Editorial Comment Acta Haematol 2014;132:199 DOI: 10.1159/000360600
Received: February 10, 2014 Accepted after revision: February 12, 2014 Published online: March 21, 2014
Endothelial Microparticles and Endothelial Damage: ‘The Tip and the Iceberg’ Andrea Piccin Haematology Department, San Maurizio Regional Hospital, Bolzano, Italy
References
1 Chan S, Chen M, Cao J, Chan GCF, Cheung Y: Carvedilol protects against iron-induced microparticle generation and apoptosis of endothelial cells. Acta Haematol 2014;132:200– 210. 2 Piccin A, Murphy WG, Smith OP: Circulating microparticles: pathophysiology and clinical implications. Blood Rev 2007;21:157–171. 3 Shet AS, Aras O, Gupta K, Hass MJ, Rausch DJ, Saba N, Koopmeiners L, Key NS, Hebbel RP: Sickle blood contains tissue factor-positive
© 2014 S. Karger AG, Basel 0001–5792/14/1322–0199$39.50/0 E-Mail [email protected] www.karger.com/aha
dy bodies. Interestingly, the presence of Gamna-Gandy bodies has also been reported in patients with haemochromatosis [5]. We believe that Gamna-Gandy bodies are the final histopathologic epiphenomenon of cell damage due to iron exposure; conversely, endothelial microparticle generation due to iron exposure may well be the true ‘tip of the iceberg’ of the pathophysiology of endothelial damage in all these conditions. The finding by Chan et al. [1] might therefore shed further light on the pathophysiology of conditions where free iron compounds are present, such as SCA, thalassaemias and haemochromatosis. Moreover, the finding of a protective action of β-blockers warrants further exploration because of important clinical implications. In addition, we believe that the measurement of endothelial modulators such as nitric oxide and endothelin-1 should be performed to clarify the action of β-blockers on endothelial cells. Clinical trials on patients with the above-mentioned conditions should be considered in order to shed further light on these findings.
Andrea Piccin, MD, PhD Haematology Department San Maurizio Regional Hospital IT–39100 Bolzano (Italy) E-Mail apiccin @ gmail.com
microparticles derived from endothelial cells and monocytes. Blood 2003;102:2678–2683. 4 Piccin A, Rizkalla H, Smith O, McMahon C, Furlan C, Murphy C, Negri G, Mc Dermott M: Composition and significance of splenic Gamna-Gandy bodies in sickle cell anemia. Hum Pathol 2012;43:1028–1036. 5 Laurent O, Lubrano J, de Beauregard M, Aubry S, Kastler B, Delabrousse É: Gamna-Gandy bodies in cirrhosis: a meaningless finding? J Radiol 2011;92:909–914. Downloaded by: Universitätsbibliothek Düsseldorf 134.99.34.168 - 3/26/2014 8:31:15 PM
We read with interest the paper by Chan et al. [1] from Hong Kong University on the in vitro study and effects of iron on human umbilical vein endothelial cells, which result in endothelial microparticle generation and increased reactive oxygen species production. The same research group also showed that when β-blockers were added, this effect was reduced. These early experimental results, if further validated, would have significant clinical potential. Microparticle generation has been reported in several clinical conditions and has been associated with endothelial damage [2]. Sickle cell anaemia (SCA) is a particularly well-known disease where cell damage occurs (haemolysis) and where free haemoglobin and iron have been reported. Furthermore, previous SCA studies have already documented that microparticle generation occurs and may participate in the haemolytic process, with release of free haemoglobin and iron [3]. Piccin et al. [4] demonstrated the presence of iron-based compounds in splenic inclusions in children with SCA undergoing recurrent crises, also known as Gamna-Gan-
Received: February 10, 2014 Accepted after revision: February 12, 2014 Published online: March 21, 2014
Endothelial Microparticles and Endothelial Damage: ‘The Tip and the Iceberg’ Andrea Piccin Haematology Department, San Maurizio Regional Hospital, Bolzano, Italy
References
1 Chan S, Chen M, Cao J, Chan GCF, Cheung Y: Carvedilol protects against iron-induced microparticle generation and apoptosis of endothelial cells. Acta Haematol 2014;132:200– 210. 2 Piccin A, Murphy WG, Smith OP: Circulating microparticles: pathophysiology and clinical implications. Blood Rev 2007;21:157–171. 3 Shet AS, Aras O, Gupta K, Hass MJ, Rausch DJ, Saba N, Koopmeiners L, Key NS, Hebbel RP: Sickle blood contains tissue factor-positive
© 2014 S. Karger AG, Basel 0001–5792/14/1322–0199$39.50/0 E-Mail [email protected] www.karger.com/aha
dy bodies. Interestingly, the presence of Gamna-Gandy bodies has also been reported in patients with haemochromatosis [5]. We believe that Gamna-Gandy bodies are the final histopathologic epiphenomenon of cell damage due to iron exposure; conversely, endothelial microparticle generation due to iron exposure may well be the true ‘tip of the iceberg’ of the pathophysiology of endothelial damage in all these conditions. The finding by Chan et al. [1] might therefore shed further light on the pathophysiology of conditions where free iron compounds are present, such as SCA, thalassaemias and haemochromatosis. Moreover, the finding of a protective action of β-blockers warrants further exploration because of important clinical implications. In addition, we believe that the measurement of endothelial modulators such as nitric oxide and endothelin-1 should be performed to clarify the action of β-blockers on endothelial cells. Clinical trials on patients with the above-mentioned conditions should be considered in order to shed further light on these findings.
Andrea Piccin, MD, PhD Haematology Department San Maurizio Regional Hospital IT–39100 Bolzano (Italy) E-Mail apiccin @ gmail.com
microparticles derived from endothelial cells and monocytes. Blood 2003;102:2678–2683. 4 Piccin A, Rizkalla H, Smith O, McMahon C, Furlan C, Murphy C, Negri G, Mc Dermott M: Composition and significance of splenic Gamna-Gandy bodies in sickle cell anemia. Hum Pathol 2012;43:1028–1036. 5 Laurent O, Lubrano J, de Beauregard M, Aubry S, Kastler B, Delabrousse É: Gamna-Gandy bodies in cirrhosis: a meaningless finding? J Radiol 2011;92:909–914. Downloaded by: Universitätsbibliothek Düsseldorf 134.99.34.168 - 3/26/2014 8:31:15 PM
We read with interest the paper by Chan et al. [1] from Hong Kong University on the in vitro study and effects of iron on human umbilical vein endothelial cells, which result in endothelial microparticle generation and increased reactive oxygen species production. The same research group also showed that when β-blockers were added, this effect was reduced. These early experimental results, if further validated, would have significant clinical potential. Microparticle generation has been reported in several clinical conditions and has been associated with endothelial damage [2]. Sickle cell anaemia (SCA) is a particularly well-known disease where cell damage occurs (haemolysis) and where free haemoglobin and iron have been reported. Furthermore, previous SCA studies have already documented that microparticle generation occurs and may participate in the haemolytic process, with release of free haemoglobin and iron [3]. Piccin et al. [4] demonstrated the presence of iron-based compounds in splenic inclusions in children with SCA undergoing recurrent crises, also known as Gamna-Gan-
