Stem Cells and Transplant Arteriosclerosis

Xu, Qingbo

doi:10.1161/circresaha.108.171488

Cited by 82 publications

(55 citation statements)

References 130 publications

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“…These SMCs then participate in the formation of neointima by decreasing the expression of SMC differentiation markers (1). Similarly, during the progression of atherosclerosis, recruited SMCs also acquired a transition to a synthetic phenotype in lesion formation (30). Studies on the mechanism of SMC de/differentiation are not only crucial for exploring human pathologies but are also useful for isolating and differentiating stem cells or vascular progenitors to SMCs, which is required for the tissue-engineered vessel.…”

Section: Discussionmentioning

confidence: 99%

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Wang

Xiao

Luo

et al. 2012

Journal of Biological Chemistry

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Background: SMC differentiation is a complicated process involving many transcription factors. Results: hnRNPA2/B1 regulates SMC differentiation gene expression transcriptionally and promotes neural crest cell migration and differentiation toward SMCs. Conclusion: hnRNPA2/B1 promotes smooth muscle differentiation and development in vitro and in vivo. Significance: This is the first report to demonstrate the functional involvements of hnRNPA2/B1 in SMC differentiation from stem cells and embryonic arteriogenesis.

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Section: Discussionmentioning

confidence: 99%

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Wang

Xiao

Luo

et al. 2012

Journal of Biological Chemistry

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“…In their 2001 article using the same transplantation model, using ␤-galactosidase-Tg mice, Shimizu et al reported that neointimal SMCs were derived from the recipient BM cells rather than those of the donor, 5 a conclusion that has since been reached by others working in different models of IH. 31 These findings have remained controversial, in part because of the disputed ability of BM-derived cells to give rise to SMCs and because recent publications have directly contradicted the earlier data. 32,33 Recently, Iwata et al, working in 3 separate models of IH including TA, reported significant numbers of recipient ␣-SMA ϩ SM22␣ ϩ cells in the neointima, but these also expressed CD115, CD11b, F4/80, and Ly-6C, markers of the monocyte/macrophage lineage rather than established markers of differentiated SMCs such as smooth muscle myosin heavy chain or calponin.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Thrombin Receptor Signaling on α-Smooth Muscle Actin ⁺ CD34 ⁺ Progenitors Leads to Repair After Murine Immune Vascular Injury

Chen

Shrivastava

et al. 2012

ATVB

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Objective-The goal of this study was to use mice expressing human tissue factor pathway inhibitor (TFPI) on ␣-smooth muscle actin (␣-SMA) ϩ cells as recipients of allogeneic aortas to gain insights into the cellular mechanisms of intimal hyperplasia (IH ϩ cells were mobilized in significant numbers after allogeneic transplantation, the majority showing sustained expression of tissue factor and protease-activated receptor-1 (PAR-1). In WT, most were CD45 ϩ myeloid progenitors coexpressing CD31, vascular endothelial growth factor receptor-2 and E-selectin; 10% of these cells coexpressed ␣-SMA and were recruited to the neointima. In contrast, the ␣-SMA

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“…On the other hand, accumulating data indicate that non-bone marrow stem/progenitor cells contribute to repair damaged endothelial cells in several animal models. 9,11,35 Thus, endothelial regeneration in apoE Ϫ/Ϫ mice by stem cells should be higher if non-bone marrow-derived stem cells are taken into account.…”

Section: Stem Cells Contribute To Endothelial Repairmentioning

confidence: 99%

Rapid Endothelial Turnover in Atherosclerosis-Prone Areas Coincides With Stem Cell Repair in Apolipoprotein E–Deficient Mice

Foteinos

Hu²,

Xiao³

et al. 2008

Circulation

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157

113

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Background-Recently, it has been shown that stem/progenitor cells may repair damaged/lost endothelial cells in vein grafts and wire-injured arteries. In the present study, we investigated endothelial cell turnover and regeneration in apolipoprotein E (apoE) Ϫ/Ϫ /transgenic mice carrying LacZ genes driven by an endothelial TIE2 promoter. Methods and Results-To assess cell proliferation on the surface of aortas in apoE Ϫ/Ϫ mice and wild-type controls, BrdU was injected into the tail vein and labeled on en face preparation. BrdU-positive cells on the aortas were observed occasionally in wild-type mice and frequently at sites prone to lesion development in apoE Ϫ/Ϫ mice (0.18Ϯ0.1% versus 1.12Ϯ0.2%; PϽ0.001). Endothelial integrity tests demonstrated that the areas with high rate of cell turnover displayed Evans blue leakage, low levels of VE-cadherin expression, and increased cell attachment, as evidenced by Evans blue dye injection, immunostaining, and scanning electron microscopy, respectively. Furthermore, immunostaining for CD34, Sca-1, Flk-1, and CD133 indicated that Ϸ3% to 5% of total cells on the aorta were positive in apoE Ϫ/Ϫ mice. En face double labeling using Ki-67 and progenitor markers revealed that 30% to 50% of progenitor ϩ cells expressed Ki-67, indicating a state of proliferation. To clarify the origin of endothelial progenitor cells participating in endothelial repair in apoE Ϫ/Ϫ mice, a chimeric mouse model was created by bone marrow transplantation between apoE Ϫ/Ϫ and LacZ ϩ/ϩ /apoE Ϫ/Ϫ mice. Ten months after bone marrow transplantation, Ϸ3% to 4% of total cells in the lesion-prone areas were ␤-gal positive in apoE Ϫ/Ϫ with apoE Ϫ/Ϫ /TIE2-LacZ bone marrow mice. When cells of aortas from chimeric mice were cultivated on Matrigel-coated plates, a capillary-like structure was found, which showed ␤-gal/CD31 or ␤-gal/von Willebrand factor double positivity. By a combined analysis of laser dissection microscopy and nest reverse transcription polymerase chain reaction, it was found that ␤-gal ϩ cells were mainly expressing CD31 and CD144. Conclusions-Our findings provide the first quantitative data on endothelial turnover and repair by progenitor cells that are, at least in part, derived from bone marrow during development of atherosclerosis in apoE Ϫ/Ϫ mice. (Circulation.

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Stem Cells and Transplant Arteriosclerosis

Abstract: Abstract-Stem

Cited by 82 publications

References 130 publications

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Inhibition of Thrombin Receptor Signaling on α-Smooth Muscle Actin ⁺ CD34 ⁺ Progenitors Leads to Repair After Murine Immune Vascular Injury

Rapid Endothelial Turnover in Atherosclerosis-Prone Areas Coincides With Stem Cell Repair in Apolipoprotein E–Deficient Mice

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Stem Cells and Transplant Arteriosclerosis

Abstract: Abstract-Stem

Cited by 82 publications

References 130 publications

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Functional Impact of Heterogeneous Nuclear Ribonucleoprotein A2/B1 in Smooth Muscle Differentiation from Stem Cells and Embryonic Arteriogenesis

Inhibition of Thrombin Receptor Signaling on α-Smooth Muscle Actin + CD34 + Progenitors Leads to Repair After Murine Immune Vascular Injury

Rapid Endothelial Turnover in Atherosclerosis-Prone Areas Coincides With Stem Cell Repair in Apolipoprotein E–Deficient Mice

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Inhibition of Thrombin Receptor Signaling on α-Smooth Muscle Actin ⁺ CD34 ⁺ Progenitors Leads to Repair After Murine Immune Vascular Injury