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Identification and characterization of VEGF-A-responsive neutrophils expressing CD49d, VEGFR1, and CXCR4 in mice and humans

Massena, Sara (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Christoffersson, Gustaf (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Vågesjö, Evelina (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
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Seignez, Cédric (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Gustafsson, Karin (author)
Uppsala universitet,Experimentell och klinisk onkologi
Binet, François (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Herrera Hidalgo, Carmen (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Giraud, Antoine (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Lomei, Jalal (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Weström, Simone (author)
Uppsala universitet,Dermatologi och venereologi
Shibuya, Masabumi (author)
Jobu Univ, Gakubunkan Inst Physiol & Med, Gunma, Japan
Claesson-Welsh, Lena (author)
Uppsala universitet,Vaskulärbiologi
Gerwins, Pär (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi,Radiologi
Welsh, Michael (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Kreuger, Johan (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
Phillipson, Mia (author)
Uppsala universitet,Institutionen för medicinsk cellbiologi
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 (creator_code:org_t)
American Society of Hematology, 2015
2015
English.
In: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 126:17, s. 2016-2026
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Vascular endothelial growth factor A (VEGF-A) is upregulated during hypoxia and is the major regulator of angiogenesis. VEGF-A expression has also been found to recruit myeloid cells to ischemic tissues where they contribute to angiogenesis. This study investigates the mechanisms underlying neutrophil recruitment to VEGF-A as well as the characteristics of these neutrophils. A previously undefined circulating subset of neutrophils shown to be CD49d(+)VEGFR1(high)CXCR4(high) was identified in mice and humans. By using chimeric mice with impaired VEGF receptor 1 (VEGFR1) or VEGFR2 signaling (Flt-1tk(-/-), tsad(-/-)), we found that parallel activation of VEGFR1 on neutrophils and VEGFR2 on endothelial cells was required for VEGF-A-induced recruitment of circulating neutrophils to tissue. Intravital microscopy of mouse microcirculation revealed that neutrophil recruitment by VEGF-A versus by the chemokine macrophage inflammatory protein 2 (MIP-2 [CXCL2]) involved the same steps of the recruitment cascade but that an additional neutrophil integrin (eg, VLA-4 [CD49d/CD29]) played a crucial role in neutrophil crawling and emigration to VEGF-A. Isolated CD49d(+) neutrophils featured increased chemokinesis but not chemotaxis compared with CD49d(-) neutrophils in the presence of VEGF-A. Finally, by targeting the integrin α4 subunit (CD49d) in a transplantation-based angiogenesis model that used avascular pancreatic islets transplanted to striated muscle, we demonstrated that inhibiting the recruitment of circulating proangiogenic neutrophils to hypoxic tissue impairs vessel neoformation. Thus, angiogenesis can be modulated by targeting cell-surface receptors specifically involved in VEGF-A-dependent recruitment of proangiogenic neutrophils without compromising recruitment of the neutrophil population involved in the immune response to pathogens.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

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