Potential role of vascular smooth muscle cell-like progenitor cell therapy in the suppression of experimental abdominal aortic aneurysms

Park, Hyung Sub; Choi, Geum Hee; Hahn, Soli; Yoo, Young Sun; Lee, Ji Youl; Lee, Taeseung

doi:10.1016/j.bbrc.2012.12.099

Cited by 21 publications

(22 citation statements)

References 34 publications

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“…The injected cells in the Cell therapy group were obtained by isolation of MDSCs from the gastrocnemius muscle of 4–6-week-old Balb/c mice using a modified preplate technique, as previously described [8, 9]. Human lymphatic endothelial cells (HLEC, ScienCell Research Laboratories) were cultured for 3 days until 80% confluence was achieved and the supernatant was moved to a new tube.…”

Section: Methodsmentioning

confidence: 99%

Modification of a Rodent Hindlimb Model of Secondary Lymphedema: Surgical Radicality versus Radiotherapeutic Ablation

Park

Jung

Choi

et al. 2013

BioMed Research International

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Secondary lymphedema is an intractable disease mainly caused by damage of the lymphatic system during surgery, yet studies are limited by the lack of suitable animal models. The purpose of this study was to create an improved model of secondary lymphedema in the hindlimbs of rodents with sustained effects and able to mimic human lymphedema. This was achieved by combining previously reported surgical methods and radiation to induce chronic lymphedema. Despite more radical surgical destruction of superficial and deep lymphatic vessels, surgery alone was not enough to sustain increased hindlimb volume. Radiotherapy was necessary to prolong these effects, with decreased lymphatic flow on lymphoscintigraphy, but hindlimb necrosis occurred after 4 weeks due to radiation toxicity. The applicability of this model for studies of therapeutic lymphangiogenesis was subsequently tested by injecting muscle-derived stem cells previously cocultured with the supernatant of human lymphatic endothelial cells in vitro. There was a tendency for increased lymphatic flow which significantly increased lymphatic vessel formation after cell injection, but attenuation of hindlimb volume was not observed. These results suggest that further refinement of the rodent hindlimb model is needed by titration of adequate radiation dosage, while stem cell lymphangiogenesis seems to be a promising approach.

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Section: Methodsmentioning

confidence: 99%

Modification of a Rodent Hindlimb Model of Secondary Lymphedema: Surgical Radicality versus Radiotherapeutic Ablation

Park

Jung

Choi

et al. 2013

BioMed Research International

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“…Arterial aneurysms are caused by two combined mechanisms that lead to progressive medial degeneration and vessel dilation: increased degradation by MMPs [ 33 ] and decreased synthesis of elastin caused by apoptosis of vascular SMCs [ 34 ]. Moreover, chronic inflammation and consequent oxidative stress promote progressive vascular wall impairment [ 35 ].…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, VW-PC may facilitate tissue damage by differentiating into inflammatory cells. VW-PC may represent a reservoir for the localized replenishment of aneurysm wall macrophages [ 33 , 36 ]. Thus, depending on the local environment and paracrine manner via cytokines and growth factors, the VW-PC could contribute to ongoing inflammation and aneurysmal degeneration or accelerate vascular repair [ 170 ].…”

Section: Resultsmentioning

confidence: 99%

Adult Vascular Wall Resident Multipotent Vascular Stem Cells, Matrix Metalloproteinases, and Arterial Aneurysms

Amato

Compagna

Amato

et al. 2015

Stem Cells International

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Evidences have shown the presence of multipotent stem cells (SCs) at sites of arterial aneurysms: they can differentiate into smooth muscle cells (SMCs) and are activated after residing in a quiescent state in the vascular wall. Recent studies have implicated the role of matrix metalloproteinases in the pathogenesis of arterial aneurysms: in fact the increased synthesis of MMPs by arterial SMCs is thought to be a pivotal mechanism in aneurysm formation. The factors and signaling pathways involved in regulating wall resident SC recruitment, survival, proliferation, growth factor production, and differentiation may be also related to selective expression of different MMPs. This review explores the relationship between adult vascular wall resident multipotent vascular SCs, MMPs, and arterial aneurysms.

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“…After blockage and permeabilization, the cells were incubated with phosphor-protein antibody overnight at 4 °C, and then an Alexa Fluor ® 555-conjugated secondary antibody was used to probe the primary antibody. The cells were washed with PBS and stained with Hoechst 33342 for 5 min [25,26] . To detect the formation of reactive oxygen species (ROS), DL0805-2 (1, 3, and 10 μmol/L) was added to VSMCs.…”

Section: Immunofluorescent Stainingmentioning

confidence: 99%

DL0805-2, a novel indazole derivative, relaxes angiotensin II-induced contractions of rat aortic rings by inhibiting Rho kinase and calcium fluxes

et al. 2016

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Aim: DL0805-2 [N-(1H-indazol-5-yl)-1-(4-methylbenzyl) pyrrolidine-3-carboxamide] is a DL0805 derivative with more potent vasorelaxant activity and lower toxicity. This study was conducted to investigate the vasorelaxant mechanisms of DL0805-2 on angiotensin II (Ang II)-induced contractions of rat thoracic aortic rings in vitro. Methods: Rat thoracic aortic rings and rat aortic vascular smooth muscle cells (VSMCs) were pretreated with DL0805-2, and then stimulated with Ang II. The tension of the aortic rings was measured through an isometric force transducer. Ang II-induced protein phosphorylation, ROS production and F-actin formation were assessed with Western blotting and immunofluorescence assays. Intracellular free Ca 2+ concentrations were detected with Fluo-3 AM. Results: Pretreatment with DL0805-2 (1-100 μmol/L) dose-dependently inhibited the constrictions of the aortic rings induced by a single dose of Ang II (10 -7 mol/L) or accumulative addition of Ang II (10 -10 -10 -7 mol/L). The vasodilatory effect of DL0805-2 was independent of endothelium. In the aortic rings, pretreatment with DL0805-2 (1, 3, and 10 μmol/L) suppressed Ang II-induced Ca 2+ influx and intracellular Ca 2+ mobilization, and Ang II-induced phosphorylation of two substrates of Rho kinase (MLC and MYPT1). In VSMCs, pretreatment with DL0805-2 (1, 3, and 10 μmol/L) also suppressed Ang II-induced Ca 2+ fluxes and phosphorylation of MLC and MYPT1. In addition, pretreatment with DL0805-2 attenuated ROS production and F-actin formation in the cells. Conclusion: DL0805-2 exerts a vasodilatory action in rat aortic rings through inhibiting the Rho/ROCK pathway and calcium fluxes.

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Potential role of vascular smooth muscle cell-like progenitor cell therapy in the suppression of experimental abdominal aortic aneurysms

Cited by 21 publications

References 34 publications

Modification of a Rodent Hindlimb Model of Secondary Lymphedema: Surgical Radicality versus Radiotherapeutic Ablation

Modification of a Rodent Hindlimb Model of Secondary Lymphedema: Surgical Radicality versus Radiotherapeutic Ablation

Adult Vascular Wall Resident Multipotent Vascular Stem Cells, Matrix Metalloproteinases, and Arterial Aneurysms

DL0805-2, a novel indazole derivative, relaxes angiotensin II-induced contractions of rat aortic rings by inhibiting Rho kinase and calcium fluxes

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