation of procoagulant activity in blood platelets

51%

Stelmach H. , Tomasiak M. , Rusak T. , Ciborowski M.

|

tom 53

|

nr Supplement 1

7

Peroxynitrite can affect platelet responses by inhibiting energy production

51%

Rusak T. , Tomasiak M. , Ciborowski M.

|

nr 4

8

Vasopressin- induced platelet procoagulant response

51%

Tomasiak M. , Stelmach H. , Rusak T. , Ciborowski M.

|

tom 53

|

nr Supplement 1

9

Cyslosporine A and platelet procoagulant activity

51%

Rusak T. , Tomasiak M. , Stelmach H. , Gacko M.

|

tom 53

|

nr Supplement 1

10

Autofagia - adaptacyjne mechanizmy molekularne w warunkach głodu

51%

Tomasiak M. , Cichacz B. , Pedrycz A.

Polish Hyperbaric Research

|

2015

|

tom nr 3(52)

71--75

PL

Autofagia jest bardzo starym procesem, podczas którego przy pomocy lizosomów usuwane są białka o długim okresie półtrwania oraz organella komórkowe. Autofagia może być wywołana przez mechanizmy stresowe dla komórki. Badania dowodzą, że autofagia odgrywa kluczową rolę w pozyskiwaniu składników odżywczych oraz w adaptacji do warunków głodu. Dzięki temu bierze udział w zachowaniu homeostazy w cytoplazmie i jądrze komórki. Osiągnięcie tego celu możliwe jest kilkoma drogami. W zależności od tego w jaki sposób substrat zostaje połączony z lizosomem mówimy o: makroautofagii oraz mikroautofagii. Dodatkowo część autorów wyróżnia również autofagię zależną od chaperonów. W niniejszym artykule opisano mechanizmy molekularne poszczególnych rodzajów autofagii ze szczególną uwagą poświeconą makroautofagii- jako najlepiej poznanemu typowi autofagii.

EN

Autophagy is an extremely old process during which long-lived proteins and cellular organelles are removed by means of lysosomes. Autophagy may be caused by cellular stress mechanisms. Research has proven that autophagy plays a key role in obtaining nutrients and adapting to the conditions of starvation. Owing to this, it takes part in maintaining homeostasis in cytoplasm and cell nucleus. This objective may be achieved through a number of ways. Depending on the manner in which a substrate connects with the lysosome, we can talk about macroautophagy and microautophagy. Additionally, some authors also distinguish a chaperone-mediated autophagy. The article presented below describes molecular mechanisms of each type of autophagy and focuses particularly on macroautophagy, which is the best understood of all the autophagy types.

11

The role of Naplus-Hplus exchanger in serotonin secretion from porcine blood platelets

51%

Tomasiak M. , Ciborowski M. , Stelmach H.

|

nr 4

EN

This study was undertaken to evaluate whether a link exists between the activation of protein kinase C (PKC), operation of Na+/H+ exchanger (NHE), cell swelling and serotonin (5-HT) secretion in porcine platelets. Activation of platelets by thrombin or phorbol 12-myristate 13-acetate (PMA), a PKC activator, initiated a rapid rise in the activity of Na+/H+ exchanger and secretion of 5-HT. Both thrombin- and PMA-evoked activation of Na+/H+ exchanger was less pronounced in the presence of ethyl-isopropyl-amiloride (EIPA), an NHE inhibitor, and by GF 109203X, a PKC inhibitor. Monensin (simulating the action of NHE) caused a dose-dependent release of 5-HT that was not abolished by GF 109203X or EGTA. Lack of Na+ in the suspending medium reduced thrombin-, PMA-, and monensin-evoked 5-HT secretion. GF 109203X nearly completely inhibited 5-HT release induced by PMA-, partly that induced by thrombin, and had no effect on 5-HT release induced by monensin. EIPA partly inhibited 5-HT release induced by thrombin and nearly totally that evoked by PMA. Electronic cell sizing measurements showed an increase in mean platelet volume upon treatment of cells with monensin, PMA or thrombin. The PMA- and thrombin-evoked rise in mean platelet volume was strongly reduced in the presence of EIPA. As judged by optical swelling assay monensin and PMA produced a rapid rise in platelet volume. The swelling elicited by PMA was inhibited by EIPA and its kinetics was similar to that observed in the presence of monensin. Hypoosmotically evoked platelet swelling did not affect platelet aggregation but significantly potentiated thrombin-evoked release of 5-HT and ATP. Taken together, these results show that in porcine platelets PKC may promote 5-HT secretion through the activation of NHE. It is hypothesized that enhanced Na+/H+ antiport may result in a rise in cell membrane tension (due to cell swelling) which in turn facilitates fusion of secretory granules with the plasma membrane leading to 5-HT secretion.

12

Involvement of Naplus-Hplus exchanger in desmopressin-induced platelet procoagulant response

51%

Tomasiak M. M. , Stelmach H. , Bodzenta-Lukaszyk A. , Tomasiak M.

Acta Biochimica Polonica

|

2004

|

tom 51

|

nr 3

EN

Desmopressin (DDAVP) action on platelets is associated with the development of procoagulant response but the underlying mechanism of this phenomenon is not known. We investigated whether this effect of DDAVP might be due to activation of plasma membrane Na+ /H+ exchanger. The DDAVP-induced platelet procoagulant response, measured as phospholipid-dependent thrombin generation, was dose dependent and significantly weaker than that produced by collagen or monensin (mimics Na+ /H+ antiport). Both the DDAVP- and collagen-produced procoagulant responses were less pronounced in the presence of EIPA, an Na+/H+ exchanger inhibitor. Flow cytometry studies revealed that in vitro treatment of platelets with DDAVP or collagen was associated with the appearance of both degranulated (and fragmented) and swollen cells. The DDAVP-evoked rise in size and granularity heterogeneity was similar to that produced by collagen or monensin and was not observed in the presence of EIPA. Using flow cytometry and annexin V-FITC as a probe for phosphatidylserine (PS) we demonstrated increased and uniform binding of this marker to all subsets of DDAVP-treated platelet population. The DDAVP-evoked PS expression was dose dependent, strongly reduced by EIPA and weaker than that caused by monensin or collagen. As judged by optical swelling assay, DDAVP in a dose dependent manner produced a rise in platelet volume. The swelling was inhibited by EIPA and its kinetics was similar to that observed in the presence of monensin. Electronic cell-sizing measurements showed an increase in mean platelet volume and a decrease in platelet count and platelet crit upon treatment with DDAVP. DDAVP elicited a slow (much slower than collagen) alkalinization of platelet cytosol. Altogether the data indicate an involvement of Na+/H+ exchanger in the generation of procoagulant activity in DDAVP-treated platelets.

13

The effect of some epsilon-aminocaproic acid derivatives on platelet responses

51%

Bruzgo I. , Tomasiak M. , Stelmach H. , Midura-Nowaczek K.

|

nr 1

EN

ε-Aminocaproic acid (EACA) is a synthetic low molecular drug with antifibrinolytic activity. However, treatment with this drug can be incidentally associated with an increased thrombotic tendency. The aim of the present work was to test synthetic EACA derivatives for their antiplatelet activities. We investigated the effect of three EACA derivatives with antifibrinolytic activity: I. ε-aminocaproyl-L-leucine hydrochloride (HCl*H-EACA-L-Leu-OH), II. ε-aminocaproyl-L-(S-benzyl)-cysteine hydrochloride (HCl*H-EACA-L-Cys(S-Bzl)-OH) and III. ε-aminocaproyl-L-norleucine (H-EACA-L-Nle-OH) on platelet responses (aggregation and adhesion) and on their integrity. It was found that: 1. as judged by LDH release test, none of the tested compounds, up to 20 mM, was toxic to platelets, 2. in comparison with EACA, all the synthetic derivatives inhibited much stronger the ADP- and collagen-induced aggregation of platelets suspended in plasma (platelet rich plasma) and aggregation of these cells in whole blood, 3. EACA and its derivatives exerted a similar inhibitory effect on the thrombin-induced adhesion of platelets to fibrinogen-coated surfaces. Since platelet activation and blood coagulation are tightly associated processes, the antiplatelet properties of EACA derivatives are expected to indicate reduced throm- botic properties of these derivatives compared to EACA.

14

The involvement of Naplus-Kplus-ATPase in the development of platelet procoagulant response

45%

Tomasiak M. , Stelmach H. , Rusak T. , Ciborowski M. , Radziwon P.

|

tom 54

|

nr 3

EN

In circulation, platelets may come into contact with both exogenous (cardiac glycoside treatment) and endogenously produced inhibitors of Na+/K+-ATPase. We examined whether blocking of platelet Na+/K+-ATPase by ouabain results in generation of procoagulant activity. It was shown that an in vitro treatment of platelets with ouabain (20-200 µM for 20 to 60 min) is associated with an intracellular accumulation of sodium ([Na+]i), generation of a weak calcium signal, and expression of procoagulant activity. The ouabain-induced procoagulant response was dose- and time-related, less pronounced than that evoked by collagen and similar to that produced by gramicidin, not affected by EDTA or aspirin, and strongly reduced in the absence of extracellular Na+ or by hyperosmolality. Flow cytometry studies revealed that ouabain treatment results in a unimodal left shift in the forward and side scatter of the entire platelet population indicating morphological changes of the plasma membrane. The shift was dose related, weaker than that evoked by collagen and similar to that produced by gramicidin. Ouabain-treated platelets express phosphatidylserine (PS). The ouabain-evoked PS expression was dose- and time-dependent, weaker than that produced by collagen and similar to that evoked by gramicidin. Electronic cell sizing measurements showed a dose-dependent increase in mean platelet volume upon treatment with ouabain. Hypoosmotically-evoked platelet swelling resulted in the appearance of procoagulant activity. Thromboelastography measurements indicate that, in whole blood, nanomolar (50-1000 nM, 15 min) concentrations of ouabain significantly accelerate the rate of clot formation initiated by contact and high extracellular concentration of calcium. We conclude that inefficiently operating platelet Na+/K+-ATPase results in a rise in [Na+]i. An increase in [Na+]i and the swelling associated with it may produce PS exposure and a rise in membrane curvature leading to the generation of a procoagulant activity.