Related Experiment Video
Updated: May 8, 2026
A Method for Labeling Vasculature in Embryonic Mice
Published on: October 7, 2011
C57BL/6 NK cell gene complex is crucially involved in vascular remodeling
M R de Vries1, L Seghers, J van Bergen
1Department of Surgery, Leiden University Medical Center, Leiden, The Netherlands; Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Natural killer (NK) cells play a key role in vascular remodeling and intimal hyperplasia. The C57BL/6 Natural Killer gene Complex (NKC) in mice significantly contributes to these cardiovascular disease processes.
Area of Science:
- Immunology
- Cardiovascular Biology
- Vascular Biology
Background:
- Natural killer (NK) cells are implicated in cardiovascular disease.
- Vascular remodeling and intimal hyperplasia vary significantly between mouse strains like C57BL/6 and BALB/c.
- Differences in immune responses and Natural Killer gene Complex (NKC) composition exist between these strains.
Purpose of the Study:
- To investigate the role of NK cells in vascular remodeling.
- To determine the specific contribution of the C57BL/6 NKC to intimal hyperplasia formation.
Main Methods:
- Utilized injury-induced cuff and vein graft models in C57BL/6, BALB/c, and CMV1(r) mice.
- Depleted NK cells in C57BL/6 mice to assess their impact on intimal hyperplasia.
- Analyzed intimal hyperplasia, leukocyte infiltration, and IFN-γ staining.
Main Results:
- NK cell depletion in C57BL/6 mice reduced intimal hyperplasia by 43% after femoral artery cuff placement.
- C57BL/6 and CMV1(r) mice exhibited profound intimal hyperplasia, unlike BALB/c mice.
- Elevated leukocyte infiltration and IFN-γ staining were observed in C57BL/6 and CMV1(r) vein grafts compared to BALB/c.
Conclusions:
- NK cells are crucial players in intimal hyperplasia and vascular remodeling.
- The C57BL/6 NKC in CMV1(r) mice promotes vascular remodeling, likely via IFN-γ-secreting NK cells.
Objective:
NK cells are known to be involved in cardiovascular disease processes. One of these processes, vascular remodeling, may strongly differ between individuals and mouse strains such as the C57BL/6 and BALB/c. Moreover, C57BL/6 and BALB/c mice vary in immune responses and in the composition of their Natural Killer gene Complex (NKC). Here we study the role of NK cells, and in particular the C57BL/6 NKC in vascular remodeling and intimal hyperplasia formation.
Methods And Results:
C57BL/6, BALB/c and CMV1(r) mice, a BALB/c strain congenic for the C57BL/6 NKC, were used in an injury induced cuff model and a vein graft model. NK cell depleted C57BL/6 mice demonstrated a 43% reduction in intimal hyperplasia after femoral artery cuff placement compared to control C57BL/6 mice (p<0.05). Cuff placement and vein grafting resulted in profound intimal hyperplasia in C57BL/6 mice, but also in CMV1(r) mice, whereas this was significantly less in BALB/c mice. Significant more leukocyte infiltrations and IFN-γ staining were seen in both C57BL/6 and CMV1(r) vein grafts compared to BALB/c vein grafts.
Conclusions:
These data demonstrate an important role for NK cells in intimal hyperplasia and vascular remodeling. Furthermore, the C57BL/6 NKC in CMV1(r) mice stimulates vascular remodeling most likely through the activation of (IFN-γ-secreting) NK-cells that modulate the outcome of vascular remodeling.
