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tional specification of ventricular myosin inducible expression in cultured neonatal light chain 2 expression in the primitive murine heart tube. Proc Natl Acad Sci USA Zou Y, Chien KR: 1995. EFIA/YB-1 is a com- Zammit PS, Kelly RG, Franco D, et al.: 2000.
and positively regulates transcription of Suppression of atrial myosin gene expres- the myosin light chain-2 v gene. Mol Cell ventricular specificity and establishes an sion occurs independently in the left and anterior-posterior gradient of expression.
Zou Y, Evans S, Chen J, et al.: 1997. CARP, a Seidman CE, Schmidt EV, Seidman JG: 2001.
Zeller R, Bloch KD, Williams BS, et al.: 1987.
Cis-dominance of rat atrial natriuretic fac- Localized expression of the atrial natriuret- tor gene regulatory sequences in transgen- ic factor gene during cardiac embryogene- Zhu H, Garcia S, Ross RS, et al.: 1991. A Small EM, Krieg PA: 1999. Expression of at- rial natriuretic factor (ANF) during Xeno- the rat cardiac myosin light chain-2 gene confers cardiac specific and a-adrenergic Small EM, Krieg PA: 1976. Transgenic analy- sis of the atrial natriuretic factor (ANF) pro-moter: Nkx2-5 and GATA-4 binding sites arerequired for atrial specific expression ofANF. Dev Biol 261:116 – 131.
Sucov HM, Dyson E, Gumeringer CL, et al.: 2002. RxRa mutant mice establish a geneticbasis for vitamin A signaling in heart mor- phogenesis. Genes Dev 8:1007 – 1018.
Takimoto E, Mizuno T, Terasaki F, et al.: 2002. Up-regulation of natriuretic peptidesin the ventricle of Csx/Nkx2-5 transgenicmice. Biochem Biophys Res Commun 270: Platelets are blood cell fragments that originate from the cytoplasm of megakaryocytes in the bone marrow and circulate in blood to play a major role in the hemostatic process and in thrombus formation after an endothelial injury. Recent studies have provided insight into platelet mRNA distribution patterns in the rat heart.
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functions in inflammation and atherosclerosis. A range of molecules, present on the platelet surface and/or stored in platelet granules, con- tributes to the cross-talk of platelets with other inflammatory cells during the vascular inflammation involved in the development and & N Rosenthal (Eds.), Heart development( pp. 357 – 369). San Diego, CA: Academic progression of atherosclerosis. This review discusses the nature of these molecules and the mechanisms involved in the participation of plate- Wang GF, Nikovits W, Schleinitz M, Stock- lets in atherosclerosis, with emphasis on P-selectin, platelet–monocyte dale FE: 1998. Atrial chamber-specific ex- interactions, chemokines, and inflammatory cytokines. (Trends pression of the slow myosin heavy chain 3gene in the embryonic heart. J Biol Chem Cardiovasc Med 2004;14:18–22) n 2004, Elsevier Inc.
Wang GF, Nikovits W Jr, Schleinitz M, Stock- dale FE 2001. A positive GATA element and a negative vitamin D receptor-like element Cardiovascular Research Center and Depart- control atrial chamber-specific expression ment of Biomedical Engineering, University of Virginia, Health Science Center, Charlot- tection of activated platelets as defined diovascular Research Center and Department Wang GF, Nikovits W Jr, Bao ZZ, Stockdale FE: 2003. Irx4 forms an inhibitory complex Virginia, Health Science Center, Box 801394, atherosclerotic disease was first reported Charlottesville, VA 22908, USA. Tel.: (+1) 434- tors to regulate cardiac chamber-specific by Fitzgerald et al. (1986). These circu- 243-9351; fax: (+1) 434-924-2828; e-mail: lating activated platelets are very likely to associate with thrombotic events. Cir- D 2004, Elsevier Inc. All rights reserved.
findings did not support a beneficial ef- fect of aspirin in atherosclerosis (Cayatte et al. 2000, Napoli et al. 2002). Also, the et al. 1998). Interestingly, most risk fac- inhibitory effect of aspirin in atheroscle- tors of atherosclerosis—including hyper- cholesterolemia (Broijersen et al. 1998), smooth muscle cells in the vessel wall.
vated platelets in circulation. The pres- platelets transiently interacting with the ble for platelet activation in atherosclero- A23187 (Frenette et al. 1995). Consistent platelet activation begins with the bind- ing of adhesive receptors to their ligands bution of platelet – endothelial inter- but robustly with atherosclerotic carotid facilitate the delivery of platelet-derived et al. 2003). These interactions are main- let – endothelial interactions in the devel- and stimulated platelets, epinephrine re- (Huo et al. 2003). Platelet P-selectin is important. Repeated injections of P-selec- phase of atherosclerosis, platelet activa- lial ligand for platelet P-selectin is un- mice accelerated the formation of athero- sclerotic lesions (Huo et al. 2003). Recon- of atherosclerosis, including superoxide, for platelet translocation and firm adhe- control mice (Burger and Wagner 2003).
sion, respectively. In addition to P-selec- atherosclerosis is controversial. In pigs ecule in both resting and activated plate- sites of arteries of rabbits with hypercho- 1980, Nichols et al. 1998). Deficiency of et al. 2002) also found GPIIb/IIIa-mediat- did not show any protective role in devel- ditionally, following formation of lesions opment of atherosclerosis (Sramek et al.
on the vessel wall, platelet activation may be initiated by ligation of GPIb with the definitions of firm adhesion are likely to influence the results. Consistent with the Platelet activation influences the devel- deficient in VWF have a defect in secretion an injection of in vitro activated platelets.
bodies. Thus, endothelial P-selectin-medi- in these VWF mutant mice (Denis et al.
luminal surfaces of atherosclerotic arter- conflicting data exist. For example, some or avidity of monocyte/leukocyte integ-rins via P-selectin glycoprotein ligand-1(PSGL-1) signaling or delivery of plate-let-derived proinflammatory factors(Figure 1B). Oxidative burst occurs onmonocytes in response to platelet bind-ing. These rapid platelet-mediated regu-lations may play a role in atherosclerosisby promoting monocyte recruitment(Figure 1B). Activated platelets are alsoable to cause a variety of slow reactions.
Resting monocytes do not express tissuefactor, a protein involved in the initia-tion of blood coagulation and the forma-tion of atherosclerotic lesions. However,upon interaction with platelet P-selectin, Figure 1. Mechanisms by which activated platelets participate in the development ofatherosclerosis. (A) No interactions occur between resting platelets and monocytes. (B) transcription of tissue factor is activated.
Activated platelets promote monocyte recruitment via platelet – monocyte interactions.
Activated platelets interacting with monocytes deliver their proinflammatory factors to monocytes. Consequently, affinity and/or avidity of monocyte integrins are upregulated and monocytes arrest on endothelium. Additionally, monocyte – platelet aggregates may employ platelet P-selectin to mediate aggregates to interact with endothelium. (C) Activated platelets promote monocyte recruitment via platelet – endothelial interactions. Activated platelets transiently interacting with endothelium may deposit their proinflammatory factors on thesurface of endothelium, causing subsequent rolling monocyte arrest. Also, platelet-derived proinflammatory factors may infiltrate into the vessel wall, triggering vascular cell prolifer- are primed by several different synergis- tic activators. Exposure of monocytes toplatelet P-selectin and platelet activating factor mobilizes the transcription factor bound to activated GPIIb/IIIa complex.
a ligand for leukocyte Mac-1 (Simon et al.
platelet – leukocyte aggregates are not sclerosis (Shpilberg et al. 2002). This is Michelson et al. (2001) found that the life crete a different set of cytokines, includ- mice. In atherosclerotic mice, deficiency shedding. In our in vivo study (Huo et al.
2003), 2 to 3 hours after an injection of activated platelets, circulating platelet – tectable and ‘‘normal’’ leukocyte subtype tions between monocytes and platelets.
P-selectin on activated platelets initiates their interactions with leukocytes. Among leukocyte subtypes interacting with acti- shed their P-selectin (Berger et al. 1998), vated platelets, monocytes have a compet- suggesting that most platelet – leukocyte activated platelets (Huo et al. 2003). The sequester into peripheral tissues or mono- tially bind platelets, a possible basis for cytes phagocytose platelets bound to their the role of activated platelets in the devel- opment of atherosclerosis, is unknown.
ly, interactions between activated plate- lets and leukocytes will be stabilized due to binding of leukocyte integrins to plate- telets are able to upregulate affinity and/ ces that are contained within the a gran- of inflammatory reactions, as do activat- sclerotic lesions, direct evidence is need- ed platelets. The role of activated platelets are endocytosed from the blood plasma.
in atherosclerotic lesions is really ‘‘plate- rosis. Platelet factor 4 (PF-4), a member derived by limited proteolysis from plate- let basic protein. PF-4 causes chemotaxis lets have recently received intense inter- Thirty years after Ross et al. (1976) pro- cent studies (Nassar et al. 2003) provide protein of the TNF family originally iden- atherosclerosis, direct evidence now sup- 4 in the development of atherosclerosis.
telets truly play an important role in the platelets in atherosclerosis, although par- tially suggested in primary studies, have cleaved over a period of minutes or hours, generating a soluble but functional frag- rived foam cells, is able to dramatically capable of initiating various inflammato- ment and progression of atherosclerosis.
ry responses on endothelial cells, includ- ing production of reactive oxygen species (Urbich et al. 2002), expression of adhe- et al. 2003, Sachais et al. 2002). RANTES sion molecules (e.g., vascular cell adhe- sion molecule 1, ICAM-1, and E-selectin), factor (Slupsky et al. 1998). In contrast to preparation of this manuscript. This work sented in its mature form on the platelet arteries, suggesting that platelet-derived Berger G, Hartwell DW, Wagner DD: 1999. P- selectin and platelet clearance. Blood 92: et al. 2003, von Hundelshausen et al.
Bowie EJ, Fuster V: 2000. Resistance to athe- rosclerosis in pigs with von Willebrand’s is a cationic polypeptide composed of two chains (A and B) that are linked by inter- Broijersen A, Hamsten A, Eriksson M, et al.: 2001a. Platelet activity in vivo in hyperlipo- jor growth factor in platelets stimulating and proliferation associated with intimal for these factors, especially for IL-1h.
Burger PC, Wagner DD: 2001b. Platelet P-se- lectin facilitates atherosclerotic lesion de- to investigate whether transient interac- Cayatte AJ, Du Y, Oliver-Krasinski J, et al.: nist S18886 but not aspirin inhibits athero- genesis in apo E-deficient mice: evidence contribute to atherosclerosis. Arterioscler Platelet microparticles, released from ac- Celi A, Pellegrini G, Lorenzet R, et al.: 1998b.
out the progression of atherosclerosis.
P-selectin induces the expression of tissue aggregates are a more sensitive marker of 1998. Activated platelets induce tissue fac- in vivo platelet activation than platelet sur- tor expression on human umbilical vein en- Cyrus T, Sung S, Zhao L, et al.: 1995. Effect of face P-selectin: studies in baboons, human dothelial cells by ligation of CD40. Thromb low-dose aspirin on vascular inflammation, plaque stability, and atherogenesis in low- Sramek A, Reiber JH, Gerrits WB, Rosendaal density lipoprotein receptor-deficient mice.
clinically relevant effect on atherogenesis: et al.: 1993. Inhibition of lung inflammatory reactions in rats by an anti-human IL-8 anti- ditary bleeding tendency. Circulation 104: DD: 1995. Defect in regulated secretion of P-selectin affects leukocyte recruitment invon Willebrand factor-deficient mice. Proc Napoli C, Ackah E, De Nigris, et al.: 2002.
Chronic treatment with nitric oxide-releas- ing aspirin reduces plasma low-density lip- platelet-endothelial cell adhesion in postca- Fitzgerald DJ, Roy L, Catella F, Fitzgerald GA: pillary venules. Arterioscler Thromb Vasc 1996. Platelet activation in unstable coro- arterial oxidation-specific epitopes, and nary disease. N Engl J Med 315:983 – 989.
Theilmeier G, Michiels C, Spaepen E, et al.: Frenette PS, Johnson RC, Hynes MR, Wagner mice. Proc Natl Acad Sci 99:12,467 – 12,470.
2002. Endothelial von Willebrand factor re- DD: 1994. Platelets roll on stimulated endo- Nassar T, Sachais BS, Akkawi S, et al.: 2003.
cruits platelets to atherosclerosis-prone thelium in vivo: an interaction mediated by Platelet factor 4 enhances the binding of sites in response to hypercholesterolemia.
endothelial P-selectin. Proc Natl Acad Sci oxidized low-density lipoprotein to vascular wall cells. J Biol Chem 278: 6187 – 6193.
Tsao PS, Theilmeier G, Singer AH, et al.: Furman MI, Benoit SE, Barnard MR, et al.: Nichols TC, Bellinger DA, Reddick RL, et al.: 1994. L-arginine attenuates platelet reactiv- 1988. Increased platelet reactivity and cir- 1998. von Willebrand factor does not influ- ity in hypercholesterolemic rabbits. Arte- ence atherogenesis in arteries subjected to patients with stable coronary artery disease.
altered shear stress. Arterioscler Thromb Urbich C, Dernbach E, Aicher A, et al.: 2002.
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