Syk contributes to PDGF-BB-mediated migration of rat aortic smooth muscle cells via MAPK pathways

Lee, Chang-Kwon; Lee, Hwan Myung; Kim, Hyo Jin; Park, Hyojun; Won, Kyung‐Jong; Roh, Hui Yul; Choi, Wahn Soo; Jeon, Byeong Hwa; Park, Tae-Kyu; Kim, Bokyung

doi:10.1016/j.cardiores.2007.01.012

Cited by 73 publications

(72 citation statements)

References 35 publications

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“…Interestingly, our results did not demonstrate any differences in the area fraction of α-SMA + SMCs in 2-week specimens, but did identify decreased SMC proliferation in the PGDF-KO group. The decreased proliferation in PGDF-KO mice is consistent with literature demonstrating the paracrine role of PDGF in promoting SMC migration and proliferation [10,[22][23][24][25]. One potential reason that no difference was observed in the total quantity of SMCs between the two groups is that we specifically targeted only the PDGF-B subtype.…”

Section: Myeloid Cell Pdgf-b and Tevg Neotissue Development Research Arsupporting

confidence: 89%

The Role of Myeloid Cell-Derived PDGF-B in Neotissue Formation in a Tissue-Engineered Vascular Graft

et al. 2017

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Aim: Inflammatory myeloid lineage cells mediate neotissue formation in tissueengineered vascular grafts, but the molecular mechanism is not completely understood. We examined the role of vasculogenic PDGF-B in tissue-engineered vascular graft neotissue development. Materials & methods: Myeloid cell-specific PDGF-B knockout mice (PDGF-KO) were generated using bone marrow transplantation, and scaffolds were implanted as inferior vena cava interposition grafts in either PDGF-KO or wildtype mice. Results: After 2 weeks, grafts from PDGF-KO mice had more remaining scaffold polymer and less intimal neotissue development. Increased macrophage apoptosis, decreased smooth muscle cell proliferation and decreased collagen content was also observed. Conclusion: Myeloid cell-derived PDGF contributes to vascular neotissue formation by regulating macrophage apoptosis, smooth muscle cell proliferation and extracellular matrix deposition. Progress in tissue engineering continues to promise a solution to the lack of tissue available for reconstructive and replacement surgery. Our lab has worked over the past several years developing a tissue-engineered vascular graft (TEVG) for use in congenital heart and vascular surgery. Traditionally used prosthetic materials in the form of Dacron ® or Gore-Tex ® pose significant risk for thromboembolic and infectious complications and also lack growth capacity, making them less ideal for use in the pediatric population. Our ability to create a TEVG with growth capacity [1,2] has therefore been an important advancement in the field, but graft stenosis continues to be a major limitation to widespread clinical application. We have therefore concentrated our efforts on understanding the underlying processes of TEVG neotissue formation and stenosis development.We developed a murine model of TEVG stenosis [3] and found that seeding the grafts with bone marrow-derived mononuclear cells prior to implantation increases graft patency [4] in a dose responsive manner [5], but the seeded cells disappear shortly after implantation [6,7]. We thus hypothesized that a paracrine mechanism, rather than proliferation of seeded cells, was responsible for the remodeling of the TEVG and then demonstrated that host endothelial and smooth muscle cells from the adjacent vessel migrate to form the TEVG neotissue.Host monocytes and macrophages were identified as key mediators of graft remodeling. They infiltrate the graft in large numbers shortly after implantation, and excessive infiltration leads to graft stenosis [8].

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Section: Myeloid Cell Pdgf-b and Tevg Neotissue Development Research Arsupporting

confidence: 89%

The Role of Myeloid Cell-Derived PDGF-B in Neotissue Formation in a Tissue-Engineered Vascular Graft

et al. 2017

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“…p38 MAPK acts as a mediator in cellular responses, including migration and proliferation in VSMCs (Kavurma & Khachigian, 2003). In our previous and current studies, we demonstrated that PDGF-BB stimulated p38 MAPK phosphorylation and also induced VSMC migration and proliferation that were inhibited by the treatment with p38 MAPK inhibitor (Lee et al, 2007a(Lee et al, , 2008a, indicating that PDGF-BB-induced migration and proliferation in VSMCs is mediated by p38 MAPK pathway.…”

Section: Discussionmentioning

confidence: 49%

“…Activation of MAPK in VSMCs is a critical response in stimulating proliferation and migration (Choi et al, 2009) and was involved in PDGFstimulated migration and proliferation in VSMCs (Bornfeldt et al, 1994;Holycross et al, 1992;Pukac et al, 1988). PDGF increased the phosphorylations of p38 MAPK and ERK1/2, and elevated the migration and proliferation in RASMCs (Lee et al, 2007a). p38 MAPK acts as a mediator in cellular responses, including migration and proliferation in VSMCs (Kavurma & Khachigian, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The activation of MAPKs is also known to be important for PDGF-stimulated VSMC migration and proliferation (Lee et al, 2007a). To investigate the mechanism of inhibitory effects of CBMFF on VSMC responses, we treated RASMCs with PDGF-BB and CBMFF.…”

Section: Effects Of the Cbmff On Phosphorylation Of Pdgfr-b Pathway Kmentioning

confidence: 99%

“…PDGF-induced activation of MAPK pathways is known to trigger VSMC migration and proliferation (Eguchi et al, 2001). Specifically, PDGFs stimulate the phosphorylation of p38 MAPK and ERK1/2 (Lee et al, 2007a), which are known to initiate migration or proliferation and growth, respectively, in VSMCs (Dubey et al, 2000;Gan et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Chrysanthemum borealeflower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells

Kim

Won

Yoon

et al. 2014

Pharmaceutical Biology

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(2015) Chrysanthemumboreale flower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells, Pharmaceutical Biology, 53:5, 725-734, DOI: 10.3109/13880209.2014 Context: Chrysanthemum boreale Makino (Compositae) (CBM) is a traditional medicine that has been used for the prevention or treatment of various disorders; it has various properties including antioxidation, anti-inflammation, and antitumor. Objective: The present study was designed to explore the in vitro effect of CBM flower floral water (CBMFF) on atherosclerosis-related responses in rat aortic smooth muscle cells (RASMCs). Materials and methods: CBMFF was extracted from CBM flower by steam distillation and analyzed using gas chromatography-mass spectrometry. The anti-atherosclerosis activity of CBMFF was tested by estimating platelet-derived growth factor (PDGF)-BB (10 ng/mL)-induced proliferation and migration levels and intracellular kinase pathways in RASMCs at CBMFF concentrations of 0.01-100 lM and analyzing ex vivo aortic ring assay. Results: Gas chromatography-mass spectrometry showed that the CBMFF contained a total of seven components. The CBMFF inhibits PDGF-BB-stimulated RASMC migration and proliferation (IC 50 : 0.010 lg/mL). Treatment of RASMCs with PDGF-BB induced PDGFR-b phosphorylation and increased the phosphorylations of MAPK p38 and ERK1/2. CBMFF addition prevented PDGF-BBinduced phosphorylation of these kinases (IC 50 : 008 and 0.018 lg/mL, for p38 MAPK and ERK1/ 2, respectively), as well as PDGFR-b (IC 50 : 0.046 lg/mL). Treatment with inhibitors of PDGFR, P38 MAPK, and ERK1/2 decreased PDGF-BB-increased migration and proliferation in RASMCs. Moreover, the CBMFF suppressed PDGF-BB-increased sprout outgrowth of aortic rings (IC 50 : 0.047 lg/mL). Discussion and conclusion: These results demonstrate that CBMFF may inhibit PDGF-BB-induced vascular migration and proliferation, most likely through inhibition of the PDGFR-b-mediated MAPK pathway; therefore, the CBMFF may be promising candidate for the development of herbal remedies for vascular disorders.

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3‐Morpholinosydnonimine participates in the attenuation of neointima formation via inhibition of annexin A2‐mediated vascular smooth muscle cell migration

et al. 2010

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3-Morpholinosydnonimine (SIN-1) affects vascular smooth muscle cell migration and proliferation, processes essential for atherosclerosis. However, the mechanism by which SIN-1 exerts these effects has not been elucidated. We used 2-DE followed by MALDI-TOF/TOF MS to identify responses in protein expression to SIN-1 in rat aortic smooth muscle. Platelet-derived growth factor-BB increased cell migration and proliferation in rat aortic smooth muscle cells, and subsequent SIN-1 treatment inhibited it. Administration of SIN-1 in vivo attenuated neointima formation in balloon-injured rat carotid arteries. Proteomic analysis showed that glutathione peroxidase and 40S ribosomal protein S12 were differentially expressed in aortic strips exposed to SIN-1. Expression of annexin A2 was decreased by SIN-1. Platelet-derived growth factor-BB-induced cell migration was increased and inhibited in rat aortic smooth muscle cells with overexpression and knockdown of annexin A2 gene, respectively. The expression of annexin A2 was increased in vascular neointima compared with the intact control, which was inhibited by SIN-1 treatment. These results demonstrate that SIN-1 may attenuate vascular neointima formation by inhibiting annexin A2-mediated migration. Therefore, annexin A2 may be a potential target for therapeutic strategies for atherosclerosis.

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Syk contributes to PDGF-BB-mediated migration of rat aortic smooth muscle cells via MAPK pathways

Abstract: These results imply that Syk is an upstream signal of the p38 MAPK/HSP27 and ERK1/2 pathways that contributes to PDGF-BB-mediated migration in RASMC.

Cited by 73 publications

References 35 publications

The Role of Myeloid Cell-Derived PDGF-B in Neotissue Formation in a Tissue-Engineered Vascular Graft

The Role of Myeloid Cell-Derived PDGF-B in Neotissue Formation in a Tissue-Engineered Vascular Graft

Chrysanthemum borealeflower floral water inhibits platelet-derived growth factor-stimulated migration and proliferation in vascular smooth muscle cells

3‐Morpholinosydnonimine participates in the attenuation of neointima formation via inhibition of annexin A2‐mediated vascular smooth muscle cell migration

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