Urotensin II Stimulates Vascular Endothelial Growth Factor Secretion From Adventitial Fibroblasts in Synergy With Angiotensin II

Song, Nana; Ding, Wenyuan; Chu, Song-Yun; Zhao, Jing; Dong, Xiao; Di, Beibing; Tang, Chaoshu

doi:10.1253/circj.cj-11-0870

Cited by 26 publications

(28 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Total protein concentrations were determined using the bicinchoninic acid (BCA) method (Nanjing Zoonbio Tech, Co., Ltd.). Western blot analysis was performed according to studies by Song et al (2012) with small modifications. Protein samples were electrophoresed on 10 % SDS-polyacrylamide gel and electroblotted to NC membrane (Bio-rad).…”

Section: Western Blotmentioning

confidence: 99%

See 1 more Smart Citation

Characterizing heat shock protein 90 gene of Apolygus lucorum (Meyer-Dür) and its expression in response to different temperature and pesticide stresses

Sun

Sheng

Bai

et al. 2014

Cell Stress and Chaperones

View full text Add to dashboard Cite

In this study, we cloned a full-length cDNA of heat shock protein (HSP) gene of Apolygus lucorum (Meyer-Dür) [AlHSP90, KC109781] and investigated its expression in response to temperature and pesticide stresses. The open reading frame (ORF) of AlHSP90 is 2,169 bp in length, encoding a 722 amino acid polypeptide with a predicted molecular weight of 82.99 kDa. Transcriptional and translational expression profiles of AlHSP90 under extreme temperature or pesticide stresses were examined by fluorescent realtime quantitative PCR and Western blot. Results showed that the expression profiles of AlHSP90 protein were in high agreement with those of AlHSP90 RNA and indicated that AlHSP90 was not only an important gene for A. lucorum adults in response to extremely high temperature, but also involved in the resistance or tolerance to cyhalothrin, imidacloprid, chlorpyrifos, and emamectin benzoate, especially for female adults to emamectin benzoate and for male adults to cyhalothrin. Transcriptional results of AlHSP90 also confirmed that AlHSP90 was an important gene involved in the resistance or tolerance to both temperature and pesticide stresses. In addition, our study also revealed that ∼24°C may be the suitable temperature range for A. lucorum survival, which is also confirmed by the results of the expression of AlHSP90, the nymph mortality, and the intrinsic rate of increase (r m ) when A. lucorum is reared at six different temperatures. Therefore, these studies are significant in elucidating the AlHSP90 in response to temperature and pesticide stresses and would provide guidance for A. lucorum management with different pesticides or temperatures in fields.

show abstract

Section: Western Blotmentioning

confidence: 99%

“…The optical density of immunoblots was determined by scanning densitometry, and the result was presented in densitometric units. Translation was calculated by dividing the normalized AlHSP90 density by the normalized β-actin density (AlHSP90/β-actin ratio) (Song et al 2012). The Western blotting was replicated three times.…”

Section: Western Blotmentioning

confidence: 99%

Characterizing heat shock protein 90 gene of Apolygus lucorum (Meyer-Dür) and its expression in response to different temperature and pesticide stresses

Sun

Sheng

Bai

et al. 2014

Cell Stress and Chaperones

View full text Add to dashboard Cite

show abstract

“…AngII has been shown to induce cardiac hypertrophy by increasing oxidative stress and UII expression (Lamarre & Tallarida 2008). Earlier studies also indicated that AngII stimulated both UII expression and genetic transcription in cardiomyocytes to cause cardiac hypertrophy (Song et al 2012). However, the expression of AngII and UII after hypoxia and the relationship between them in regulating genetic transcription in cardiomyocytes under hypoxia have not been well defined.…”

mentioning

confidence: 99%

Angiotensin II and the JNK pathway mediate urotensin II expression in response to hypoxia in rat cardiomyocytes

Chiu¹,

Wang²,

Shyu³

2014

Journal of Endocrinology

View full text Add to dashboard Cite

Cardiomyocyte hypoxia causes cardiac hypertrophy through cardiac-restricted gene expression. Urotensin II (UII) cooperates with activating protein 1 (AP1) to regulate cardiomyocyte growth in response to myocardial injuries. Angiotensin II (AngII) stimulates UII expression, reactive oxygen species (ROS) production, and cardiac hypertrophy. This study aimed to evaluate the expression of UII, ROS, and AngII as well as their genetic transcription after hypoxia treatment in neonatal cardiomyocytes. Cultured neonatal rat cardiomyocytes were subjected to hypoxia for different time periods. UII (Uts2) protein levels increased after 2.5% hypoxia for 4 h with earlier expression of AngII and ROS. Both hypoxia and exogenously added AngII or Dp44mT under normoxia stimulated UII expression, whereas AngII receptor blockers, JNK inhibitors (SP600125), JNK siRNA, or N-acetyl-L-cysteine (NAC) suppressed UII expression. The gel shift assay indicated that hypoxia induced an increase in DNA-protein binding between UII and AP1. The luciferase assay confirmed an increase in transcription activity of AP1 to the UII promoter under hypoxia. After hypoxia, an increase in 3 H-proline incorporation in the cardiomyocytes and expression of myosin heavy chain protein, indicative of cardiomyocyte hypertrophy, were observed. In addition, hypoxia increased collagen I expression, which was inhibited by SP600125, NAC, and UII siRNA. In summary, hypoxia in cardiomyocytes increases UII and collagen I expression through the induction of AngII, ROS, and the JNK pathway causing cardiomyocyte hypertrophy and fibrosis.

show abstract

“…7,[53][54][55] For example, in carotid artery vein grafts and arterial allografts, activated adventitial fibroblasts were able to migrate to the intima.…”

Section: Discussionmentioning

confidence: 99%

Monocyte Chemoattractant Protein 1–Mediated Migration of Mesenchymal Stem Cells Is a Source of Intimal Hyperplasia

Grudzińska

Kurzejamska

Bojakowski

et al. 2013

ATVB

View full text Add to dashboard Cite

Objective-Intimal hyperplasia is considered to be a healing response and is a major cause of vessel narrowing after injury, where migration of vascular progenitor cells contributes to pathological events, including transplant arteriosclerosis. Approach and Results-In this study, we used a rat aortic-allograft model to identify the predominant cell types associated with transplant arteriosclerosis and to identify factors important in their recruitment into the graft. Transplantation of labeled adventitial tissues allowed us to identify the adventitia as a major source of cells migrating to the intima. RNA microarrays revealed a potential role for monocyte chemoattractant protein 1 (MCP-1), stromal cell-derived factor 1, regulated on activation, normal T cell expressed and secreted, and interferon-inducible protein 10 in the induced vasculopathy. MCP-1 induced migration of adventitial fibroblast cells. CCR2, the receptor for MCP-1, was coexpressed with CD90, CD44, NG2, or sca-1 on mesenchymal stem cells. In vivo experiments using MCP-1-deficient and CCR2-deficient mice confirmed an important role of MCP-1 in the formation of intimal hyperplasia in a mouse model of vascular injury. The aim of this study was to examine the contribution of MSCs in intimal hyperplasia and to identify relevant factors that affect their recruitment. We found that local inflammation in transplanted vessels exerts an effect on surrounding tissue and vessels that leads to phenotypic modulation of SMCs; however, those cells did not migrate to the intima and did not contribute to the intimal hyperplasia. Rather, as shown by transplantation of labeled cells, adventitial progenitor cells seemed to be a prominent source of host-derived cells in the lesion, and MCP-1 exhibits an important role in their recruitment and the pathological process of intimal hyperplasia. Conclusions-The Materials and MethodsMaterials and Methods are available in the online-only Supplement. Results Transplantation of Allografts Leads to Structural Changes in Adjacent TissuesRejection of transplanted organs is associated with inflammation, and the production of factors that may activate cells in surrounding tissues. To determine how allografts influence the adjacent vessel tissues, we transplanted a fragment of rat isogenic (from F344 rats) or allogenic (from LEW rats) aortic graft into the abdominal aorta of F344 rats. Samples of aortic allografts and adjacent vessel segments were collected at 1, 2, 4, 8, and 12 weeks and analyzed separately; isograft samples were collected at 8 weeks.In 2-week-old allografts, immunohistochemical staining for α-smooth muscle actin was decreasing in the media, and α-smooth muscle actin positive cells had migrated to the neointima. Similar, but less prominent, changes were observed in adjacent vessels ( Figure 1A). At 1 to 2 weeks after transplantation, electron microscopy revealed distinct structural alterations in SMCs in the inner layer of the media and progressive de-endothelization of the allograft. Most of the SMCs were contracti...

show abstract

Urotensin II Stimulates Vascular Endothelial Growth Factor Secretion From Adventitial Fibroblasts in Synergy With Angiotensin II

Cited by 26 publications

References 28 publications

Characterizing heat shock protein 90 gene of Apolygus lucorum (Meyer-Dür) and its expression in response to different temperature and pesticide stresses

Characterizing heat shock protein 90 gene of Apolygus lucorum (Meyer-Dür) and its expression in response to different temperature and pesticide stresses

Angiotensin II and the JNK pathway mediate urotensin II expression in response to hypoxia in rat cardiomyocytes

Monocyte Chemoattractant Protein 1–Mediated Migration of Mesenchymal Stem Cells Is a Source of Intimal Hyperplasia

Contact Info

Product

Resources

About