The role of complement in the trafficking of hematopoietic stem/progenitor cells

Janowska‐Wieczorek, Anna; Marquez‐Curtis, Leah A.; Shirvaikar, Neeta; Ratajczak, Mariusz Z.

doi:10.1111/j.1537-2995.2012.03636.x

Cited by 14 publications

(13 citation statements)

References 90 publications

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“…Within this time frame mobilization of hematopoietic, pluripotent, and cardiac stem cells is severely attenuated in C3 KO mice compared to WT controls demonstrating that C3 is necessary for mobilization of BM cells after MI. We have previously shown that G‐CSF and AMD3100 activate the CC where it then promotes mobilization . Thus a role for C3 in myocardial regeneration can be derived from its effect on stem/progenitor cell mobilization.…”

Section: Discussionmentioning

confidence: 98%

“…CC activation in BM was necessary for stress‐induced BM hematopoiesis but not homeostasis. Regeneration of BM hematopoiesis after hematopoietic stem/progenitor cell (HSPC) transplantation was impaired in C3, C5, C3aR, and C5aR KO mice and was also associated with impaired HSPC homing . Recent studies suggest that CC might favor bone formation where C3a and C5a influence bone cell migration, osteoblast–osteoclast interaction, and modulation of the inflammatory response by osteoblasts .…”

Section: Introductionmentioning

confidence: 99%

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Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction

Wysoczynski¹,

Solanki²,

Borkowska

et al. 2014

Stem Cells

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Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kitpos cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67pos CSPCs and decreased formation of new BrdUpos/α-sarcomeric actinpos myocytes and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate the CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction

Wysoczynski¹,

Solanki²,

Borkowska

et al. 2014

Stem Cells

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“…96 Ratajczak e t al. have provided updated information about chemoattractant properties of components of the complement system, 13,97–101 but the cognate receptors are not expressed on HSPCs. Recently, a role for S1P in HSPC mobilization was suggested, although whether S1P targets HSPCs directly, or whether S1P exerts its effect on HSPC egress indirectly, through mature hematopoietic or BM stroma cells currently remains elusive (see above).…”

Section: Cellular and Molecular Targets For Stem Cell Mobilizationmentioning

confidence: 99%

Hematopoietic stem cell mobilization: updated conceptual renditions

2012

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Despite its specific clinical relevance, the field of hematopoietic stem cell mobilization has received broad attention, owing mainly to the belief that pharmacologic stem cell mobilization might provide clues as to how stem cells are retained in their natural environment, the bone marrow ‘niche’. Inherent to this knowledge is also the desire to optimally engineer stem cells to interact with their target niche (such as after transplantation), or to lure malignant stem cells out of their protective niches (in order to kill them), and in general to decipher the niche’s structural components and its organization. Whereas, with the exception of the recent addition of CXCR4 antagonists to the armamentarium for mobilization of patients refractory to granulocyte colony-stimulating factor alone, clinical stem cell mobilization has not changed significantly over the last decade or so, much effort has been made trying to explain the complex mechanism(s) by which hematopoietic stem and progenitor cells leave the marrow. This brief review will report some of the more recent advances about mobilization, with an attempt to reconcile some of the seemingly inconsistent data in mobilization and to interject some commonalities among different mobilization regimes.

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“…Die Fähigkeit zirkulierender hämatopoietischer Stammzellen zum Repopulieren entfernter Knochenmarksregionen durch hämatogene Aussaat ist direkt belegt durch Teilkörperbestrahlungs-und Parabiose-Experimente in der Maus [23][24][25][26][27][28]. Eine Vielzahl von Stimuli, darunter exogene hämatopoietische Wachstumsfaktoren [29], Chemokine [30][31][32][33][34][35][36] und Chemokinrezeptor-Antagonisten [37,38], der myeloische Rebound nach zytoreduktiver Chemotherapie [39,40], Integrinrezeptorblocker [41][42][43], bakterielle Toxine [44][45][46][47], aber auch körperliche Anstrengung [48,49], Tageszeit [50][51][52], adrenerge Signale des autonomen Nervensystems [52][53][54][55][56] oder nicht primär hämatologische pathologische Zustände wie Entzündung [44,57], Gewebeschädigung [58], Komplementaktivierung [59,60], Gerinnungsaktivierung [61], können erhöhte Zahlen zirkulierender Stammzellen induzieren. [30,32,33,…”

Section: Grundlagen Der Biologie Hämatopoietischer Stammzellenunclassified

Mobilisierung hämatopoietischer Stammzellen

Karpova

Wiercinska

Bönig

2013

Transfusionsmedizin

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Zusammenfassung Als Stammzellmobilisierung wird der pharmakologisch induzierte Egress h?matopoietischer Stammzellen aus dem Knochenmark in das Peripherblut bezeichnet. Die klinische Bedeutung der Stammzellmobilisierung liegt darin, dass mobilisierte Stammzellen mittels Leukapherese aus dem Blut extrahiert und als Transplantat f?r entsprechend konditionierte Patienten verwendet werden k?nnen. Heute werden fast alle autologen und ca. 80?% der allogenen Transplantationen mit ?mobilisierten Stammzellen? durchgef?hrt. Obwohl eine Vielzahl Stammzellen mobilisierender Substanzen bekannt ist, haben bisher lediglich das myelopoietische Zytokin Granulozytenkolonien stimulierender Faktor (G-CSF) und, bei schlecht mobilisierenden Patienten, der CXCR4-Antagonist Plerixafor klinische Bedeutung erlangt. Durch die Aufnahme der Stammzellherstellung in das Arzneimittelgesetz ist vielen Ortes die Verantwortung f?r die Herstellung von Stammzellpr?paraten und damit auch f?r die Stammzellmobilisierung an die Transfusionsmedizin ?bergegangen. Dieses fokussierte Review skizziert den Stand des Wissens zu Mechanismen der Stammzellmobilisierung speziell bez?glich der heute in der Klinik eingesetzten Agenzien und fasst die klinischen Erfahrungen und arzneimittelrechtlichen Aspekte der klinischen Stammzellmobilisierung zusammen.

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The role of complement in the trafficking of hematopoietic stem/progenitor cells

Cited by 14 publications

References 90 publications

Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction

Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction

Hematopoietic stem cell mobilization: updated conceptual renditions

Mobilisierung hämatopoietischer Stammzellen

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