Emerging role of polymerase-1 and transcript release factor (PTRF/ Cavin-1) in health and disease

Low, Jin-Yih; Nicholson, Helen

doi:10.1007/s00441-014-1964-z

Cited by 23 publications

(19 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[124,125] In prostate cancer cells, down expression of Cavin1 induced cell migration and contributed significantly to tumor progression and metastasis. [123,126] These effects are mediated through reduced expression of matrix metalloproteases and altered secretion of proteases, cytokines and growth regulatory proteins.…”

Section: Caveolae New Partners and Cancermentioning

confidence: 99%

Caveolae and cancer: A new mechanical perspective

Lamaze¹,

Torrino²

2015

Biomed J

View full text Add to dashboard Cite

Section: Caveolae New Partners and Cancermentioning

confidence: 99%

Caveolae and cancer: A new mechanical perspective

Lamaze¹,

Torrino²

2015

Biomed J

View full text Add to dashboard Cite

“…Loss of Cavin‐1/polymerase I and transcript release factor resulted in decreased caveolae formation and the altered associations of signaling pathways within the membrane. Within caveolae, Cavin‐1 is co‐localized with CAV‐1 . CAV‐1 has been reported to interact directly with ERK through its residues 32 to 95.…”

Section: Discussionmentioning

confidence: 99%

“…Within caveolae, Cavin-1 is co-localized with CAV-1. 52 CAV-1 has been reported to interact directly with ERK through its residues 32 to 95. Peptides derived from this region inhibit the kinase activity of ERK.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Cavin‐1 Expression via Increasing Caveolin‐1 Degradation Prompts the Proliferation and Migration of Vascular Smooth Muscle Cells in Balloon Injury–Induced Neointimal Hyperplasia

Zhou

Chen

Liu

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundPercutaneous coronary intervention has been widely used in the treatment of ischemic heart disease, but vascular restenosis is a main limitation of percutaneous coronary intervention. Our previous work reported that caveolin‐1 had a key functional role in intimal hyperplasia, whereas whether Cavin‐1 (another important caveolae‐related protein) was involved is still unknown. Therefore, we will investigate the effect of Cavin‐1 on neointimal formation.Methods and ResultsBalloon injury markedly reduced Cavin‐1 protein and enhanced ubiquitin protein expression accompanied with neointimal hyperplasia in injured carotid arteries, whereas Cavin‐1 mRNA had no change. In cultured vascular smooth muscle cells (VSMCs), Cavin‐1 was downregulated after inhibition of protein synthesis by cycloheximide, which was distinctly prevented by pretreatment with proteasome inhibitor MG132 but not by lysosomal inhibitor chloroquine, suggesting that proteasomal degradation resulted in Cavin‐1 downregulation. Knockdown of Cavin‐1 by local injection of Cavin‐1 short hairpin RNA (shRNA) into balloon‐injured carotid arteries in vivo promoted neointimal formation. In addition, inhibition or overexpression of Cavin‐1 in cultured VSMCs in vitro prompted or suppressed VSMC proliferation and migration via increasing or decreasing extracellular signal‐regulated kinase phosphorylation and matrix‐degrading metalloproteinases‐9 activity, respectively. However, under basic conditions, the effect of Cavin‐1 on VSMC migration was stronger than on proliferation. Moreover, our results indicated that Cavin‐1 regulated caveolin‐1 expression via lysosomal degradation pathway.ConclusionsOur study revealed the role and the mechanisms of Cavin‐1 downregulation in neointimal formation by promoting VSMC proliferation, migration, and synchronously enhancing caveolin‐1 lysosomal degradation. Cavin‐1 may be a potential therapeutic target for the treatment of postinjury vascular remodeling.

show abstract

“…Ptrf knockout mice present a mildly fatty liver on a normal diet, and the level of liver fat is not exacerbated by high fat feeding . Human PTRF mutations have been associated with congenital generalized lipodystrophy, insulin resistance and dyslipidemia . These observations suggest that PTRF has an important role in lipogenesis.…”

Section: Introductionmentioning

confidence: 99%

Ptrf transgenic mice exhibit obesity and fatty liver

Bai

Shi

et al. 2018

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Polymerase I and transcript release factor (Ptrf, also known as Cavin1) is an essential component in the biogenesis and function of caveolae. Ptrf knockout mice or patients with PTRF mutations exhibit numerous pathologies including markedly aberrant fuel metabolism, lipodystrophy and muscular dystrophy. In this study, we generated Ptrf transgenic mice to explore its function in vivo. Compared with wild-type (WT) mice, we found that the Ptrf transgenic mice showed obesity with an increased level of ALT (alanine aminotransferase) and AST (aspartate transaminase). Ptrf transgenic mice exhibited severe fat degeneration and a higher degree of fat accumulation in the liver compared with WT mice. Consistently, we found that the expression of the fat synthesis gene, Fasn, was increased in the liver of Ptrf transgenic mice. Thus, Ptrf transgenic mice would be a good model for investigating the molecular mechanism and therapeutic targets of obesity and fatty liver associated diseases.

show abstract

Emerging role of polymerase-1 and transcript release factor (PTRF/ Cavin-1) in health and disease

Cited by 23 publications

References 64 publications

Caveolae and cancer: A new mechanical perspective

Caveolae and cancer: A new mechanical perspective

Downregulation of Cavin‐1 Expression via Increasing Caveolin‐1 Degradation Prompts the Proliferation and Migration of Vascular Smooth Muscle Cells in Balloon Injury–Induced Neointimal Hyperplasia

Ptrf transgenic mice exhibit obesity and fatty liver

Contact Info

Product

Resources

About