Alpha-smooth muscle actin, a differentiation marker of smooth muscle cells, is present in microfilamentous bundles of pericytes.

Skalli, Omar; Pelte, Marie‐Françoise; Peclet, M C; Gabbiani, Giulio; Gugliotta, Patrizia; Bussolati, Gianni; Ravazzola, Mariella; Orci, Lelio

doi:10.1177/37.3.2918221

Cited by 335 publications

(198 citation statements)

References 22 publications

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“…It seems that HIF-1α, although a sustained expression can improve wound healing and revascularization in normal [33] and diabetic mice [42], is more rapidly degraded [43] and displays a reduced activity under hyperglycemic conditions [30,44] due to the methylglyoxylation of its transcriptional cofactor p300. In concordance, we observed that Pecam1 and Acta2, which encode the blood vessel markers CD31 and α-SMA [45,46], were induced in healthy animals 3 and 7 days after wounding after condensate application but less pronounced in diabetic animals. Released VEGF 165 protein -a potent inducer of endothelial cell proliferation and recruitment [45] -seems to be rapidly diluted and degraded [36] and hardly affects Pecam1 expression levels.…”

supporting

confidence: 68%

The angiogenic response to PLL-g-PEG-mediated HIF-1α plasmid DNA delivery in healthy and diabetic rats

et al. 2013

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Impaired angiogenesis is a major clinical problem and affects wound healing especially in diabetic patients. Improving angiogenesis is a reasonable strategy to increase diabetes-impaired wound healing. Recently, our lab described a system of transient gene expression due to pegylated poly-l-lysine (PLL-g-PEG) polymer-mediated plasmid DNA delivery in vitro. Here we synthesized peptide-modified PLL-g-PEG polymers with two functionalities, characterized them in vitro and utilized them in vivo via a fibrin-based delivery matrix to induce dermal wound angiogenesis in diabetic rats. The two peptides were 1) a TG-peptide to covalently bind these nanocondensates to the fibrin matrix (TG-peptide) for a sustained release and 2) a polyR peptide to improve cellular uptake of these nanocondensates. In order to induce angiogenesis in vivo we condensed modified and non-modified polymers with plasmid DNA encoding a truncated form of the therapeutic candidate gene hypoxia-inducible transcription factor 1 (HIF-1 ). HIF-1 is the primarily oxygen-dependent regulated subunit of the heterodimeric transcription factor HIF-1, which controls angiogenesis among other physiological pathways. The truncated form of HIF-1 lacks the oxygen-dependent degradation domain (ODD) and therefore escapes degradation under normoxic conditions. PLL-g-PEG polymer-mediated HIF-1 -ΔODD plasmid DNA delivery was found to lead to a transiently induced gene expression of angiogenesis-related genes Acta2 and Pecam1 as well as the HIF-1 target gene Vegf in vivo. Furthermore, HIF-1 gene delivery was shown to enhance the number endothelial cells and smooth muscle cells -precursors for mature blood vessels -during wound healing. We show that -depending on the selection of the therapeutic target gene -PLL-g-PEG nanocondensates are a promising alternative to viral DNA delivery approaches, which might pose a risk to health. AbstractImpaired angiogenesis is a major clinical problem and affects wound healing especially in diabetic patients. Improving angiogenesis is a reasonable strategy to increase diabetes-impaired wound healing. Recently, our lab described a system of transient gene expression due to pegylated poly-L-lysine (PLL-g-PEG) polymermediated plasmid DNA delivery in vitro. Here we synthesized peptide-modified PLLg-PEG polymers with two functionalities, characterized them in vitro and utilized them in vivo via a fibrin-based delivery matrix to induce dermal wound angiogenesis in diabetic rats. The two peptides were 1) a TG-peptide to covalently bind these nanocondensates to the fibrin matrix (TG-peptide) for a sustained release and 2) a polyR peptide to improve cellular uptake of these nanocondensates. In order to induce angiogenesis in vivo we condensed modified and non-modified polymers with plasmid DNA encoding a truncated form of the therapeutic candidate gene hypoxiainducible transcription factor 1α (HIF-1α). HIF-1α is the primarily oxygen-dependent regulated subunit of the hetero-dimeric transcription factor HIF-1, which controls angiogenesis...

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supporting

confidence: 68%

The angiogenic response to PLL-g-PEG-mediated HIF-1α plasmid DNA delivery in healthy and diabetic rats

et al. 2013

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“…Generally, MLCK is known to phosphorylate the serine-19 residue of myosin regulatory light chain, which would enhance the actomyosin contraction via the RhoA pathway [33,34]. SMA is localized in microfilament bundles, strengthening the contraction of smooth muscle cells, but not in cardiac myocytes [35,36]. ACTA1 is a major constituent of the contractile apparatus, which can be found in skeletal muscle, but poorly expressed in cardiac myocytes [37].…”

Section: Resultsmentioning

confidence: 99%

Insights into the Role of Focal Adhesion Modulation in Myogenic Differentiation of Human Mesenchymal Stem Cells

Lui

Xiong

et al. 2013

Stem Cells and Development

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We report the establishment of a novel platform to induce myogenic differentiation of human mesenchymal stem cells (hMSCs) via focal adhesion (FA) modulation, giving insights into the role of FA on stem cell differentiation. Micropatterning of collagen type I on a polyacrylamide gel with a stiffness of 10.2 kPa efficiently modulated elongated FA. This elongated FA profile preferentially recruited the b 3 integrin cluster and induced specific myogenic differentiation at both transcription and translation levels with expression of myosin heavy chain and a-sarcomeric actin. This was initiated with elongation of FA complexes that triggered the RhoA downstream signaling toward a myogenic lineage commitment. This study also illustrates how one could partially control myogenic differentiation outcomes of similar-shaped hMSCs by modulating FA morphology and distribution. This technology increases our toolkit choice for controlled differentiation in muscle engineering.

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“…[16–18] The results of this study showed that massive ROS was produced after exposure to PQ, which indicated strong oxidative stress on the cells. UTI could significantly reduce the increase of ROS induced by PQ, and the effect was stronger as the concentration of UTI increased.…”

Section: Discussionmentioning

confidence: 99%

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Meng¹,

Wang²,

Gao³

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND:Ulinastatin (UTI) is a urinary trypsin inhibitor extracted and purified from urine of males. This study aimed to explore the effects of UTI on paraquat-induced-oxidative stress in human type II alveolar epithelial cells.METHODS:The human type II alveolar epithelial cells, A549 cells, were cultured in vitro. The A549 cells were treated with different concentrations of paraquat (200, 400, 600, 800, 1 000, 1 200 µmol/L) and ulinastatin(0, 2 000, 4 000, 6 000, 8 000 U/mL) for 24 hours, the cell viability was measured by cell counting kit-8 and the median lethal concentration was selected. In order to establish an in vitro model of paraquat intoxication and to determine the safe dose of ulinastatin, we calculated LD50 using cell counting kit-8 to determine the survival rate of the cells. A549 cells were divided into normal control group, paraquat group and paraquat+ulinastatin group. The levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were detected by biochemistry colorimetry, while the level of reactive oxygen spies (ROS) was detected by DCFH-DA assay.RESULTS:The survival rate of A549 cells treated with different concentrations of paraquat decreased in a concentration-dependent manner. Whereas there was no decrease in the survival rate of cells treated with 0–4 000 U/mL ulinastatin. The levels of MDA, MPO, and ROS were significantly higher in the paraquat group than in the normal control group after 24-hour-exposure. And the survival rate of the paraquat+ulinastatin group was higher than that of the paraquat group, but lower than that of the normal control group. The levels of MDA, MPO, and ROS were lower than those of the paraquat group.CONCLUSION:Ulinastatin can alleviate the paraquat-induced A549 cell damage by reducing oxidative stress.

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Alpha-smooth muscle actin, a differentiation marker of smooth muscle cells, is present in microfilamentous bundles of pericytes.

Cited by 335 publications

References 22 publications

The angiogenic response to PLL-g-PEG-mediated HIF-1α plasmid DNA delivery in healthy and diabetic rats

The angiogenic response to PLL-g-PEG-mediated HIF-1α plasmid DNA delivery in healthy and diabetic rats

Insights into the Role of Focal Adhesion Modulation in Myogenic Differentiation of Human Mesenchymal Stem Cells

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

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