Integrin α9 regulates smooth muscle cell phenotype switching and vascular remodeling

Jain, Manish; Doddapattar, Prakash; Kawa, Shigeyuki; Dhanesha, Nirav; Chauhan, Anil K.

doi:10.1172/jci.insight.147134

Cited by 20 publications

(19 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Integrin signaling plays an essential role in SMC biology by regulating adhesion, migration, proliferation, contraction, and differentiation [ 10 , 16 , 18 , 19 , 20 , 21 ]. Several proteins such as integrin-associated protein, integrin-linked kinase, focal adhesion kinase (FAK), tetraspanin CD9, and urokinase-type plasminogen activator receptor modulate integrin-mediated cell motility and adhesion in SMCs [ 10 , 22 , 23 , 24 , 25 ].…”

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

“…The major α-integrin subunits present in SMC are α1, α3, α5, α8, and α9 [ 10 , 33 ], whereas β subunits are β1, β3, and β5. The expression of integrins is dynamic and varies dramatically in SMC with different phenotypes [ 21 , 33 ]. Few integrins are upregulated in activated SMC, while expression levels are very low or undetectable in differentiated quiescent SMCs [ 21 ].…”

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

“…The expression of integrins is dynamic and varies dramatically in SMC with different phenotypes [ 21 , 33 ]. Few integrins are upregulated in activated SMC, while expression levels are very low or undetectable in differentiated quiescent SMCs [ 21 ]. For example, integrin α1β1 is a collagen-binding integrin that is highly expressed in resting SMCs, and its expression is significantly downregulated in culture conditions [ 34 ].…”

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

“…In quiescent murine and human aortic SMCs, α9 is expressed at low levels and is mainly restricted to a membrane lining. After stimulation with PDGF-BB, which is known to modulate the membrane mobility and trafficking of integrins [ 85 ], a higher expression of α9 was detected in the cytoplasm ( Figure 2 ) [ 21 ]. SMC-specific deletion of α9 significantly reduces SMC proliferation, migration, phenotypic switching, and injury-mediated pathological remodeling [ 21 ].…”

Section: Role Of α9β1 In Smc Proliferation and Neointimal Hyperplasiamentioning

confidence: 99%

See 3 more Smart Citations

Role of Integrins in Modulating Smooth Muscle Cell Plasticity and Vascular Remodeling: From Expression to Therapeutic Implications

Jain

Chauhan

2022

Cells

Self Cite

View full text Add to dashboard Cite

Smooth muscle cells (SMCs), present in the media layer of blood vessels, are crucial in maintaining vascular homeostasis. Upon vascular injury, SMCs show a high degree of plasticity, undergo a change from a “contractile” to a “synthetic” phenotype, and play an essential role in the pathophysiology of diseases including atherosclerosis and restenosis. Integrins are cell surface receptors, which are involved in cell-to-cell binding and cell-to-extracellular-matrix interactions. By binding to extracellular matrix components, integrins trigger intracellular signaling and regulate several of the SMC function, including proliferation, migration, and phenotypic switching. Although pharmacological approaches, including antibodies and synthetic peptides, have been effectively utilized to target integrins to limit atherosclerosis and restenosis, none has been commercialized yet. A clear understanding of how integrins modulate SMC biology is essential to facilitate the development of integrin-based interventions to combat atherosclerosis and restenosis. Herein, we highlight the importance of integrins in modulating functional properties of SMCs and their implications for vascular pathology.

show abstract

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

Section: Role Of Integrins In Smc Biologymentioning

confidence: 99%

Section: Role Of α9β1 In Smc Proliferation and Neointimal Hyperplasiamentioning

confidence: 99%

See 2 more Smart Citations

Role of Integrins in Modulating Smooth Muscle Cell Plasticity and Vascular Remodeling: From Expression to Therapeutic Implications

Jain

Chauhan

2022

Cells

Self Cite

View full text Add to dashboard Cite

show abstract

“…Many factors such as oxidative stress damage, hyperphosphatemic environment, and inflammation increase the indices related to bone formation in VSMCs and promote their transformation into osteoblasts (Voelkl et al, 2018a). On the other hand, a variety of biochemical factors are involved in the phenotype switching of VSMCs, i.e., the growth factors platelet-derived growth factor (PDGF-BB) and transforming growth factor-β1 (TGF-β1) could promote the phenotype switching of VSMCs (Jain et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Matrix Vesicles as a Therapeutic Target for Vascular Calcification

Zhang

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Vascular calcification (VC) is linked to an increased risk of heart disease, stroke, and atherosclerotic plaque rupture. It is a cell-active process regulated by vascular cells rather than pure passive calcium (Ca) deposition. In recent years, extracellular vesicles (EVs) have attracted extensive attention because of their essential role in the process of VC. Matrix vesicles (MVs), one type of EVs, are especially critical in extracellular matrix mineralization and the early stages of the development of VC. Vascular smooth muscle cells (VSMCs) have the potential to undergo phenotypic transformation and to serve as a nucleation site for hydroxyapatite crystals upon extracellular stimulation. However, it is not clear what underlying mechanism that MVs drive the VSMCs phenotype switching and to result in calcification. This article aims to review the detailed role of MVs in the progression of VC and compare the difference with other major drivers of calcification, including aging, uremia, mechanical stress, oxidative stress, and inflammation. We will also bring attention to the novel findings in the isolation and characterization of MVs, and the therapeutic application of MVs in VC.

show abstract

Vascular smooth muscle- and myeloid cell-derived integrin α9β1 does not directly mediate the development of atherosclerosis in mice

Jung¹,

Elenbaas²,

Burks³

et al. 2022

Atherosclerosis

View full text Add to dashboard Cite

Integrin α9 regulates smooth muscle cell phenotype switching and vascular remodeling

Cited by 20 publications

References 53 publications

Role of Integrins in Modulating Smooth Muscle Cell Plasticity and Vascular Remodeling: From Expression to Therapeutic Implications

Role of Integrins in Modulating Smooth Muscle Cell Plasticity and Vascular Remodeling: From Expression to Therapeutic Implications

Matrix Vesicles as a Therapeutic Target for Vascular Calcification

Vascular smooth muscle- and myeloid cell-derived integrin α9β1 does not directly mediate the development of atherosclerosis in mice

Contact Info

Product

Resources

About