Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF‐β1/SMAD and myocardin/serum response factor

Wang, Wen; Zhang, Wei; Lu, Yao Wei; Tou, Emiley; Ye, Jiemei; Gao, Ping; Jourd’heuil, David; Singer, Harold A.; Wu, Mingfu; Long, Xiaochun

doi:10.1096/fj.201601021r

Cited by 27 publications

(33 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PDGF induces the synthetic phenotype of VSMCs ( Fig 1A ) [ 1 ]. Data from HCASMs overexpressing myocardin (MYOCD) (GSE77120) and those cells treated with TGFβ (GSE85910) were obtained [ 22 ]. Both MYOCD and TGFβ were reported to induce a contractile phenotype ( Fig 1A ) [ 1 , 2 ].…”

Section: Resultsmentioning

confidence: 99%

Identification of long noncoding RNAs involved in muscle differentiation

et al. 2018

View full text Add to dashboard Cite

Long noncoding RNAs (lncRNAs) are a large class of regulatory RNAs with diverse roles in cellular processes. Thousands of lncRNAs have been discovered; however, their roles in the regulation of muscle differentiation are unclear because no comprehensive analysis of lncRNAs during this process has been performed. In the present study, by combining diverse RNA sequencing datasets obtained from public database, we discovered lncRNAs that could behave as regulators in the differentiation of smooth or skeletal muscle cells. These analyses confirmed the roles of previously reported lncRNAs in this process. Moreover, we discovered dozens of novel lncRNAs whose expression patterns suggested their possible involvement in the phenotypic switch of vascular smooth muscle cells. The comparison of lncRNA expression change suggested that many lncRNAs have common roles during the differentiation of smooth and skeletal muscles, while some lncRNAs may have opposite roles in this process. The expression change of lncRNAs was highly correlated with that of their neighboring genes, suggesting that they may function as cis-acting lncRNAs. Furthermore, within the lncRNA sequences, there were binding sites for miRNAs with expression levels inversely correlated with the expression of corresponding lncRNAs during differentiation, suggesting a possible role of these lncRNAs as competing endogenous RNAs. The lncRNAs identified in this study will be a useful resource for future studies of gene regulation during muscle differentiation.

show abstract

Section: Resultsmentioning

confidence: 99%

Identification of long noncoding RNAs involved in muscle differentiation

et al. 2018

View full text Add to dashboard Cite

show abstract

“…More than one half of TSPANs family genes are significantly reduced by TGF-β1, while only TSPAN2, 12, 13, and 22 are up-regulated, and TSPAN2 shows the most dramatic change by TGF-β1 (Zhao et al, 2017). Myocardin, which is another master regulator of VSMCs differentiation, increases 8 TSPANs genes expression, including TSPAN2,7,10,11,12,15,21,33, and TSPAN2 showed the greatest up-regulation (Zhao et al, 2017). The expression profiles of TSPANs family genes in ECs and VSMCs indicate that they may play critical roles in vascular biology, such as migration ( Table 2).…”

Section: The Current Understanding Of Tetraspanins Family In Vascularmentioning

confidence: 97%

“…They found that HUVECs expressed 23 TSPANs and human liver endothelium expressed 17 TSPANs. The RNA-seq analyses and RNA-arrays for TSPANs family genes expressed in HCASMCs, MASMCs and mouse carotid arteries indicate that all TSPANs except for TSPAN16 and TSPAN19 are detectable in these cells and tissue (Zhao et al, 2017). More than one half of TSPANs family genes are significantly reduced by TGF-β1, while only TSPAN2, 12, 13, and 22 are up-regulated, and TSPAN2 shows the most dramatic change by TGF-β1 (Zhao et al, 2017).…”

Section: The Current Understanding Of Tetraspanins Family In Vascularmentioning

confidence: 97%

“…The RNA-seq analyses and RNA-arrays for TSPANs family genes expressed in HCASMCs, MASMCs and mouse carotid arteries indicate that all TSPANs except for TSPAN16 and TSPAN19 are detectable in these cells and tissue (Zhao et al, 2017). More than one half of TSPANs family genes are significantly reduced by TGF-β1, while only TSPAN2, 12, 13, and 22 are up-regulated, and TSPAN2 shows the most dramatic change by TGF-β1 (Zhao et al, 2017). Myocardin, which is another master regulator of VSMCs differentiation, increases 8 TSPANs genes expression, including TSPAN2,7,10,11,12,15,21,33, and TSPAN2 showed the greatest up-regulation (Zhao et al, 2017).…”

Section: The Current Understanding Of Tetraspanins Family In Vascularmentioning

confidence: 98%

“…TSPAN2 is extensively expressed in medial layer VSMCs of aortas, bladder, brain, lung, skeletal muscle, stomach, heart, spleen, kidney and liver, however, the levels of TSPAN2 is decreased in mouse carotid arteries after ligation injury and in failed human arteriovenous fistula samples after occlusion by dedifferentiated neointimal VSMCs (Zhao et al, 2017). TSPAN2 acts as a suppressor of VSMCs proliferation and migration, and plays important role in the pathogenesis of occlusive vascular diseases (Zhao et al, 2017).…”

Section: The Current Understanding Of Tetraspanins Family In Vascularmentioning

confidence: 99%

See 2 more Smart Citations

Migrasome and Tetraspanins in Vascular Homeostasis: Concept, Present, and Future

Zhang

Wang

Ding³

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Cell migration plays a critical role in vascular homeostasis. Under noxious stimuli, endothelial cells (ECs) migration always contributes to vascular repair, while enhanced migration of vascular smooth muscle cells (VSMCs) will lead to pathological vascular remodeling. Moreover, vascular activities are involved in communication between ECs and VSMCs, between ECs and immune cells, et al. Recently, Ma et al. (2015) discovered a novel migration-dependent organelle "migrasome," which mediated release of cytoplasmic contents, and this process was defined as "migracytosis." The formation of migrasome is precisely regulated by tetraspanins (TSPANs), cholesterol and integrins. Migrasomes can be taken up by neighboring cells, and migrasomes are distributed in many kinds of cells and tissues, such as in blood vessel, human serum, and in ischemic brain of human and mouse. In addition, the migrasome elements TSPANs are wildly expressed in cardiovascular system. Therefore, TSPANs, migrasomes and migracytosis might play essential roles in regulating vascular homeostasis. In this review, we will discuss the discoveries of migration-dependent migrasome and migracytosis, migrasome formation, the basic differences between migrasomes and exosomes, the distributions and functions of migrasome, the functions of migrasome elements TSPANs in vascular biology, and discuss the possible roles of migrasomes and migracytosis in vascular homeostasis.

show abstract

DNA Methylation Analysis Identifies Loci for Blood Pressure Regulation

Richard

Huan

Ligthart

et al. 2017

The American Journal of Human Genetics

177

170

View full text Add to dashboard Cite

Genome-wide association studies have identified hundreds of genetic variants associated with blood pressure (BP), but sequence variation accounts for a small fraction of the phenotypic variance. Epigenetic changes may alter the expression of genes involved in BP regulation and explain part of the missing heritability. We therefore conducted a two-stage meta-analysis of the cross-sectional associations of systolic and diastolic BP with blood-derived genome-wide DNA methylation measured on the Infinium HumanMethylation450 BeadChip in 17,010 individuals of European, African American, and Hispanic ancestry. Of 31 discovery-stage cytosine-phosphate-guanine (CpG) dinucleotides, 13 replicated after Bonferroni correction (discovery: N = 9,828, p < 1.0 × 10; replication: N = 7,182, p < 1.6 × 10). The replicated methylation sites are heritable (h > 30%) and independent of known BP genetic variants, explaining an additional 1.4% and 2.0% of the interindividual variation in systolic and diastolic BP, respectively. Bidirectional Mendelian randomization among up to 4,513 individuals of European ancestry from 4 cohorts suggested that methylation at cg08035323 (TAF1B-YWHAQ) influences BP, while BP influences methylation at cg00533891 (ZMIZ1), cg00574958 (CPT1A), and cg02711608 (SLC1A5). Gene expression analyses further identified six genes (TSPAN2, SLC7A11, UNC93B1, CPT1A, PTMS, and LPCAT3) with evidence of triangular associations between methylation, gene expression, and BP. Additional integrative Mendelian randomization analyses of gene expression and DNA methylation suggested that the expression of TSPAN2 is a putative mediator of association between DNA methylation at cg23999170 and BP. These findings suggest that heritable DNA methylation plays a role in regulating BP independently of previously known genetic variants.

show abstract

Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF‐β1/SMAD and myocardin/serum response factor

Cited by 27 publications

References 58 publications

Identification of long noncoding RNAs involved in muscle differentiation

Identification of long noncoding RNAs involved in muscle differentiation

Migrasome and Tetraspanins in Vascular Homeostasis: Concept, Present, and Future

DNA Methylation Analysis Identifies Loci for Blood Pressure Regulation

Contact Info

Product

Resources

About