Generation of an Adult Smooth Muscle Cell–Targeted Cre Recombinase Mouse Model

Zhang, Jifeng; Zhong, Wei; Cui, Taixing; Yang, Maozhou; Hu, Xing; Xu, Kefeng; Xie, Changqing; Xue, Changhu; Gibbons, Gary H.; Liu, Chengyu; Li, Li; Chen, Yuqing E.

doi:10.1161/01.atv.0000202661.61837.93

Cited by 52 publications

(75 citation statements)

References 7 publications

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“…Third, the 24-hour mRNA oscillations of period circadian clock 1 (Per1) and period circadian clock 2 (Per2), 2 BMAL1 target genes, were abolished in mesenteric arteries by Bmal1 deletion (Figure 1, D and E). In addition, in agreement with the literature (19,20), we also found that Cre recombinase was indeed expressed in heart but at a much lower level than in smooth muscle (Z. Guo and M. Gong, unpublished observations). In contrast to the drastic effect of Bmal1 deletion in the mesenteric artery, Bmal1 deletion in the heart had no effect on Per1 and Per2 mRNA 24-hour oscillation (Figure 1, F and G).…”

Section: +supporting

confidence: 92%

See 1 more Smart Citation

Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation

Xie¹,

Su²,

Liu³

et al. 2014

J. Clin. Invest.

143

144

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Section: +supporting

confidence: 92%

“…We generated a smooth-muscle-specific Bmal1-knockout mouse model (SM-Bmal1-KO) by crossing Bmal1 flox/flox mice (18) with smooth-muscle-specific SM22α-Cre mice (19). SM-Bmal1-KO mice were viable, fertile, and grossly normal.…”

Section: Resultsmentioning

confidence: 99%

Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation

Xie¹,

Su²,

Liu³

et al. 2014

J. Clin. Invest.

143

144

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“…For example, Cre recombinase was knocked into the endogenous Sm22a gene and the mouse line showed only adult SMC-restricted activity; no activity was seen in the embryonic heart or blood vessels. 58 This Cre driver therefore represents a valuable tool to circumvent the embryonic lethality of knocking out SRF with a conventional Sm22a promoter-driven Cre. 32 Moreover, a tamoxifen-inducible, smooth-muscle myosin heavy-chain promoter-driven Cre will be of utility to inactivate SRF at any time during embryonic or postnatal development.…”

Section: Blood Vesselsmentioning

confidence: 99%

Role of serum response factor in the pathogenesis of disease

Miano

2010

Laboratory Investigation

118

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Serum response factor (SRF) is a ubiquitously expressed transcription factor that binds to a DNA cis element known as the CArG box, which is found in the proximal regulatory regions of over 200 experimentally validated target genes. Genetic deletion of SRF is incompatible with life in a variety of animals from different phyla. In mice, loss of SRF throughout the early embryo results in gastrulation defects precluding analyses in individual organ systems. Genetic inactivation studies using conditional or inducible promoters directing the expression of the bacteriophage Cre recombinase have shown a vital role for SRF in such cellular processes as contractility, cell migration, synaptic activity, inflammation, and cell survival. A growing number of experimental and human diseases are associated with changes in SRF expression, suggesting that SRF has a role in the pathogenesis of disease. This review summarizes data from experimental model systems and human pathology where SRF expression is either deliberately or naturally altered. Genomic DNA is a quaternary code comprising proteincoding and non-protein-coding sequences. While the protein-coding sequences are well-defined and increasingly understood, we are only beginning to elucidate the hidden information within the vast landscape of the non-proteincoding sequences. The field of comparative genomics has facilitated the identification of transcription factor-binding sites (TFBS) and microRNAs (miRs), which, aside from repetitive DNA sequences, are among the more easily decipherable non-protein-coding sequences in the human genome. Together, TFBS and miRs have essential roles in cell fate determination and cellular homeostasis of most life forms. Sequence variations (eg, single-nucleotide polymorphisms, SNPs) in the TFBS, miRs, and miR target sequences alter gene/protein expression and thus disturb homeostasis leading to disease. 1-4 A major imperative, therefore, is decoding the non-protein-coding genome relating to gene regulation to gain a full understanding of how DNA-binding transcription factors and the estimated one million or more TFBS direct normal biological processes.Serum response factor (SRF) is the founding member of the MADS-box family of transcription factors 5 and is one of the best understood DNA-binding proteins in the human proteome. The DNA-binding properties of SRF and its molecular cloning were first defined in the laboratory of Richard Treisman. 6,7 SRF has relatively low intrinsic transcriptional activity, but its interaction with over 60 cofactors confers strong transactivation potential in a cell-and context-specific manner. At least two major signaling pathways converge upon SRF to direct the programs of gene expression. 8,9 The classic pathway involves growth factor stimulation and mitogen-activated protein kinase signaling leading to the phosphorylation of the SRF cofactor, ELK1, and the activation of growth-related genes. 10,11 The second regulatory pathway occurs through Rho-dependent changes in actin dynamics. 12 In this pathway, si...

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“…The Msx1 lox conditional mutant allele (Fu et al, 2007) was a generous gift from Dr Robert Maxson (Los Angeles, CA, USA) and the Tie2-Cre transgenic mouse (Kisanuki et al, 2001) from Dr Masashi Yanagisawa (Dallas, TX, USA). The Sm22-Cre (Zhang et al, 2006) and Rosa mT/mG (Muzumdar et al, 2007) engineered mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). The Msx1…”

Section: Micementioning

confidence: 99%

“…To inactivate both genes in blood vessels, we combined a null (Lallemand et al, 2005) and a floxed (Bensoussan et al, 2008) Msx2 allele and the Sm22-Cre (Sm22 is also known as transgelinMouse Genome Informatics) transgene (Zhang et al, 2006), together with Msx1 lacZ null alleles. Using this strategy, Msx1 is inactivated in the two layers of the blood vessel, whereas Msx2 is inactivated only in the VSMCs.…”

Section: Msx1 and Msx2 Expression In The Mouse Embryo Head Vessels Anmentioning

confidence: 99%

Msx genes define a population of mural cell precursors required for head blood vessel maturation

et al. 2011

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SUMMARYVessels are primarily formed from an inner endothelial layer that is secondarily covered by mural cells, namely vascular smooth muscle cells (VSMCs) CreERT2 allele, we demonstrated by lineage tracing that the primary defect lies in a population of VSMC precursors. The abnormal phenotype that ensues is a consequence of impaired BMP signaling in the VSMC precursors that leads to downregulation of the metalloprotease 2 (Mmp2) and Mmp9 genes, which are essential for cell migration and integration into the mural layer. Improper coverage by VSMCs secondarily leads to incomplete maturation of the endothelial layer. Our results demonstrate that both Msx1 and Msx2 are required for the recruitment of a population of neural crest-derived VSMCs.

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Generation of an Adult Smooth Muscle Cell–Targeted Cre Recombinase Mouse Model

Cited by 52 publications

References 7 publications

Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation

Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation

Role of serum response factor in the pathogenesis of disease

Msx genes define a population of mural cell precursors required for head blood vessel maturation

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