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Jean Marc Herbert

Bio: Jean Marc Herbert is an academic researcher from University of Michigan. The author has contributed to research in topics: Myocyte & Vascular smooth muscle. The author has an hindex of 1, co-authored 1 publications receiving 241 citations.

Papers
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Journal ArticleDOI
01 Jan 2001
TL;DR: A technique for isolating smooth muscle cells from a single mouse aorta is described, particularly useful when material is limiting, as is frequently the case when genetically modified animals are being characterized.
Abstract: The vascular smooth muscle cell plays a significant role in many important cardiovascular disorders, and smooth muscle biology is therefore important to cardiovascular research. The mouse is critical to basic cardiovascular research, largely because techniques for genetic manipulation are more fully developed in the mouse than in any other mammalian species. We describe here a technique for isolating smooth muscle cells from a single mouse aorta. This technique is particularly useful when material is limiting, as is frequently the case when genetically modified animals are being characterized.

250 citations


Cited by
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Journal ArticleDOI
TL;DR: Smooth muscle cells were filtration seeded in the scaffolds and it was shown that both scaffolds supported cell adhesion and growth, with smooth muscle cells growing more extensively in the PEUU scaffold.

675 citations

Journal ArticleDOI
TL;DR: The results show that the miR-143/145 gene cluster has a critical role during SMC differentiation and strongly suggest its involvement in the reversion of the VSMC differentiation phenotype that occurs during vascular disease.
Abstract: Mechanisms controlling vascular smooth muscle cell (VSMC) plasticity and renewal still remain to be elucidated completely. A class of small RNAs called microRNAs (miRs) regulate gene expression at the post-transcriptional level. Here, we show a critical role of the miR-143/145 cluster in SMC differentiation and vascular pathogenesis, also through the generation of a mouse model of miR-143 and -145 knockout (KO). We determined that the expression of miR-143 and -145 is decreased in acute and chronic vascular stress (transverse aortic constriction and in aortas of the ApoE KO mouse). In human aortic aneurysms, the expression of miR-143 and -145 was significantly decreased compared with control aortas. In addition, overexpression of miR-143 and -145 decreased neointimal formation in a rat model of acute vascular injury. An in-depth analysis of the miR-143/145 KO mouse model showed that this miR cluster is expressed mostly in the SMC compartment, both during development and postnatally, in vessels and SMC-containing organs. Loss of miR-143 and miR-145 expression induces structural modifications of the aorta, because of an incomplete differentiation of VSMCs. In conclusion, our results show that the miR-143/145 gene cluster has a critical role during SMC differentiation and strongly suggest its involvement in the reversion of the VSMC differentiation phenotype that occurs during vascular disease.

530 citations

Journal ArticleDOI
25 Jan 2010-PLOS ONE
TL;DR: The study suggests that interventional tools able to revert the MØ infiltrate towards the M2 phenotype may exert an atheroprotective action.
Abstract: As in human disease, macrophages (MO) are central players in the development and progression of experimental atherosclerosis. In this study we have evaluated the phenotype of MO associated with progression of atherosclerosis in the apolipoprotein E (ApoE) knockout (KO) mouse model.We found that bone marrow-derived MO submitted to M1 and M2 polarization specifically expressed arginase (Arg) II and Arg I, respectively. This distinct arginase expression was used to evaluate the frequency and distribution of M1 and M2 MO in cross-sections of atherosclerotic plaques of ApoE KO mice. Early lesions were infiltrated by Arg I(+) (M2) MO. This type of MO favored the proliferation of smooth muscle cells, in vitro. Arg II(+) (M1) MO appeared and prevailed in lesions of aged ApoE KO mice and lesion progression was correlated with the dominance of M1 over the M2 MO phenotype. In order to address whether the M2->M1 switch could be due to a phenotypic switch of the infiltrated cells, we performed in vitro repolarization experiments. We found that fully polarized MO retained their plasticity since they could revert their phenotype. The analysis of the distribution of Arg I- and Arg II-expressing MO also argued against a recent recruitment of M1 MO in the lesion. The combined data therefore suggest that the M2->M1 switch observed in vivo is due to a conversion of cells already present in the lesion. Our study suggests that interventional tools able to revert the MO infiltrate towards the M2 phenotype may exert an atheroprotective action.

485 citations

Journal ArticleDOI
TL;DR: An intact form of UBM can be successfully solubilized without purification steps and induced to repolymerize into a gel form of the UBM biologic scaffold material, which supported the adhesion and growth of rat aortic smooth muscle cells when cultured under static in vitro conditions.

451 citations

Journal ArticleDOI
TL;DR: Electrospraying vascular smooth muscle cells (SMCs) concurrently with electrospinning a biodegradable, elastomeric poly(ester urethane)urea (PEUU) matrix embodies a novel tissue engineering approach that could be applied to fabricate high cell density elastic tissue mimetics, blood vessels or other cardiovascular tissues.

410 citations