Immunohistologic labeling of murine endothelium

Ismail, Jitka A.; Poppa, Veronica; Kemper, Lynn E.; Scatena, Marta; Giachelli, Cecilia M.; Coffin, J. Douglas; Murry, Charles E.

doi:10.1016/s1054-8807(02)00166-7

Cited by 56 publications

(48 citation statements)

References 20 publications

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“…No analgesia was used, and all experiments were performed during the light phase of the circadian cycle between zeitgeber time 3 and 9. The surgical procedure is described in more detail elsewhere (19,30).…”

Section: Animalsmentioning

confidence: 99%

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Attenuation of myocardial injury in mice with functional deletion of the circadian rhythm gene mPer2

Virag¹,

Dries²,

Easton³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Animalsmentioning

confidence: 99%

“…553371; 1:2,000) for endothelial cells in infarcted hearts, isolectin B4 (Vector, No. B-1205) for endothelial cells in control hearts (19), anti-CD45 (PharMingen, No. 550539; 1:2,000) for leukocytes, and antiLy6G (BD PharMingen, No.…”

Section: Animalsmentioning

confidence: 99%

Attenuation of myocardial injury in mice with functional deletion of the circadian rhythm gene mPer2

Virag¹,

Dries²,

Easton³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…The distribution of animals in each group and time point is indicated in Table 1. Extracted hearts were sectioned into 2 mm thick slices and fixed in zinc fixative [11,12]. Blinded histological assessment for infarct size, cell proliferation and vascular density was performed.…”

Section: Tissue Collection Histology and Analysismentioning

confidence: 99%

Absence of regeneration in the MRL/MpJ mouse heart following infarction or cryoinjury

Robey

Murry

2008

Cardiovascular Pathology

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SummaryThe MRL/MpJ mouse has been reported to exhibit minimal scarring and subsequent cardiac regeneration after cryoinjury of the right ventricle. We studied the temporal evolution of infarcts and cryoinjuries in MRL/MpJ and C57BL/6 control mice. Both types of injury in MRL/MpJ mice heal similarly to controls by typical scar formation rather than muscle regeneration, and no differences in cell proliferation, angiogenesis or scar contraction between the two mouse strains were observed.Background-Myocardial infarcts in mammals heal by scar formation rather than formation of new muscle tissue. The MRL/MpJ mouse, however, has been reported to exhibit minimal scarring and subsequent cardiac regeneration after cryoinjury of the right ventricle. Other groups have reported that permanent and temporary ligation of the coronary artery resulted in scarring without regeneration.Methods-To clarify these contradictory results, we studied the temporal evolution of infarcts in MRL/MpJ and C57BL/6 control mice from 1 to 90 days post-injury, and the effects of intrathoracic cryoinjury to 28 days.Results-After infarction, the conversion from necrotic myocardium to granulation tissue and then to scar proceeded identically in the two groups. Infarct DNA synthesis, measured by incorporation of a BrdU pulse, peaked at 4 days in both strains and did not differ between strains at any time point. Endothelial cell and total vascular density in the both the infarcted and non-infarcted cardiac tissue did not differ between groups at any time. Histological analysis of directly cryoinjured right and left ventricular myocardium showed indistinguishable wound healing in both strains, and final scar size was identical in each group.Conclusions-These studies demonstrate that both myocardial infarcts and cryoinjuries in MRL/ MpJ mice heal by typical scar formation rather than muscle regeneration, in a manner very similar to C57BL/6 controls. We conclude that the MRL mouse is not a model for myocardial regeneration.

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“…Previous evidence from murine experiments has shown that a proportion of CD34-positive cells are endothelial cells. 7,18,19 Location of the vascular endothelial growth factor receptor-2 (VEGFR2, FLK-1) was used to confirm an endothelial cell phenotype. 9,20 PerCP-CY5.5-conjugated rat anti-mouse antibody was used to detect CD45 ϩ hematopoietic cells.…”

Section: Flow Cytometrymentioning

confidence: 99%

Endothelial Progenitor Cells Are Recruited Into Resolving Venous Thrombi

et al. 2005

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Background-The purpose of this study was to determine whether endothelial cells of bone marrow origin are involved in thrombus recanalization. Methods and Results-Irradiated mice were reconstituted with bone marrow from transgenic donors expressing green fluorescent protein (GFP) linked to the Tie2 promoter. Thrombi were formed in 2 groups of 6 mice. GFP-expressing cells were located and quantified in sections of the thrombi taken after 7 and 14 days. The cell markers Mac-3, F4/80, CD68 (macrophage), and vascular endothelial growth factor receptor 2 (VEGFR2; endothelial cells) were used to determine colocalization with GFP expression in tissue sections and peritoneal macrophages. The markers CD34 and VEGFR2 were used to quantify changes in circulating endothelial cells by flow cytometry of blood from 3 cohorts of wild-type animals that had either a thrombus induced (nϭ18), a sham operation (nϭ18), or no operation (nϭ10). The number of GFP-expressing cells was found to increase by Ϸ3-fold in thrombi formed in transplanted animals between 7 and 14 days after induction (Pϭ0.0022

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Immunohistologic labeling of murine endothelium

Cited by 56 publications

References 20 publications

Attenuation of myocardial injury in mice with functional deletion of the circadian rhythm gene mPer2

Attenuation of myocardial injury in mice with functional deletion of the circadian rhythm gene mPer2

Absence of regeneration in the MRL/MpJ mouse heart following infarction or cryoinjury

Endothelial Progenitor Cells Are Recruited Into Resolving Venous Thrombi

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